FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Shayestehpour, M
   Ehsani, M
   Dadkhah, D
   Zamani, B
AF Shayestehpour, Mohammad
   Ehsani, Majid
   Dadkhah, Davood
   Zamani, Batool
TI A Case of Antiphospholipid Syndrome Following Gastric Signet Ring Cell
   Adenocarcinoma
SO AMERICAN JOURNAL OF CASE REPORTS
LA English
DT Article
DE Antibodies, Anticardiolipin; Antiphospholipid Syndrome; Stomach
   Neoplasms
ID ANTIBODIES; CANCER
AB Objective: Rare disease
   Background: Antiphospholipid syndrome (APS) is a rare autoimmune disease characterized by arterial, venous, and small-vessel thrombosis, pregnancy-related morbidity and the presence of antiphospholipid antibodies such as anticardiolipin antibody, and/or anti-beta2-glycoprotein I. In the recent years, APS was observed in patients with solid tumors and the renal cancer, lung carcinoma and breast tumors were the most common tumors linked with APS.
   Case Report: A 53-year-old female presented with pain and pitting edema of left lower extremity that had begun 6 months prior to hospitalization. Deep vein thrombosis (DVT) in the popliteal vein diagnosed by Doppler ultrasonography and the patient was treated with heparin followed by warfarin. Following subdural hematoma, anticoagulant therapy was stopped, and the patient underwent craniotomy. One month later, the patient returned with pain and DVT diagnosed in its right leg. Laboratory tests showed high levels of lupus anticoagulant, IgM and IgG anticardiolipin antibodies. Following a high alkaline phosphatase, diffuse bone marrow involvement was found by whole body bone scan. Looking to find primary tumor, a large infilterable lesion in gastric was seen by endoscopic images, and biopsy histopathology showed a signet ring cell adenocarcinoma. The patient refused chemotherapy and died 6 months after diagnosis.
   Conclusions: APS is associated with gastric signet ring cell adenocarcinoma.
C1 [Shayestehpour, Mohammad; Ehsani, Majid; Dadkhah, Davood; Zamani, Batool] Kashan Univ Med Sci, Autoimmune Dis Res Ctr, Kashan, Iran.
   [Shayestehpour, Mohammad] Kashan Univ Med Sci, Fac Med, Dept Microbiol & Immunol, Kashan, Iran.
RP Zamani, B (corresponding author), Kashan Univ Med Sci, Autoimmune Dis Res Ctr, Kashan, Iran.
EM batol_zamani2007@yahoo.com
RI Zamani, Batool/F-8319-2017; Ehsani, Majid/G-1140-2017; Shayestehpour,
   Mohammad/M-8321-2017
OI Shayestehpour, Mohammad/0000-0002-9654-5544
CR Chénard-Poirier M, 2019, DRUGS, V79, P1, DOI 10.1007/s40265-018-1032-1
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NR 9
TC 1
Z9 1
U1 0
U2 1
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
EI 1941-5923
J9 AM J CASE REP
JI Am. J. Case Rep.
PD JAN 18
PY 2020
VL 21
AR e919037
DI 10.12659/AJCR.919037
PG 4
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA KD5KM
UT WOS:000507903300001
PM 31953377
OA Green Published
DA 2025-06-01
ER

PT J
AU Hoft, SG
   Noto, CN
   DiPaolo, RJ
AF Hoft, Stella G.
   Noto, Christine N.
   DiPaolo, Richard J.
TI Two Distinct Etiologies of Gastric Cancer: Infection and Autoimmunity
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE immunology; gastric cancer; gastric adenocarcinoma; H; pylori; AIG =
   autoimmune gastritis; autoimmunity; gastritis
ID HELICOBACTER-PYLORI INFECTION; DENDRITIC CELLS; T-CELLS; COSTIMULATORY
   MOLECULES; PERNICIOUS-ANEMIA; IMMUNE-RESPONSES; EPITHELIAL-CELLS;
   B-CELL; PREVALENCE; EXPRESSION
AB Gastric cancer is a leading cause of mortality worldwide. The risk of developing gastric adenocarcinoma, which comprises >90% of gastric cancers, is multifactorial, but most associated with Helicobacter pylori infection. Autoimmune gastritis is a chronic autoinflammatory syndrome where self-reactive immune cells are activated by gastric epithelial cell autoantigens. This cause of gastritis is more so associated with the development of neuroendocrine tumors. However, in both autoimmune and infection-induced gastritis, high risk metaplastic lesions develop within the gastric mucosa. This warrants concern for carcinogenesis in both inflammatory settings. There are many similarities and differences in disease progression between these two etiologies of chronic gastritis. Both diseases have an increased risk of gastric adenocarcinoma development, but each have their own unique comorbidities. Autoimmune gastritis is a primary cause of pernicious anemia, whereas chronic infection typically causes gastrointestinal ulceration. Both immune responses are driven by T cells, primarily CD4(+) T cells of the IFN-gamma producing, Th1 phenotype. Neutrophilic infiltrates help clear H. pylori infection, but neutrophils are not necessarily recruited in the autoimmune setting. There have also been hypotheses that infection with H. pylori initiates autoimmune gastritis, but the literature is far from definitive with evidence of infection-independent autoimmune gastric disease. Gastric cancer incidence is increasing among young women in the United States, a population at higher risk of developing autoimmune disease, and H. pylori infection rates are falling. Therefore, a better understanding of these two chronic inflammatory diseases is needed to identify their roles in initiating gastric cancer.
C1 [Hoft, Stella G.; Noto, Christine N.; DiPaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63103 USA.
C3 Saint Louis University
RP Hoft, SG; DiPaolo, RJ (corresponding author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63103 USA.
EM stella.hoft@health.slu.edu; richard.dipaolo@health.slu.edu
OI DiPaolo, Richard/0000-0002-2191-6689
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NR 112
TC 17
Z9 18
U1 0
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD NOV 26
PY 2021
VL 9
AR 752346
DI 10.3389/fcell.2021.752346
PG 10
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA XM7KS
UT WOS:000729001700001
PM 34900999
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Patiroglu, T
   Gungor, HE
   Arslan, D
   Deniz, K
   Unal, E
   Coskun, A
AF Patiroglu, Turkan
   Gungor, Hatice Eke
   Arslan, Duran
   Deniz, Kemal
   Unal, Ekrem
   Coskun, Abdulhakim
TI Gastric Signet Ring Carcinoma in a Patient With Ataxia-Telangiectasia: A
   Case Report and Review of the Literature
SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY
LA English
DT Article
DE ataxia-telangiectasia; gastric signet ring cell carcinoma; Hashimoto
   thyroiditis
ID STOMACH
AB Ataxia-telangiectasia (A-T) is an autosomal recessive primary immunodeficiency disease characterized by progressive cerebellar ataxia, telangiectasia, sinopulmoner recurrent infections, and cancer susceptibility. Individuals with A-T are known to be at increased risk of certain malignancies including leukemia, lymphoma, and breast and gastric cancer. We present an 18-year-old case of A-T with Hashimoto thyroiditis who admitted with complaints of nausea, vomiting, anorexia, and weight loss. An upper endoscopic biopsy revealed gastric signet ring cell carcinoma. To the best of our knowledge, we report the first case of signet ring cell carcinoma in the patient with A-T. Our experience with occurrence of Hashimoto thyroiditis and gastric signet ring cell carcinoma in the same case of A-T underlines that the clinicians handling A-T must be vigilant about both malignancy and autoimmune disorders.
C1 [Patiroglu, Turkan; Unal, Ekrem] Erciyes Univ, Dept Pediat, Div Pediat Hematol & Oncol, TR-25300 Kayseri, Turkey.
   [Patiroglu, Turkan; Gungor, Hatice Eke] Erciyes Univ, Dept Pediat, Div Pediat Allergy & Immunol, TR-25300 Kayseri, Turkey.
   [Arslan, Duran] Erciyes Univ, Dept Pediat, Div Pediat Gastroenterol, TR-25300 Kayseri, Turkey.
   [Deniz, Kemal] Erciyes Univ, Dept Pathol, TR-25300 Kayseri, Turkey.
   [Coskun, Abdulhakim] Erciyes Univ, Dept Radiol, Fac Med, Div Pediat Radiol, TR-25300 Kayseri, Turkey.
C3 Erciyes University; Erciyes University; Erciyes University; Erciyes
   University; Erciyes University
RP Gungor, HE (corresponding author), Erciyes Univ, Fevzi MERCAN Children Hosp, Fac Med, Dept Pediat,Div Pediat Allergy & Immunol, 38039 Melikgazi, TR-25300 Kayseri, Turkey.
EM haticeekegungor@hotmail.com
RI Deniz, Kemal/Q-3486-2019; ARSLAN, DURAN/AAL-9828-2021; UNAL,
   Ekrem/A-5099-2019
OI ARSLAN, DURAN/0000-0002-1906-7999; UNAL, Ekrem/0000-0002-2691-4826
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NR 22
TC 12
Z9 12
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1077-4114
EI 1536-3678
J9 J PEDIAT HEMATOL ONC
JI J. Pediatr. Hematol. Oncol.
PD NOV
PY 2013
VL 35
IS 8
BP E341
EP E343
DI 10.1097/MPH.0b013e318279b3f7
PG 3
WC Oncology; Hematology; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology; Pediatrics
GA 292WW
UT WOS:000329934400008
PM 23211692
DA 2025-06-01
ER

PT J
AU Nguyen, TLM
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   DiPaolo, RJ
AF Nguyen, Thanh-Long M.
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   Capoccia, Benjamin J.
   Sagartz, John E.
   Kesman, Russell A., Jr.
   Mills, Jason C.
   DiPaolo, Richard J.
TI Autoimmune Gastritis Mediated by CD4+ T Cells Promotes the Development
   of Gastric Cancer
SO CANCER RESEARCH
LA English
DT Article
ID HELICOBACTER-PYLORI ERADICATION; PERNICIOUS-ANEMIA; CARCINOID-TUMORS;
   TRANSGENIC MICE; HIGH PREVALENCE; METAPLASIA; MODEL; RISK;
   DIFFERENTIATION; AUTOANTIBODIES
AB Chronic inflammation is a major risk factor for cancer, including gastric cancers and other gastrointestinal cancers. For example, chronic inflammation caused by autoimmune gastritis (AIG) is associated with an increased risk of gastric polyps, gastric carcinoid tumors, and possibly adenocarcinomas. In this study, we characterized the progression of gastric cancer in a novel mouse model of AIG. In this model, disease was caused by CD4(+) T cells expressing a transgenic T-cell receptor specific for a peptide from the H+/K+ ATPase proton pump, a protein expressed by parietal cells in the stomach. AIG caused epithelial cell aberrations that mimicked most of those seen in progression of human gastric cancers, including chronic gastritis followed by oxyntic atrophy, mucous neck cell hyperplasia, spasmolytic polypeptide-expressing metaplasia, dysplasia, and ultimately gastric intraepithelial neoplasias. Our work provides the first direct evidence that AIG supports the development of gastric neoplasia and provides a useful model to study how inflammation drives gastric cancer. Cancer Res; 73(7); 2117-26. (C)2013 AACR.
C1 [Nguyen, Thanh-Long M.; Bellone, Clifford J.; Kesman, Russell A., Jr.; DiPaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA.
   [Sagartz, John E.] St Louis Univ, Sch Med, Dept Comparat Med, St Louis, MO 63104 USA.
   [Khurana, Shradha S.; Capoccia, Benjamin J.; Mills, Jason C.] Washington Univ, Sch Med, Div Gastroenterol, St Louis, MO 63110 USA.
C3 Saint Louis University; Saint Louis University; Washington University
   (WUSTL)
RP DiPaolo, RJ (corresponding author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63104 USA.
EM rdipaolo@slu.edu
RI Nguyen, Thanh-Luan/AAR-7199-2021; Mills, Jason/AAA-6688-2021
OI DiPaolo, Richard/0000-0002-2191-6689; Mills, Jason/0000-0002-0402-4662
FU ACS [RSG-12-171-01-LIB]; Digestive Diseases Research Core Center
   [NIH2P30 DK052574-12]; AGA Funderburg Research Scholar Award; Siteman
   Cancer Pathways Award;  [ACSDDC-115769];  [NIHDK094989-01]
FX R.J. DiPaolo was supported by ACS:RSG-12-171-01-LIB, Digestive Diseases
   Research Core Center: NIH2P30 DK052574-12; J.C. Mills by ACSDDC-115769,
   NIHDK094989-01; AGA Funderburg Research Scholar Award; Digestive
   Diseases Research Core Center: NIH2P30 DK052574-12; and S.S. Khurana by
   Siteman Cancer Pathways Award.
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NR 47
TC 45
Z9 50
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 2013
VL 73
IS 7
BP 2117
EP 2126
DI 10.1158/0008-5472.CAN-12-3957
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 118AU
UT WOS:000316995600010
PM 23378345
OA Bronze, Green Accepted
DA 2025-06-01
ER

PT J
AU Findakly, D
AF Findakly, Dawood
TI Peritoneal Carcinomatosis in an Adult With Sjogren's Syndrome: A
   Diagnostic Dilemma Revealing a Rare Association With Primary Gastric
   Adenocarcinoma
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE sjogren syndrome; autoimmune disease; peritoneal carcinomatosis; gastric
   adenocarcinoma; solid tumors
ID CANCER; RISK; MALIGNANCY
AB Sjogren's syndrome (SS) is a systemic autoimmune disease that mainly affects middle-aged women. It is rarely associated with solid neoplasms. We report a 60-year-old woman with a past medical history relevant for SS who was diagnosed with advanced-stage gastric adenocarcinoma upon evaluating for peritoneal carcinomatosis and succumbed two months after her original diagnosis. This case highlights the significance of considering gastrointestinal (GI) malignancy as an essential differential, particularly when evaluating patients with SS who fail conservative treatment for their GI symptoms.
C1 [Findakly, Dawood] Creighton Univ Arizona Hlth Educ Alliance, Valleywise Hlth Med Ctr, Internal Med, Phoenix, AZ 85012 USA.
RP Findakly, D (corresponding author), Creighton Univ Arizona Hlth Educ Alliance, Valleywise Hlth Med Ctr, Internal Med, Phoenix, AZ 85012 USA.
EM dawood_findakly@yahoo.com
RI Findakly, Dawood/AAE-7488-2022
OI Findakly, Dawood/0000-0001-5586-7072
CR Anderson LA, 2009, INT J CANCER, V125, P398, DOI 10.1002/ijc.24287
   Brito-Zerón P, 2017, J HEMATOL ONCOL, V10, DOI 10.1186/s13045-017-0464-5
   BROWN A, 2014, AM J RESP CRIT CARE, V189
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NR 12
TC 1
Z9 1
U1 0
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD MAY 14
PY 2020
VL 12
IS 5
AR e8123
DI 10.7759/cureus.8123
PG 7
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA LN0EF
UT WOS:000532618300017
PM 32426201
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Inoue, T
   Hayama, M
   Kobayashi, S
   Oyaizu, T
   Nakazato, Y
   Honma, K
   Chida, M
AF Inoue, Takashi
   Hayama, Makio
   Kobayashi, Satoru
   Oyaizu, Takeshi
   Nakazato, Yoshimasa
   Honma, Koichi
   Chida, Masayuki
TI Lung Cancer Complicated with IgG4-related Disease of the Lung
SO ANNALS OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article
DE IgG4-related disease; lung cancer; gastric cancer
ID SCLEROSING PANCREATITIS; AUTOIMMUNE PANCREATITIS; DACRYOADENITIS
AB Few have reported a concomitant malignant neoplasm with immunoglobulin G4 (IgG4)-related diseases. We describe a case of lung cancer and gastric cancer accompanied with IgG4-related disease. A 78-year-old man had an area of ground-glass opacity with central collapse in right upper lobe and a gastric cancer. The patient underwent a right upper lobectomy following a gastrectomy for the gastric cancer. Histological examination of the resected lung specimen revealed a lepidic pattern of an adenocarcinoma and a large amount of plasmacyte infiltration around the tumor. In immunohistochemical findings, the plasmacytes were stained for IgG4. Therefore, the lung tumor was considered to have associated with IgG4-related interstitial lesions.
C1 [Inoue, Takashi; Hayama, Makio; Kobayashi, Satoru; Oyaizu, Takeshi; Chida, Masayuki] Dokkyo Med Univ, Dept Gen Thorac Surg, Shimotsuga, Tochigi 3210293, Japan.
   [Nakazato, Yoshimasa; Honma, Koichi] Dokkyo Med Univ, Dept Anat & Diagnost Pathol, Shimotsuga, Tochigi 3210293, Japan.
C3 Dokkyo Medical University; Dokkyo Medical University
RP Chida, M (corresponding author), Dokkyo Med Univ, Dept Gen Thorac Surg, 880 Kitakobayashi, Shimotsuga, Tochigi 3210293, Japan.
EM chida-ths@umin.ac.jp
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NR 14
TC 17
Z9 21
U1 0
U2 2
PU MEDICAL TRIBUNE INC
PI TOKYO
PA ED COMM ANNALS THORACIC CARDIOVASCULAR SURG, 2-1-30 KUDAN MINAMI,
   CHIYODA-KU, TOKYO, 102-0074, JAPAN
SN 1341-1098
J9 ANN THORAC CARDIOVAS
JI Ann. Thorac. Cardiovasc. Surg.
PY 2014
VL 20
SU S
BP 474
EP 477
DI 10.5761/atcs.cr.12.02208
PG 4
WC Cardiac & Cardiovascular Systems; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Surgery
GA AZ1AO
UT WOS:000347973000013
PM 23574998
OA Green Submitted, gold
DA 2025-06-01
ER

PT J
AU Lahner, E
   Esposito, G
   Pilozzi, E
   Galli, G
   Corleto, VD
   Di Giulio, E
   Annibale, B
AF Lahner, Edith
   Esposito, Gianluca
   Pilozzi, Emanuela
   Galli, Gloria
   Corleto, Vito D.
   Di Giulio, Emilio
   Annibale, Bruno
TI Gastric cancer in patients with type I gastric carcinoids
SO GASTRIC CANCER
LA English
DT Article
DE Gastric cancer; Type I gastric carcinoids; Atrophic body gastritis;
   Pernicious anemia; Autoimmune gastritis
ID ATROPHIC BODY GASTRITIS; FOLLOW-UP; PERNICIOUS-ANEMIA; SYNCHRONOUS
   OCCURRENCE; RISK-FACTORS; TUMORS; STOMACH; CLASSIFICATION; DYSPLASIA;
   LESIONS
AB Atrophic body gastritis (ABG) is associated with both type I gastric carcinoids (T1-GCs) and intestinal-type gastric cancer. The occurrence of gastric cancer in ABG patients with type I gastric carcinoids has not yet been described.
   To describe the occurrence at follow-up of gastric cancer in ABG patients with type I gastric carcinoid in a retrospective case series in a single tertiary referral center.
   Between 1994 and 2012, 17 new cases of T1-GCs were diagnosed among a cohort of ABG patients in a single tertiary referral center for ABG. The clinical charts of these 17 T1-GC patients were retrospectively evaluated for the occurrence of gastric cancer at follow-up (median 4.2 years, range 0.5-13).
   In 4 (23.5 %)/17 T1-GCs patients (3 females, age 40-78 years), gastric cancer occurred (median follow-up 5.9 years, range 5.1-13). Three cases were intestinal-type adenocarcinomas and one a signet-ring cell diffuse gastric cancer, localized in three cases in the antrum. In two patients, it was detected on random biopsies during follow-up gastroscopy; in the other two, gastroscopy was performed because of new symptoms. All patients with gastric cancer had associated autoimmune features (pernicious anemia, autoimmune thyroid disease and a spared antrum) compared to 77, 46 and 54 % of those without gastric cancer, although statistical significance was not reached.
   This case series shows that in patients with T1-GCs, gastric cancer may frequently occur at long-term follow-up. Thus, these patients should be monitored by a long-term surveillance program, including an accurate bioptic sampling of the antral mucosa.
C1 [Lahner, Edith; Esposito, Gianluca; Galli, Gloria; Annibale, Bruno] Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Digest & Liver Dis, I-00189 Rome, Italy.
   [Pilozzi, Emanuela] Sapienza Univ Rome, St Andrea Hosp, Sch Med 2, Dept Pathol, I-00189 Rome, Italy.
   [Corleto, Vito D.; Di Giulio, Emilio] Sapienza Univ Rome, St Andrea Hosp, Sch Med 2, Dept Digest Endoscopy, I-00189 Rome, Italy.
   [Corleto, Vito D.] Osped S Pietro, Ctr Ric S Pietro, Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza
   University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza University
   Rome; Azienda Ospedaliera Sant'Andrea
RP Annibale, B (corresponding author), Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Digest & Liver Dis, Via Grottarossa 1035-1039, I-00189 Rome, Italy.
EM bruno.annibale@uniroma1.it
RI Lahner, Edith/AAM-1039-2021; Annibale, Bruno/A-5372-2008; PILOZZI,
   Emanuela/AAC-1854-2022; Esposito, Gianluca/J-7200-2019
OI Esposito, Gianluca/0000-0002-2242-5048; GALLI,
   GLORIA/0000-0003-3547-1067; annibale, bruno/0000-0001-9120-5957
FU Sapienza University of Rome
FX Declaration of personal interests: None. Declaration of funding
   interests: This study was supported by grants from the Sapienza
   University of Rome, 2011 and 2013.
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NR 43
TC 24
Z9 26
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1436-3291
EI 1436-3305
J9 GASTRIC CANCER
JI Gastric Cancer
PD JUL
PY 2015
VL 18
IS 3
BP 564
EP 570
DI 10.1007/s10120-014-0393-8
PG 7
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA CN3KL
UT WOS:000358325000013
PM 24890255
OA Bronze
DA 2025-06-01
ER

PT J
AU Maddalo, G
   Spolverato, Y
   Rugge, M
   Farinati, F
AF Maddalo, Gemma
   Spolverato, Ylenia
   Rugge, Massimo
   Farinati, Fabio
TI Gastrin: from pathophysiology to cancer prevention and treatment
SO EUROPEAN JOURNAL OF CANCER PREVENTION
LA English
DT Review
DE autoimmune gastritis; G17DT; gastric atrophy; gastric carcinoids;
   hypochlorhydria; neuroendocrine tumors; vaccine
ID HELICOBACTER-PYLORI; ATROPHIC GASTRITIS; CARCINOID-TUMORS; EXPRESSION;
   RECEPTOR; HYPERGASTRINEMIA; MANAGEMENT; G17DT; CELLS; RISK
AB Gastrin has been identified as the principal effector of gastric secretion, but several studies have demonstrated its role as a biomarker of cancer risk and as a growth factor for colorectal, stomach, liver, and pancreatic cancer. Hypergastrinemia characterizes autoimmune gastritis, with body and fundic gland atrophy and increased risk for both gastric adenocarcinoma and neuroendocrine tumors. Gastric type I carcinoids develop in the context of autoimmune gastritis because of the stimulus exerted by gastrin on enterochromaffin-like cells and remain gastrin-sensitive for long durations because the removal of hypergastrinemia leads to tumor regression. The treatment of gastric carcinoid is still open to debate, but when the disease frequently relapses, or is multicentric or infiltrating, surgery is advocated or, in the alternative, a costly and long-lasting treatment with long-acting somatostatin analogues is prescribed. A technology allowing the preparation of an immunogen eliciting an immune system response with generation of antibodies against G17 has been developed. This vaccine has been tested in patients with colorectal, pancreatic or advanced gastric cancer. The vaccine has also been used in the treatment of gastric type I carcinoids, and the administration of G17DT in patients harboring these lesions leads to carcinoid regression. Antigastrin vaccination in the treatment of gastrointestinal cancer obviously needs validation, but this immunotherapy may well represent a simple, inexpensive, and active `adjuvant' treatment. (C) 2014 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Maddalo, Gemma; Spolverato, Ylenia; Farinati, Fabio] Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, I-35128 Padua, Italy.
   [Rugge, Massimo] Univ Padua, Dept Med, Padua, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua
RP Farinati, F (corresponding author), Padua Univ Hosp, Dept Surg Oncol & Gastroenterol, Via Giustiniani 2, I-35128 Padua, Italy.
EM fabio.farinati@unipd.it
RI Farinati, Fabio/A-8267-2012; Rugge, Massimo/K-7525-2016
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NR 62
TC 24
Z9 27
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0959-8278
EI 1473-5709
J9 EUR J CANCER PREV
JI Eur. J. Cancer Prev.
PD JUL
PY 2014
VL 23
IS 4
BP 258
EP 263
DI 10.1097/CEJ.0000000000000008
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AI9XP
UT WOS:000337300400004
PM 24469263
DA 2025-06-01
ER

PT J
AU Soykan, I
   Er, RE
   Baykara, Y
   Kalkan, C
AF Soykan, Irfan
   Er, Ramazan Erdem
   Baykara, Yigit
   Kalkan, Cagdas
TI Unraveling the Mysteries of Autoimmune Gastritis
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Anti-parietal cell antibody; autoimmune gastritis; gastrin;
   neuroendocrine tumor type 1
ID FATTY LIVER-DISEASE; MEAN PLATELET VOLUME; LATERAL STARTING POSITION;
   GROWTH-FACTOR 21; ATROPHIC GASTRITIS; COLORECTAL-CANCER; DONOR LIVER;
   H+,K+-ADENOSINE TRIPHOSPHATASE; GASTROESOPHAGEAL-REFLUX; COLONOSCOPE
   WITHDRAWAL
AB Autoimmune gastritis is an immune-mediated disease characterized by the destruction of parietal cells and atrophy of the oxyntic mucosa due to anti-parietal cell antibodies. It may lead to serious conditions including iron/vitamin 812 and micronutrient deficiencies, neurological disorders, and gastric malignancies. The exact mechanism of this disease is not exactly understood; however, dysregulated immunological mechanisms appear to be major contributors. Patients with this disease are often asymptomatic but may present with gastrointestinal symptoms and/or iron/vitamin 812 deficiencies. Although important serological markers are available and despite advanced endoscopic techniques, the definitive diagnosis relies on histopathological examination of gastric corporal biopsy specimens. Autoimmune gastritis is closely related with increased risk of gastric neuroendocrine tumors and gastric adenocarcinoma. Patients with autoimmune gastritis do not benefit from specific treatments, thus, management is directed to restore micronutrient deficiencies and to prevent occurrence of neoplastic transformation with appropriate endoscopic surveillance.
C1 [Soykan, Irfan; Er, Ramazan Erdem] Ankara Univ Med Sch, Ibn i Sina Hosp, Gastroenterol, Ankara, Turkiye.
   [Baykara, Yigit] Stanford Med Transfus Med & Blood Banking, Dept Pathol, Stanford, CA USA.
   [Kalkan, Cagdas] Bilkent City Hosp, Dept Gastroenterol, Minist Hlth, Ankara, Turkiye.
C3 Ankara University; Ministry of Health - Turkey
RP Soykan, I (corresponding author), Ankara Univ Med Sch, Ibn i Sina Hosp, Gastroenterol, Ankara, Turkiye.
EM isoykan@medicine.ankara.edu.tr
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NR 211
TC 1
Z9 1
U1 7
U2 7
PU AVES
PI SISLI
PA BUYUKDERE CAD 105-9, MECIDIYEKOY, SISLI, ISTANBUL 34394, Turkiye
EI 2148-5607
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD MAR
PY 2025
VL 36
IS 3
DI 10.5152/tjg.2024.24563
PG 71
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0HL0I
UT WOS:001447453000002
PM 39632655
OA gold
DA 2025-06-01
ER

PT J
AU Raderer, M
   Püspök, A
   Stummvoll, G
   Längle, F
   Chott, A
AF Raderer, M
   Püspök, A
   Stummvoll, G
   Längle, F
   Chott, A
TI Early cancer of the stomach arising after successful treatment of
   gastric MALT lymphoma in patients with autoimmune disease
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmune disease; MALT lymphoma; signet ring cell carcinoma
ID HELICOBACTER-PYLORI INFECTION; B-CELL LYMPHOMA; MALIGNANT-LYMPHOMA;
   SJOGRENS-SYNDROME; TISSUE MALT; FOLLOW-UP; ADENOCARCINOMA; ERADICATION;
   REGRESSION; REMISSION
AB Background: Extranodal marginal zone B-cell lymphoma of the mucosa associated lymphoid tissue ( MALT lymphoma) arises in lymphoid tissue acquired through chronic antigenic stimulation as exemplified by Helicobacter pylori. Secondary development of gastric cancer, however, is thought to be a rare event. The detection of a signet ring cell carcinoma during follow-up endoscopy after successful therapy of MALT lymphoma in a patient with Sjogren's syndrome prompted us to analyse the frequency of subsequent gastric cancer in patients with underlying autoimmune disease ( AD). Methods: Patients with early stage MALT lymphoma and an underlying AD were evaluated for the occurrence of a secondary gastric cancer during the course of follow-up. Data analysed included the type of AD, stage of MALT lymphoma, H. pylori status, treatment for MALT lymphoma and response, follow-up, the presence of a secondary cancer, and time to development of cancer. In all patients, histologic samples were reassessed for the extent of gastritis, presence of intestinal metaplasia or focal atrophy at the time of lymphoma diagnosis. Results: A total of eight patients with overt AD at the time of diagnosis of MALT lymphoma were identified. All patients were women aged between 56 and 77 years; 5 had Sjogren's syndrome, 2 had autoimmune thyroiditis ( 1 along with psoriasis) and 1 suffered from polymyalgia rheumatica. All patients had early stage MALT lymphoma restricted to the mucosa and submucosa at the time of diagnosis, and the presence of H. pylori was found in all cases. Two of these patients achieved complete remission (CR) of the lymphoma following H. pylori eradication, while six were judged unresponsive and underwent chemotherapy, resulting in CR in all cases. One patient died from stroke while being in CR for 2 months following chemotherapy. Two patients (25%) developed early cancer limited to the gastric mucosa while being in CR from lymphoma for 9 and 27 months, respectively, and underwent partial gastrectomy. Final staging of gastric cancer revealed pT1pN0M0 in both cases. Of the remaining 5 cases, 1 patient had a local lymphoma relapse 18 months after CR and was salvaged with radiotherapy. In the remaining 4 patients, no evidence of lymphoma recurrence or a second malignancy has been found so far by regular follow-up every 3 months for a time-span between 52 and 63 months after initial diagnosis. Conclusion: Patients with concurrent MALT lymphoma and an underlying autoimmune condition show not only an impaired response to H. pylori eradication but might also be at increased risk for the development of gastric cancer. In view of this, such patients should be followed closely by regular endoscopies after remission of MALT lymphoma.
C1 Univ Vienna, Dept Internal Med 1, Div Oncol, AT-1090 Vienna, Austria.
   Univ Vienna, Div Gastroenterol, AT-1090 Vienna, Austria.
   Univ Vienna, Div Rheumatol Surg & Pathol, AT-1090 Vienna, Austria.
C3 University of Vienna; University of Vienna; University of Vienna
RP Univ Vienna, Dept Internal Med 1, Div Oncol, Waehringer Guertel 18-20, AT-1090 Vienna, Austria.
EM markus.raderer@akh-wien.ac.at
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NR 27
TC 11
Z9 11
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAR
PY 2003
VL 38
IS 3
BP 294
EP 297
DI 10.1080/00365520310000582
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 662YP
UT WOS:000181977200011
PM 12737445
DA 2025-06-01
ER

PT J
AU Boone, ATS
   Martínez, MGT
   Herrera, GL
   Portilla, JOD
   Padilla, SEE
   Rosales, FJE
   Reyes, SOL
AF Staines Boone, Aide Tamara
   Torres Martinez, Maria Guadalupe
   Herrera, Gabriela Lopez
   de Leija Portilla, Julia O.
   Espinosa Padilla, Sara Elva
   Espinosa Rosales, Francisco J.
   Lugo Reyes, Sau Oswaldo
TI Gastric Adenocarcinoma in the Context of X-linked Agammaglobulinemia
SO JOURNAL OF CLINICAL IMMUNOLOGY
LA English
DT Article
DE Cancer; solid tumor; gastric adenocarcinoma; primary immunodeficiency;
   X-linked agammaglobulinemia; antibody defect; Bruton
ID COMMON VARIABLE IMMUNODEFICIENCY; MULTIPLE COLORECTAL NEOPLASMS; CHRONIC
   ATROPHIC GASTRITIS; HELICOBACTER-PYLORI; TYROSINE KINASE; CANCER;
   HYPOGAMMAGLOBULINEMIA; DEFICIENCY; BOY
AB The hallmarks of X-linked Agammaglobulinemia (XLA) are panhypogammaglobulinemia, absent B-cells, and recurrent sinopulmonary and gastrointestinal infections starting at an early age, as well as other infections like cellulitis, meningitis, arthritis and sepsis. A number of noninfectious complications have been reported in these patients, including autoimmune diseases and malignancy, especially lymphomas. Here, we report the case of a 30-year old man who developed gastric adenocarcinoma in the context of XLA. Previous reports of, and hypotheses addressing the development of cancer in patients with XLA, are also summarized. Solid cancer in XLA affects mainly the gastrointestinal tract and seems to be related to chronic infection. A natural evolution can be traced back from gastric adenocarcinoma to megaloblastic anemia due to achlorhydria in the context of chronic infection; periodic endoscopy thus seems justified to detect and treat carcinoma in early stages.
C1 [Staines Boone, Aide Tamara; Torres Martinez, Maria Guadalupe] Northeast Natl Med Ctr, Clin Immunol & Allergol Dept, High Specialty Med Unit IMSS 25, Monterrey, NL, Mexico.
   [de Leija Portilla, Julia O.] Northeast Natl Med Ctr, Dept Pathol, High Specialty Med Unit IMSS 25, Monterrey, NL, Mexico.
   [Herrera, Gabriela Lopez; Espinosa Padilla, Sara Elva; Espinosa Rosales, Francisco J.; Lugo Reyes, Sau Oswaldo] Natl Inst Pediat, Immunodeficiencies Res Unit, Mexico City, DF, Mexico.
RP Boone, ATS (corresponding author), Northeast Natl Med Ctr, Clin Immunol & Allergol Dept, High Specialty Med Unit IMSS 25, Monterrey, NL, Mexico.
EM tamarastaines@gmail.com
RI Lopez-Herrera, Gabriela/HHN-1429-2022
OI LOPEZ HERRERA, GABRIELA/0000-0002-5498-6739
FU CONACYT [70062]; CSL Behring Pharmaceutical
FX The Immunodeficiencies Research Unit is supported in part by grants from
   CONACYT (BTK Grant # 70062), an unrestricted annual support from CSL
   Behring Pharmaceutical, as well as the continued support of Fundacion
   Mexicana para Nin@s con Inmunodeficiencias primarias (FUMENI), A.C.
   Edith Gonzalez Serrano reviewed an early draft for correction and
   clarity.
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NR 28
TC 14
Z9 14
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0271-9142
EI 1573-2592
J9 J CLIN IMMUNOL
JI J. Clin. Immunol.
PD FEB
PY 2014
VL 34
IS 2
BP 134
EP 137
DI 10.1007/s10875-013-9971-5
PG 4
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AH3SK
UT WOS:000336045400004
DA 2025-06-01
ER

PT J
AU Waldum, H
   Mjones, P
AF Waldum, Helge
   Mjones, Patricia
TI The central role of gastrin in gastric cancer
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE gastric cancer; types of gastric cancer; neuroendocrine carcinoma;
   Helicobacter pylori; gastrin
ID HELICOBACTER-PYLORI INFECTION; ENTEROCHROMAFFIN-LIKE CELL; MULTIPLE
   ENDOCRINE NEOPLASIA; ZOLLINGER-ELLISON-SYNDROME; LONG-TERM USE;
   ACID-SECRETION; PERNICIOUS-ANEMIA; CARCINOID-TUMORS; FOLLOW-UP; ATROPHIC
   GASTRITIS
AB The prevalence of gastric cancer has markedly declined, but due to the high mortality rates associated with gastric cancer, it is still a serious disease. The preferred classification of gastric cancer is according to Lauren into either the intestinal type, which has a glandular growth pattern, or the diffuse type, which does not have glandular structures. Both types have been classified as adenocarcinomas, with the latter type based on periodic acid-Schiff (PAS) positivity presumed to reflect mucin. However, the presence of mucin in the diffuse type, in contrast to neuroendocrine/enterochromaffin-like (ECL) cell markers, has not been confirmed by immunohistochemistry and in situ hybridization. The ECL cells are probably prone to becoming cancerous because they do not express E-cadherin. Gastric cancer is unique in that a bacterium, Helicobacter pylori, is thought to be its main cause. H. pylori predisposes infected individuals to cancer only after having caused oxyntic atrophy leading to gastric hypoacidity and hypergastrinemia. No single H. pylori factor has been convincingly proved to be carcinogenic. It is probable that gastrin is the pathogenetic factor for gastric cancer due to H. pylori, autoimmune gastritis, and long-term prolonged inhibition of gastric acid secretion. Hypergastrinemia induces ECL cell hyperplasia, which develops into neuroendocrine tumors (NETs) and then into neuroendocrine carcinomas in rodents, a sequence that has also been described in humans. During carcinogenesis, the tumor cells lose specific traits, requiring that sensitive methods be used to recognize their origin. Gastric cancer occurrence may hopefully be prevented by H. pylori eradication at a young age, and by the reduced use of inhibitors of acid secretion and use of a gastrin antagonist in those with previous long-term H. pylori infection and those with autoimmune gastritis.
C1 [Waldum, Helge; Mjones, Patricia] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, Trondheim, Norway.
   [Mjones, Patricia] Trondheim Reg & Univ Hosp, St Olavs Hosp, Dept Pathol, Trondheim, Norway.
C3 Norwegian University of Science & Technology (NTNU); Norwegian
   University of Science & Technology (NTNU)
RP Waldum, H (corresponding author), Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, Trondheim, Norway.
EM helge.waldum@ntnu.no
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NR 159
TC 14
Z9 14
U1 1
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD OCT 24
PY 2023
VL 13
AR 1176673
DI 10.3389/fonc.2023.1176673
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA X6GA4
UT WOS:001099402200001
PM 37941554
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Vanoli, A
   Parente, P
   Fassan, M
   Mastracci, L
   Grillo, F
AF Vanoli, Alessandro
   Parente, Paola
   Fassan, Matteo
   Mastracci, Luca
   Grillo, Federica
TI Gut inflammation and tumorigenesis: every site has a different tale to
   tell
SO INTERNAL AND EMERGENCY MEDICINE
LA English
DT Review
DE Cancer; Celiac disease; Esophagitis; Gastritis; Inflammatory bowel
   disease
ID SMALL-BOWEL ADENOCARCINOMA; COLORECTAL-CANCER; CROHNS-DISEASE;
   NONCONVENTIONAL DYSPLASIA; ULCERATIVE-COLITIS; BARRETTS-ESOPHAGUS;
   RISK-FACTORS; INDIVIDUALS; CARCINOMAS; LYMPHOMA
AB Gut inflammation has been correlated with cancerogenesis by disrupting gastrointestinal homeostasis. Numerous chronic inflammatory disorders of the tubular gastrointestinal tract (e.g., gastroesophageal reflux disease, Helicobacter pylori-induced and autoimmune chronic gastritis, celiac disease, and inflammatory bowel diseases) have been variably associated with an increased neoplastic risk. Gastrointestinal inflammation-induced neoplasms include epithelial tumors (esophageal squamous cell carcinoma and adenocarcinoma, gastric adenocarcinoma and neuroendocrine tumors, small bowel adenocarcinoma and neuroendocrine tumors, and colorectal cancer) and lymphomas (such as gastric marginal zone lymphomas and enteropathy-associated T cell lymphoma). In the last decades, numerous studies have investigated the pathogenetic mechanisms and the microenvironmental/microbiome changes that trigger genetic and/or epigenetic alterations eventually leading to tumorigenesis, often through a histologically recognizable inflammation-dysplasia-carcinoma cancerogenic sequence. In the present review, an overview of the current knowledge on the links between inflammatory diseases and neoplasms of the tubular GI tract, applying a site-by-site approach, is provided.
C1 [Vanoli, Alessandro] Univ Pavia, Dept Mol Med, Anat Pathol Unit, Via Carlo Forlanini 16, I-27100 Pavia, Italy.
   [Vanoli, Alessandro] IRCCS San Matteo Hosp, Anat Pathol Unit, Pavia, Italy.
   [Parente, Paola] Fdn IRCCS Osped Casa Sollievo Sofferenza, Unit Pathol, San Giovanni Rotondo, FG, Italy.
   [Fassan, Matteo] Univ Hosp Padua, Dept Med DIMED, Surg Pathol Unit, Padua, Italy.
   [Fassan, Matteo] Veneto Inst Oncol IOV IRCCS, Padua, Italy.
   [Mastracci, Luca; Grillo, Federica] IRCCS Osped Policlin San Martino, Genoa, Italy.
   [Mastracci, Luca; Grillo, Federica] Univ Genoa, Dept Surg Sci & Integrated Diagnost DISC, Anat Pathol, Genoa, Italy.
C3 University of Pavia; IRCCS Fondazione San Matteo; University of Padua;
   Azienda Ospedaliera - Universita di Padova; IRCCS Istituto Oncologico
   Veneto (IOV); University of Genoa; IRCCS AOU San Martino IST; University
   of Genoa
RP Vanoli, A (corresponding author), Univ Pavia, Dept Mol Med, Anat Pathol Unit, Via Carlo Forlanini 16, I-27100 Pavia, Italy.; Vanoli, A (corresponding author), IRCCS San Matteo Hosp, Anat Pathol Unit, Pavia, Italy.
EM alessandro.vanoli@unipv.it
RI Grillo, Federica/AAA-6422-2020; Mastracci, Luca/AAA-6411-2020; Vanoli,
   Alessandro/J-4469-2016; Fassan, Matteo/F-5152-2012; Parente,
   Paola/AAY-6963-2020
OI Vanoli, Alessandro/0000-0002-2976-7032; Grillo,
   Federica/0000-0001-6477-3182; Fassan, Matteo/0000-0001-6515-5482;
   Parente, Paola/0000-0003-0591-6723
FU Universita~degli Studi di Pavia
FX Open access funding provided by Universita degli Studi di Pavia within
   the CRUI-CARE Agreement. None.
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NR 73
TC 7
Z9 8
U1 2
U2 8
PU SPRINGER-VERLAG ITALIA SRL
PI MILAN
PA VIA DECEMBRIO, 28, MILAN, 20137, ITALY
SN 1828-0447
EI 1970-9366
J9 INTERN EMERG MED
JI Intern. Emerg. Med.
PD NOV
PY 2023
VL 18
IS 8
BP 2169
EP 2179
DI 10.1007/s11739-023-03320-w
EA MAY 2023
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HC1N4
UT WOS:000998044100004
PM 37249755
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Fornasarig, M
   Magris, R
   De Re, V
   Bidoli, E
   Canzonieri, V
   Maiero, S
   Viel, A
   Cannizzaro, R
AF Fornasarig, Mara
   Magris, Raffaella
   De Re, Valli
   Bidoli, Ettore
   Canzonieri, Vincenzo
   Maiero, Stefania
   Viel, Alessandra
   Cannizzaro, Renato
TI Molecular and Pathological Features of Gastric Cancer in Lynch Syndrome
   and Familial Adenomatous Polyposis
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE gastric cancer; lynch syndrome; familial adenomatous polyposis (FAP);
   helicobacter pylori infection; autoimmune gastritis; fundic gland polyps
   (FGPs)
ID NONPOLYPOSIS COLORECTAL-CANCER; PYLORIC-GLAND-ADENOMAS; SYNDROME HNPCC;
   NEOPLASMS; FAP; GUIDELINES; MANAGEMENT; MUTATION; GENETICS
AB Lynch syndrome (LS) and familial adenomatous polyposis (FAP) are autosomal dominant hereditary diseases caused by germline mutations leading to the development of colorectal cancer. Moreover, these mutations result in the development of a spectrum of different tumors, including gastric cancers (GCs). Since the clinical characteristics of GCs associated with LS and FAP are not well known, we investigated clinical and molecular features of GCs occurring in patients with LS and FAP attending our Institution. The Hereditary Tumor Registry was established in 1994 at the Department of Oncologic Gastroenterology, CRO Aviano National Cancer Institute, Italy. It includes 139 patients with LS and 86 patients with FAP. Patients were recruited locally for prospective surveillance. Out of 139 LS patients, 4 developed GC3 in the presence of helicobacter pylori infection and 1 on the background of autoimmune diseases. All GCs displayed a high microsatellite instability (MSI-H) and loss of related mismatch repair (MMR) protein. One of the FAP patients developed a flat adenoma, displaying low-grade dysplasia at the gastric body, and another poorly differentiated adenocarcinoma with signet ring cells like Krukenberg without HP infection. LS carriers displayed a risk of GC. The recognition of HP infection and autoimmune diseases would indicate those at higher risk for an endoscopic surveillance. Regarding FAP, the data suggested the need of suitable endoscopic surveillance in long survivals with diffuse fundic gland polyps.
C1 [Fornasarig, Mara; Magris, Raffaella; Maiero, Stefania; Cannizzaro, Renato] Ctr Riferimento Oncol IRCSS, SOC Gastroenterol Oncol, I-33081 Aviano, Italy.
   [De Re, Valli] Ctr Riferimento Oncol IRCSS, SOSD Immunopatol & Biomarcatori Oncol, I-33081 Aviano, Italy.
   [Bidoli, Ettore] Ctr Riferimento Oncol IRCSS, SOC Epidemiol, I-33081 Aviano, Italy.
   [Canzonieri, Vincenzo] Ctr Riferimento Oncol IRCSS, SOSD Anat Patol, I-33081 Aviano, Italy.
   [Viel, Alessandra] Ctr Riferimento Oncol IRCSS, SOSD Oncogenet & Oncogen Funz, I-33081 Aviano, Italy.
RP Fornasarig, M (corresponding author), Ctr Riferimento Oncol IRCSS, SOC Gastroenterol Oncol, I-33081 Aviano, Italy.
EM mfornasarig@cro.it; raffaella.magris@cro.it; vdere@cro.it;
   bidolie@cro.it; vcanzonieri@cro.it; smaiero@cro.it; aviel@cro.it;
   rcannizzaro@cro.it
RI De Re, Valli/K-4121-2016; Canzonieri, Vincenzo/AAA-7951-2019; Viel,
   Alessandra/J-7116-2018; DE RE, VALLI/AAA-1374-2019; Fornasarig,
   Mara/ABD-5093-2020; Magris, Raffaella/ABD-7791-2020; Cannizzaro,
   Renato/V-3804-2018; Maiero, Stefania/ABD-6092-2020; Canzonieri,
   Vincenzo/K-3141-2018; Bidoli, Ettore/AAC-1762-2020
OI Viel, Alessandra/0000-0003-2804-0840; DE RE, VALLI/0000-0001-6100-9373;
   Fornasarig, Mara/0000-0003-3388-0676; Magris,
   Raffaella/0000-0002-6137-7296; Cannizzaro, Renato/0000-0002-2020-222X;
   Maiero, Stefania/0000-0001-5085-1549; Canzonieri,
   Vincenzo/0000-0001-6010-0976; Bidoli, Ettore/0000-0001-8273-9084
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NR 25
TC 25
Z9 26
U1 0
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUN
PY 2018
VL 19
IS 6
AR 1682
DI 10.3390/ijms19061682
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GK8UZ
UT WOS:000436506600137
PM 29882764
OA Green Submitted, Green Published, gold
DA 2025-06-01
ER

PT J
AU Genta, RM
AF Genta, RM
TI The gastritis connection - Prevention and early detection of gastric
   neoplasms
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE gastric; gastric lymphoma; gastric cancer
ID HELICOBACTER-PYLORI INFECTION; HYPERTROPHIC LYMPHOCYTIC GASTRITIS;
   GASTROESOPHAGEAL REFLUX DISEASE; LOCALIZED MENETRIERS-DISEASE; BENIGN
   ULCER DISEASE; PARTIAL GASTRECTOMY; PATHOLOGICAL FEATURES; LYMPHOID
   FOLLICLES; PERNICIOUS-ANEMIA; BIOPSY SPECIMENS
AB Most gastric polyps, adenocarcinomas, carcinoids, and B cell lymphomas arise on a gastric mucosa damaged by long-standing chronic gastritis. The most common form of chronic gastritis is caused by infection with Helicobacter pylori. All patients with H. pylori infection develop lymphoid aggregates with germinal centers that interact intimally with the gastric mucosa (mucosaassociated lymphoid tissue [MALT]); these follicles are the condition sine qua non for the development of primary B cell mantle lymphomas, also known as MALT lymphomas. As the infection progresses, atrophy of the gastric mucosa develops in a subset of patients, which is replaced by an intestinal-type epithelium (intestinal metaplasia). On this background, dysplasia and adenocarcinomas of the intestinal type may develop. When atrophy is sufficiently severe to impair acid production, the gastrinproducing cells of the antrum increase their secretion of gastrin and stimulate endocrine cells in the corpus, which may eventually proliferate, become dysplastic, and give raise to carcinoids. This development is more frequent in advanced cases of autoimmune gastritis associated with pernicious anemia. On this background, there is also extensive epithelial hyperplasia and the formation of hyperplastic or inflammatory polyps, a small percentage of which may become dysplastic and progress to adenocarcinoma. Chronic exposure of the corpus mucosa to pancreaticoduodenal secretions ("bile reflux") causes reactive mucosal changes that may predispose to neoplasia. Thus, the progression of inflammation to atrophy to metaplasia, and in some cases chronic chemical injury, may give rise, at different times and under the influence of other, unknown stimuli, to. most types of gastric tumors. Other types of gastritis, including lymphocytic and granulomatous gastritis, are rare and have not been associated with gastric neoplasia. Awareness of these associations, appropriate treatment policies, and implementation of endoscopic surveillance programs would dramatically reduce the incidence of most types of gastric neoplasms and would allow the detection of many tumors at a stage when endoscopic resection or conservative treatment would still be possible.
C1 HUG, Dept Clin Pathol, CH-1211 Geneva 14, Switzerland.
C3 University of Geneva
RP HUG, Dept Clin Pathol, Rue Mucheli Du Crest,24, CH-1211 Geneva 14, Switzerland.
EM robert.genta@medecine.unige.ch
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NR 55
TC 14
Z9 16
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAY-JUN
PY 2003
VL 36
IS 5
BP S44
EP S49
DI 10.1097/00004836-200305001-00008
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 670XQ
UT WOS:000182435700008
PM 12702965
DA 2025-06-01
ER

PT J
AU Barakat, S
   Abdallah, B
   Finianos, A
   Al Mahmasani, L
AF Barakat, Salim
   Abdallah, Batoul
   Finianos, Antoine
   Al Mahmasani, Layal
TI Tumor Lysis Syndrome: A Rare Complication of Metastatic Gastric Cancer
   and a Possible Indicator of Disease Progression
SO CLINICAL MEDICINE INSIGHTS-CASE REPORTS
LA English
DT Article
DE Tumor lysis syndrome; cancer; progression
AB Tumor lysis syndrome (TLS) is an oncologic emergency that is usually associated with hematologic malignancies either spontaneously or following early chemotherapy and is caused by massive tumor cell lysis. However. it has been rarely reported in solid tumors. We report a case of 25-year-old lady recently diagnosed with metastatic gastric adenocarcinoma who developed TLS after the fourth cycle of chemoimmunotherapy (FOLFOX plus Nivolumab). She presented with abdominal pain. decrease in oral intake and decreased urine output. Laboratory studies showed acute kidney injury with electrolyte disturbances and was diagnosed initially with autoimmune nephritis secondary to Nivolumab but was later found to have TLS and recovered after appropriate treatment. Soon after this complication, our patient was found to have disease progression on imaging which makes the incidence of TLS an indicator of disease progression.
C1 [Barakat, Salim; Abdallah, Batoul] Amer Univ Beirut, Dept Internal Med, Med Ctr, Beirut, Lebanon.
   [Finianos, Antoine; Al Mahmasani, Layal] Amer Univ Beirut, Dept Internal Med, Div Hematol Oncol, Med Ctr, Cairo St,POB 11-0236, Beirut 11072020, Lebanon.
C3 American University of Beirut; American University of Beirut
RP Al Mahmasani, L (corresponding author), Amer Univ Beirut, Dept Internal Med, Div Hematol Oncol, Med Ctr, Cairo St,POB 11-0236, Beirut 11072020, Lebanon.
EM la108@aub.edu.lb
OI Al Mahmasani, Layal/0000-0002-0661-4383
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   Kobayashi Tomoki, 2012, Nihon Shokakibyo Gakkai Zasshi, V109, P1372
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NR 12
TC 0
Z9 0
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1179-5476
J9 CLIN MED INSIGHT-CAS
JI Clin. Med. Insights-Case Rep.
PD OCT
PY 2022
VL 15
AR 11795476221129238
DI 10.1177/11795476221129238
PG 3
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 5N1NI
UT WOS:000871556000001
PM 36277906
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Chinnadurai, A
   Strum, S
   Ghassemian, A
   Fortin, D
   Foster, C
   Breadner, D
AF Chinnadurai, Anu
   Strum, Scott
   Ghassemian, Artin
   Fortin, Dalilah
   Foster, Cheryl
   Breadner, Daniel
TI A Rare Association of Mixed Autoimmune Hemolytic Anemia with Gastric
   Carcinoma
SO CASE REPORTS IN ONCOLOGY
LA English
DT Article
DE Gastric carcinoma; Autoimmune hemolytic anemia; Mixed autoimmune
   hemolytic anemia
ID DIAGNOSIS
AB This case report outlines a 70-year-old female patient who presented with a concurrent mixed autoimmune hemolytic anemia (AIHA) and a gastric adenocarcinoma. Her treatment course of these two diseases is summarized, which included supportive care, neoadjuvant chemotherapy for her gastric adenocarcinoma, steroids, rituximab, and surgical resection of the tumor. This approach ultimately led to the stabilization of her AIHA and primary cure for her solid malignancy. We briefly review both AIHA and gastric adenocarcinoma as clinical entities, propose working causes of hemolytic anemia including gastric adenocarcinoma, and outline a successful treatment pathway for these two concurrent conditions.
C1 [Chinnadurai, Anu; Strum, Scott; Ghassemian, Artin; Foster, Cheryl; Breadner, Daniel] Western Univ, Schulich Sch Med & Dent, Dept Med, London, ON, Canada.
   [Strum, Scott; Ghassemian, Artin; Foster, Cheryl; Breadner, Daniel] Victoria Hosp, London Reg Canc Program, London Hlth Sci Ctr, London, ON, Canada.
   [Fortin, Dalilah] Western Univ, Schulich Sch Med & Dent, Dept Surg, London, ON, Canada.
C3 Western University (University of Western Ontario); Western University
   (University of Western Ontario); University Western Ontario Hospital;
   London Health Sciences Centre; University of Victoria; Western
   University (University of Western Ontario)
RP Breadner, D (corresponding author), Western Univ, Schulich Sch Med & Dent, Dept Med, London, ON, Canada.; Breadner, D (corresponding author), Victoria Hosp, London Reg Canc Program, London Hlth Sci Ctr, London, ON, Canada.
EM Daniel.breadner@lhsc.on.ca
RI Breadner, Daniel/AAJ-9843-2021
OI Strum, Scott/0000-0003-3618-9936; Breadner, Daniel/0000-0001-5379-7621
FX Y
CR Agrawal K, 2017, CASE REP ONCOL MED, V2017, DOI 10.1155/2017/8414602
   Barcellini W, 2018, EXPERT REV CLIN IMMU, V14, P857, DOI 10.1080/1744666X.2018.1521722
   Berentsen S, 2004, BLOOD, V103, P2925, DOI 10.1182/blood-2003-10-3597
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NR 14
TC 0
Z9 0
U1 0
U2 0
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1662-6575
J9 CASE REP ONCOL
JI Case Rep. Oncol.
PY 2023
VL 16
IS 1
BP 1209
EP 1216
DI 10.1159/000534278
PG 8
WC Oncology
WE Emerging Sources Citation Index (ESCI)
SC Oncology
GA NW4F6
UT WOS:001203472100162
PM 37900792
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Coati, I
   Fassan, M
   Farinati, F
   Graham, DY
   Genta, RM
   Rugge, M
AF Coati, Irene
   Fassan, Matteo
   Farinati, Fabio
   Graham, David Y.
   Genta, Robert M.
   Rugge, Massimo
TI Autoimmune gastritis: Pathologist's viewpoint
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune gastritis; Metaplasia; Carcinoids; Operative link for
   gastritis assessment staging
ID CHRONIC ATROPHIC GASTRITIS; PYLORIC GLAND ADENOMA; PERNICIOUS-ANEMIA;
   T-CELLS; CANCER; METAPLASIA; CLASSIFICATION; PREVALENCE; DISEASES;
   STOMACH
AB Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic (and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and (intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integrating endoscopy, serology, histology and molecular profiling.
C1 [Coati, Irene; Fassan, Matteo; Rugge, Massimo] Univ Padua, Dept Med DIMED, Surg Pathol Unit, I-35121 Padua, Italy.
   [Farinati, Fabio] Univ Padua, Dept Surg Oncol & Gastroenterol, Gastroenterol Unit, I-35121 Padua, Italy.
   [Graham, David Y.] Baylor Coll Med, Dept Med, Vet Adm Hosp, Houston, TX 77030 USA.
   [Genta, Robert M.] Miraca Life Sci Res Inst, Irving, TX 75039 USA.
   [Genta, Robert M.] VA North Texas Hlth Care Syst, Dept Pathol, Dallas, TX 75390 USA.
   [Genta, Robert M.] VA North Texas Hlth Care Syst, Dept Med, Dallas, TX 75390 USA.
   [Genta, Robert M.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
C3 University of Padua; University of Padua; Baylor College of Medicine; US
   Department of Veterans Affairs; Veterans Health Administration (VHA);
   Michael E DeBakey VA Medical Center; US Department of Veterans Affairs;
   Veterans Health Administration (VHA); VA North Texas Health Care System;
   US Department of Veterans Affairs; Veterans Health Administration (VHA);
   VA North Texas Health Care System; University of Texas System;
   University of Texas Southwestern Medical Center Dallas
RP Fassan, M (corresponding author), Univ Padua, Dept Med DIMED, Pathol, Surg Pathol Unit, Via Gabelli 61, I-35121 Padua, Italy.
EM matteo.fassan@unipd.it
RI Farinati, Fabio/A-8267-2012; Rugge, Massimo/K-7525-2016; Graham,
   David/AAL-2165-2021; Fassan, Matteo/F-5152-2012
OI FARINATI, FABIO/0000-0002-2944-1374; Fassan, Matteo/0000-0001-6515-5482
FU Italian Association for Cancer Research (AIRC Regional grant) [6421];
   Healthy Stomach Initiative (HIS)
FX Supported by A grant from the Italian Association for Cancer Research
   (partly, AIRC Regional grant 2008 No. 6421); and published under the
   auspices of the Healthy Stomach Initiative (HIS)
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NR 60
TC 108
Z9 112
U1 3
U2 28
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 14
PY 2015
VL 21
IS 42
BP 12179
EP 12189
DI 10.3748/wjg.v21.i42.12179
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW5HC
UT WOS:000365025300026
PM 26576102
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Zurleni, T
   Altomare, M
   Serio, G
   Catalano, F
AF Zurleni, Tommaso
   Altomare, Michele
   Serio, Giovanni
   Catalano, Filippo
TI Multifocal early gastric cancer in a patient with atrophic gastritis and
   pernicious anemia
SO INTERNATIONAL JOURNAL OF SURGERY CASE REPORTS
LA English
DT Article
DE Multifocal early gastric cancer; Pernicious anemia; Autoimmune
   metaplastic atrophic gastritis; Subtotal gastrectomy
ID RISK; STOMACH; CARCINOMA
AB INTRODUCTION: Pernicious anemia (PA) caused by vitamin B12 deficiency is associated with Autoimmune Metaplastic Atrophic Gastritis (AMAG). Patients with AMAG have threefold risk of the development of gastric cancer.
   PRESENTATION OF CASE: We describe a case of a 66 year old man with a history of PA and atrophic antral-corpus gastritis. After endoscopic and chromoendoscopic evaluation the patient was treated with subtotal gastrectomy plus D2 lymphadenectomy. The tumor was diagnosed as Stage Ia; pT1a pN0 pM0 G2 with multiple foci of high grade dysplasia and intramucosal adenocarcinoma.
   DISCUSSION: Multifocal Early Gastric Cancer can be a problem for minimally invasive treatment such as endoscopic excision.
   Surgical management where it is not possible Endoscopic Mucosal Resection or Submucosal Resection (EMR/ESD) should include D1 or more type of lymphadenectomy because of the risk of nodes metastases.
   The chromoendoscopic evaluation may be helpful in the preoperative work-up and during the follow-up period.
   CONCLUSION: Multidisciplinary approach is very important to reduce the under-treatment risk in multifocal early gastric cancer. Further studies will be needed to evaluate the safety of Subtotal vs Total Gastrectomy in this kind of disease. (C) 2020 The Authors. Published by Elsevier Ltd on behalf of IJS Publishing Group Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
C1 [Zurleni, Tommaso; Altomare, Michele] Busto Arsizio Hosp, ASST Valle Olona, Dept Gen Surg, Busto Arsizio, Italy.
   [Serio, Giovanni] Busto Arsizio Hosp, ASST Valle Olona, Dept Anat Pathol, Busto Arsizio, Italy.
   [Catalano, Filippo] Borgo Trento City Hosp, Emergency Endoscopy Unit, Verona, Italy.
C3 Ospedale di Busto Arsizio; Ospedale di Busto Arsizio; University of
   Verona; Azienda Ospedaliera Universitaria Integrata Verona
RP Zurleni, T (corresponding author), Busto Arsizio Hosp, ASST Valle Olona, Dept Gen Surg, Busto Arsizio, Italy.
EM tzurleni@yahoo.it
RI Altomare, Michele/AAE-7981-2022
OI Serio, Giovanni/0000-0001-7800-6793; Altomare,
   Michele/0000-0002-3879-2678
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NR 23
TC 4
Z9 4
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2210-2612
J9 INT J SURG CASE REP
JI Int. J. Surg. Case Rep.
PY 2020
VL 72
BP 433
EP 437
DI 10.1016/j.ijscr.2020.06.010
PG 5
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA MK6WM
UT WOS:000548926300021
PM 32563836
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Li, GY
   Li, QJ
   Ping, MM
   Jiao, ZY
   Wang, XX
   Cheng, J
   Guo, JZ
   Cheng, Y
AF Li, Guangyao
   Li, Qijiao
   Ping, Miaomiao
   Jiao, Ziying
   Wang, Xingxing
   Cheng, Juan
   Guo, Jizheng
   Cheng, Ya
TI SLAMF8 can predict prognosis of pan-cancer and the immunotherapy
   response effectivity of gastric cancer
SO AGING-US
LA English
DT Article
DE SLAMF8; pan-cancer; biomarker; TME; immunotherapy
ID EXPRESSION; INNATE; FAMILY; TIGIT; LAG-3; CD96; SAP
AB SLAMF8, the eighth member of the Signaling Lymphocytic Activation Molecule Family (SLAMF), functions in the regulation of the development and activity of diverse immune cells as a costimulatory receptor within the SLAMF family. Studies had revealed that SLAMF8 is expressed higher in several autoimmune inflammation diseases and tumors. Nevertheless, the connection between SLAMF8 and pan-cancer remains undisclosed. The research investigated the correlation between SLAMF8 and various factors including the immune microenvironment, microsatellite instability, immune novel antigen, gene mutation, immune regulatory factors, immune blockade TMB, and immune or molecular subtypes of SLAMF8 in verse cancer types. Immunohistochemistry was ultimately employed to validate the presence of the SLAMF8 gene in various tumor types including hepatocellular carcinoma, prostate adenocarcinoma, and kidney renal clear cell carcinoma. Furthermore, the relationship between SLAMF8 expression and the therapeutic efficacy of the PD1 blockade agent, Sintilimab, treatment in gastric cancer was validated. The result of differential analysis suggested that SLAMF8 was over-expressed in pan-cancer compared with paracancerous tissues. The analysis of survival indicated a connection between SLAMF8 and the overall prognosis in different types of cancers, where higher levels of SLAMF8 were found to be significantly linked to unfavorable outcomes in patients but favorable outcome of immunotherapy in gastric cancer. Significant correlations were observed between SLAMF8 levels and pan-cancer tumorigenesis, tumor metabolism, and immunity. As a result, SLAMF8 may become an important prognostic biomarker in the majority of tumors and a hopeful gene target for immunotherapy against gastric cancer.
C1 [Li, Guangyao] Second Peoples Hosp Wuhu, Dept Gastrointestinal Surg, Wuhu 241000, Anhui, Peoples R China.
   [Li, Qijiao; Ping, Miaomiao; Jiao, Ziying; Wang, Xingxing; Cheng, Juan; Guo, Jizheng] Anhui Med Univ, Sch Basic Med Sci, Hefei 230032, Anhui, Peoples R China.
   [Cheng, Ya] Anhui Med Univ, Affiliated Hosp 1, Dept Emergency Surg, Hefei 230032, Anhui, Peoples R China.
C3 Anhui Medical University; Anhui Medical University
RP Cheng, J; Guo, JZ (corresponding author), Anhui Med Univ, Sch Basic Med Sci, Hefei 230032, Anhui, Peoples R China.; Cheng, Y (corresponding author), Anhui Med Univ, Affiliated Hosp 1, Dept Emergency Surg, Hefei 230032, Anhui, Peoples R China.
EM juancheng@ahmu.edu.cn; guojizheng@ahmu.edu.cn;
   2336020145@stu.ahmu.edu.cn
FU Anhui Provincial Health Commission Provincial Financial Support for
   Youth Programs [AHWJ2023A30159]
FX This work is funded by the Anhui Provincial Health Commission Provincial
   Financial Support for Youth Programs (AHWJ2023A30159) .
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NR 40
TC 2
Z9 2
U1 2
U2 3
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD MAY 30
PY 2024
VL 16
IS 10
BP 8944
EP 8964
PG 21
WC Cell Biology; Geriatrics & Gerontology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Geriatrics & Gerontology
GA TB6F2
UT WOS:001238829900032
PM 38787377
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Miehlke, S
   Hackelsberger, A
   Meining, A
   vonArnim, U
   Muller, P
   Ochsenkuhn, T
   Lehn, N
   Malfertheiner, P
   Stolte, M
   Bayerdorffer, E
AF Miehlke, S
   Hackelsberger, A
   Meining, A
   vonArnim, U
   Muller, P
   Ochsenkuhn, T
   Lehn, N
   Malfertheiner, P
   Stolte, M
   Bayerdorffer, E
TI Histological diagnosis of Helicobacter pylori gastritis is predictive of
   a high risk of gastric carcinoma
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
ID INFECTION; CANCER; PREVALENCE; ADENOCARCINOMA; ANTIBODY; STOMACH;
   DISEASE; BODY
AB Chronic Helicobacter pylori infection has been identified as a major risk factor for the subsequent development of gastric carcinoma. On the basis of seroepidemiological studies the relative risk for infected persons was estimated to range between 3 and 6. Our study attempted to determine the relative risk of gastric carcinoma in H. pylori-infected individuals based on the histological evaluation of gastritis in gastric carcinoma patients in the light of a declining prevalence of H. pylori infection in Western countries. We histologically determined the H. pylori infection rate in 215 patients with early gastric carcinoma (tumor stage pT1), and compared it with that of 215 asymptomatic persons matched by age and sex who were tested by the 13C urea breath test. On the basis of these data an odds ratio of 16.7 (CI 9.6-29.1) was calculated for the relative risk of developing gastric carcinoma in H. pylori-infected people. The histological diagnosis of gastritis permits a separate risk assessment for patients with autoimmune gastritis, and by excluding these patients from the analysis we calculated an odds ratio for H. pylori-infected persons of 150 (CI 36.4-622.9). The endoscopic-histological diagnosis of H. pylori infection is associated with an increased risk of the subsequent development of gastric carcinoma of approximately 150-fold compared with H. pylori-negative patients who do not have chronic atrophic corpus gastritis of the autoimmune type (type A gastritis). (C) 1997 Wiley-Liss, Inc.
C1 UNIV MAGDEBURG,DEPT GASTROENTEROL HEPATOL & INFECT DIS,D-39106 MAGDEBURG,GERMANY.
   UNIV MUNICH,KLINIKUM GROSSHADERN,DEPT MED 2,D-8000 MUNICH,GERMANY.
   KLINIKUM BAYREUTH,INST PATHOL,BAYREUTH,GERMANY.
   UNIV REGENSBURG,INST MICROBIOL,D-8400 REGENSBURG,GERMANY.
C3 Otto von Guericke University; University of Munich; Klinikum Bayreuth;
   University of Regensburg
RI Malfertheiner, Peter/AEZ-6553-2022
CR *AM JOINT COMM CAN, 1993, MAN STAG CANC
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NR 28
TC 38
Z9 42
U1 0
U2 0
PU WILEY-LISS
PI NEW YORK
PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD DEC 10
PY 1997
VL 73
IS 6
BP 837
EP 839
PG 3
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA YJ834
UT WOS:A1997YJ83400012
PM 9399662
DA 2025-06-01
ER

PT J
AU Murphy, G
   Dawsey, SM
   Engels, EA
   Ricker, W
   Parsons, R
   Etemadi, A
   Lin, SW
   Abnet, CC
   Freedman, ND
AF Murphy, Gwen
   Dawsey, Sanford M.
   Engels, Eric A.
   Ricker, Winnie
   Parsons, Ruth
   Etemadi, Arash
   Lin, Shih-Wen
   Abnet, Christian C.
   Freedman, Neal D.
TI Cancer Risk After Pernicious Anemia in the US Elderly Population
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Chronic Atrophic Autoimmune Gastritis; Acid Secretion; Parietal Cells;
   Stomach Cancer
ID GASTRIC CARCINOID-TUMORS; SERUM PEPSINOGENS; COHORT; CARCINOGENESIS;
   ADENOCARCINOMA; PREVENTION; PREVALENCE; HISTOLOGY; STOMACH; DISEASE
AB BACKGROUND & AIMS: Pernicious anemia, a result of autoimmune gastritis, is the most common cause of vitamin B-12 deficiency, affecting 2% to 5% of the elderly population. Treatment with vitamin B-12 cures the anemia, but not the gastritis. Findings from small studies have indicated that patients with pernicious anemia could have an increased risk of cancer.
   METHODS: We performed a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, comparing 1,138,390 cancer cases (age, 66-99 y) with 100,000 matched individuals without cancer (controls). Individuals with pernicious anemia were identified based on their medical claims within the year before selection for the study. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using unconditional logistic regression, and models were adjusted for sex, age, and calendar year of diagnosis and selection.
   RESULTS: Compared with controls, we found individuals with pernicious anemia to be at increased risk for noncardia gastric adenocarcinoma (OR, 2.18; 95% CI, 1.94-2.45) and gastric carcinoid tumors (OR, 11.43; 95% CI, 8.90-14.69). In addition, people with pernicious anemia have an increased risk of developing tonsilar cancer (OR, 2.00; 95% CI, 1.40-2.85), hypopharyngeal cancer (OR, 1.92; 95% CI, 1.35-2.73), esophageal squamous cell carcinoma (OR, 2.12; 95% CI, 1.76-2.55), small intestinal cancer (OR, 1.63; 95% CI, 1.32-2.02), liver cancer (OR, 1.49; 95% CI, 1.28-1.73), myeloma (OR, 1.55; 95% CI, 1.37-1.75), acute myeloid leukemia (OR, 1.68; 95% CI, 1.46-1.93), and myelodysplastic syndrome (OR, 2.87; 95% CI, 2.53-3.26). People with pernicious anemia have a lower risk of rectal cancer than the general population (OR, 0.82; 95% CI, 0.74-0.92).
   CONCLUSIONS: In a population-based, case-control study of individuals in the Surveillance, Epidemiology, and End Results-Medicare database, we found individuals with pernicious anemia to have significantly increased risks of gastric carcinoid tumors, adenocarcinomas, and other cancers located throughout the body.
C1 [Murphy, Gwen; Dawsey, Sanford M.; Engels, Eric A.; Etemadi, Arash; Lin, Shih-Wen; Abnet, Christian C.; Freedman, Neal D.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
   [Ricker, Winnie; Parsons, Ruth] Informat Management Serv Inc, Calverton, MD USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); NIH National Cancer Institute- Division of Cancer Epidemiology &
   Genetics; Information Management Services, Inc.
RP Murphy, G (corresponding author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E314, Bethesda, MD 20892 USA.
EM murphygw@mail.nih.gov
RI Etemadi, Arash/Y-7082-2018; Murphy, Gwen/GQB-3897-2022; Abnet,
   Christian/JAC-5179-2023; Murphy, Gwen/AFR-8275-2022; Etemadi,
   Arash/C-1386-2016; Freedman, Neal/B-9741-2015; Abnet,
   Christian/C-4111-2015
OI Murphy, Gwen/0000-0003-0118-5337; Etemadi, Arash/0000-0002-3458-1072;
   Freedman, Neal/0000-0003-0074-1098; Abnet, Christian/0000-0002-3008-7843
FU National Cancer Institute at the US National Institutes of Health;
   National Cancer Institute [ZIACP010127] Funding Source: NIH RePORTER
FX This work was supported by the Intramural Research Program of the
   National Cancer Institute at the US National Institutes of Health.
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NR 31
TC 105
Z9 107
U1 1
U2 17
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2015
VL 13
IS 13
BP 2282
EP +
DI 10.1016/j.cgh.2015.05.040
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CW7PK
UT WOS:000365191300016
PM 26079040
OA Bronze, Green Accepted
DA 2025-06-01
ER

PT J
AU Sano, Y
   Yoshida, K
   Hibi, E
   Sekiya, A
   Watanabe, Y
   Shibata, D
AF Sano, Yuriko
   Yoshida, Kosuke
   Hibi, Erina
   Sekiya, Atsushi
   Watanabe, Yuriko
   Shibata, Daijiro
TI A rare case of signet ring cell carcinoma with diffuse cutaneous
   systemic sclerosis: A case report
SO JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH
LA English
DT Article
DE case reports; signet ring cell carcinoma; squamous cell carcinoma;
   systemic scleroderma; uterine cervical neoplasms
ID CERVIX
AB Systemic sclerosis, an autoimmune disease characterized by fibrosis and vasculopathy of the skin and other multiple organs has been associated with an increased risk of malignancy. We present the case of a 74-year-old woman who had diffused cutaneous systemic sclerosis and uterine cervical cancer. The patient was initially diagnosed with stage IIB squamous cell carcinoma and concurrent chemoradiotherapy was planned. However, cisplatin could not be administered due to acute renal failure, so the patient was treated solely with radiotherapy. However, complications of systemic sclerosis progressed rapidly, and the patient died 63 days later from pulmonary edema. An autopsy later revealed that uterine cervix had primary signet ring cell carcinoma. We suspected that this patient had a combination of signet ring cell carcinoma and squamous cell carcinoma, with squamous cell carcinoma disappearing after radiotherapy. This case highlighted the importance of systemic management for cancers associated with systemic sclerosis.
C1 [Sano, Yuriko; Yoshida, Kosuke; Hibi, Erina; Sekiya, Atsushi; Watanabe, Yuriko; Shibata, Daijiro] Chubu Rosai Hosp, Dept Obstet & Gynecol, Nagoya, Japan.
   [Yoshida, Kosuke] Nagoya Univ, Dept Obstet & Gynecol, Grad Sch Med, Tsuruma Cho 65,Showa Ku, Nagoya 4668550, Japan.
C3 Nagoya University
RP Yoshida, K (corresponding author), Nagoya Univ, Dept Obstet & Gynecol, Grad Sch Med, Tsuruma Cho 65,Showa Ku, Nagoya 4668550, Japan.
EM yoshida.kousuke@med.nagoya-u.ac.jp
RI YOSHIDA, Kosuke/AAM-6507-2020
OI Yoshida, Kosuke/0000-0003-1484-4872
CR [Anonymous], 2015, Nat Rev Dis Primers, V1, P15053, DOI 10.1038/nrdp.2015.53
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NR 10
TC 1
Z9 1
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1341-8076
EI 1447-0756
J9 J OBSTET GYNAECOL RE
JI J. Obstet. Gynaecol. Res.
PD OCT
PY 2023
VL 49
IS 10
BP 2549
EP 2552
DI 10.1111/jog.15715
EA JUN 2023
PG 4
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA T9KN3
UT WOS:001012204700001
PM 37344106
DA 2025-06-01
ER

PT J
AU Hughes, JW
   Muegge, BD
   Tobin, GS
   Litvin, M
   Sun, L
   Saenz, JB
   Gyawali, CP
   McGill, JB
AF Hughes, Jing W.
   Muegge, Brian D.
   Tobin, Garry S.
   Litvin, Marina
   Sun, Lulu
   Saenz, Jose B.
   Gyawali, C. Prakash
   McGill, Janet B.
TI HIGH-RISK GASTRIC PATHOLOGY AND PREVALENT AUTOIMMUNE DISEASES IN
   PATIENTS WITH PERNICIOUS ANEMIA
SO ENDOCRINE PRACTICE
LA English
DT Article
ID FOLLOW-UP; ATROPHIC GASTRITIS; CANCER-RISK; CARCINOMA; STOMACH;
   MANAGEMENT; ASSOCIATION; POPULATION; CHILDREN; LESIONS
AB Objective: Pernicious anemia (PA) develops from atrophic gastritis due to autoimmune destruction of parietal cells and results in achlorhydria, vitamin B12 and iron deficiencies, anemia, neurologic deficits, and premalignant and malignant stomach lesions. We report the presentation, diagnosis and gastric complications of PA in patients from an endocrinology practice.
   Methods: Thirty-four patients (31 female, 3 male) with PA who underwent esophagogastroduodenoscopy (EGD) or gastrectomy were identified. Pertinent clinical, laboratory, and pathology findings were reviewed and summarized.
   Results: The mean age of patients was 58.6 +/- 14.2 years; the onset of PA was age 50.2 +/- 15.3 years. Anemia reflected vitamin B12 and/or iron deficiencies. Parietal cell antibodies (PCA) were detected in 97% of patients, and intrinsic factor blocking antibody (IFBA) was found in 52%. Fasting gastrin and chromogranin A levels were elevated (1,518.0 +/- 1,588.3 pg/mL, and 504.9.1 +/- 1,524.9 ng/mL respectively). Autoimmune or immunologic diseases (AIDs) were present in 32/34 patients. Stomach pathology showed premalignant or malignant lesions in 26 patients, including gastric neuroendocrine tumors (GNETs) in 6 and adenocarcinoma in 1. One patient presented with neurologic symptoms and subacute combined degeneration of the posterior column of the spinal cord.
   Conclusion: PA should be suspected in patients with unexplained anemia or neurologic symptoms. The diagnosis of PA relies on fasting gastrin and gastric auto-antibody testing, in addition to hematologic evaluation. EGD with measurement of gastric pH and biopsies of the fundus and antrum identifies patients with achlorhydria, atrophic gastritis, and premalignant and malignant stomach lesions. EGD surveillance of patients with high-risk stomach lesions is recommended.
C1 [Hughes, Jing W.; Muegge, Brian D.; Tobin, Garry S.; Litvin, Marina; McGill, Janet B.] Washington Univ, Sch Med, Div Endocrinol Metab & Lipid Res, St Louis, MO USA.
   [Sun, Lulu] Washington Univ, Sch Med, Div Anat & Mol Pathol, St Louis, MO USA.
   [Saenz, Jose B.; Gyawali, C. Prakash] Washington Univ, Sch Med, Div Gastroenterol, St Louis, MO 63110 USA.
C3 Washington University (WUSTL); Washington University (WUSTL); Washington
   University (WUSTL)
RP McGill, JB (corresponding author), Div Endocrinol, Med, Campus Box 8127,660 S Euclid Ave, St Louis, MO 63110 USA.
EM jmcgill@wustl.edu
OI Muegge, Brian/0000-0002-0044-3704; Sun, Lulu/0000-0001-7543-1532
FU NIDDK NIH HHS [T32 DK101363] Funding Source: Medline
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NR 36
TC 17
Z9 17
U1 1
U2 8
PU AMER ASSOC CLINICAL ENDOCRINOLOGISTS
PI JACKSONVILLE
PA 245 RIVERSIDE AVENUE, STE 200, JACKSONVILLE, FL 32202 USA
SN 1530-891X
EI 1934-2403
J9 ENDOCR PRACT
JI Endocr. Pract.
PD NOV
PY 2017
VL 23
IS 11
BP 1297
EP 1303
DI 10.4158/EP-2017-0056
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA FP1RL
UT WOS:000417391700002
PM 29190137
DA 2025-06-01
ER

PT J
AU Miyagawa, K
   Kumamoto, K
   Shinohara, N
   Watanabe, T
   Kumei, S
   Yoneda, A
   Nebuya, S
   Koya, Y
   Oe, S
   Kume, K
   Yoshikawa, I
   Harada, M
AF Miyagawa, Koichiro
   Kumamoto, Keiichiro
   Shinohara, Nobuhiko
   Watanabe, Tatsuyuki
   Kumei, Shinsuke
   Yoneda, Akitoshi
   Nebuya, Satoru
   Koya, Yudai
   Oe, Shinji
   Kume, Keiichiro
   Yoshikawa, Ichiro
   Harada, Masaru
TI Autoimmune Pancreatitis with Gastric Cancer: Some IgG4-related Diseases
   May Be Paraneoplastic Syndrome
SO INTERNAL MEDICINE
LA English
DT Article
DE autoimmune pancreatitis; early gastric cancer; paraneoplastic syndrome
ID DIAGNOSIS; RISK; MALIGNANCIES; ASSOCIATION; MECHANISMS; CARCINOMA
AB A 70-year-old man was referred to our department for the treatment of early gastric cancer. Contrastenhanced computed tomography (CT) incidentally showed diffuse enlargement of the pancreas with a capsule-like rim, and blood tests showed elevated serum IgG4 levels, leading to a diagnosis of autoimmune pancreatitis (AIP). Endoscopic treatment for gastric cancer was performed, and pathological findings showed adenocarcinoma with abundant IgG4-positive plasma cell infiltration. Thereafter, the serum IgG4 levels normalized, and the findings of AIP disappeared on CT without steroid treatment. These findings suggest that the gastric cancer activated an IgG4-related immune response, resulting in the development of AIP.
C1 [Miyagawa, Koichiro; Kumamoto, Keiichiro; Shinohara, Nobuhiko; Watanabe, Tatsuyuki; Kumei, Shinsuke; Yoneda, Akitoshi; Nebuya, Satoru; Koya, Yudai; Oe, Shinji; Kume, Keiichiro; Harada, Masaru] Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Fukuoka, Japan.
   [Yoshikawa, Ichiro] Univ Hosp Occupat & Environm Hlth, Dept Endoscopy, Kitakyushu, Fukuoka, Japan.
C3 University of Occupational & Environmental Health - Japan; University of
   Occupational & Environmental Health - Japan
RP Miyagawa, K (corresponding author), Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Fukuoka, Japan.
EM koichiro@med.uoeh-u.ac.jp
RI Koya, Yudai/ABA-3809-2022
FU Grants-in-Aid for Scientific Research [21K07926] Funding Source: KAKEN
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NR 29
TC 6
Z9 7
U1 0
U2 2
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2022
VL 61
IS 14
BP 2155
EP 2160
DI 10.2169/internalmedicine.8590-21
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 3D2WP
UT WOS:000829168700001
PM 35850987
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Chen, WC
   Warner, RRP
   Harpaz, N
   Zhu, HF
   Roayaie, S
   Kim, MK
AF Chen, William C.
   Warner, Richard R. P.
   Harpaz, Noam
   Zhu, Hongfa
   Roayaie, Sasan
   Kim, Michelle Kang
TI Gastric Neuroendocrine Tumor and Duodenal Gastrinoma With Chronic
   Autoimmune Atrophic Gastritis
SO PANCREAS
LA English
DT Article
DE chronic autoimmune atrophic gastritis; duodenal gastrinoma; gastric
   neuroendocrine tumor
ID ZOLLINGER-ELLISON-SYNDROME; HELICOBACTER-PYLORI GASTRITIS; DIAGNOSIS;
   CARCINOIDS; GUIDELINES; FEATURES; MUCOSA
AB Our group observed the first case of synchronous gastric neuroendocrine tumor (NET) and duodenal gastrinoma with autoimmune chronic atrophic gastritis (CAG), in the absence of Helicobacter pylori infection. Demographic, clinical, endoscopic, and pathologic data were abstracted from the electronic medical record at Mount Sinai Hospital from 2013 to 2015. The patient's anonymity was carefully protected, and informed consent was obtained for publication of protected health information. A 53-year-old woman with hypertension presented to Mount Sinai Hospital in June 2013 for a second opinion for management of gastric and duodenal NETs. After evaluation by gastroenterology and surgery, repeat upper endoscopy with ultrasound and fine-needle aspiration revealed multiple diminutive type I gastric NETs and 2 duodenal NETs, against a background of autoimmune CAG, with biopsy pathology negative for H. pylori. She subsequently underwent a transduodenal resection of the duodenal NETs, confirming low-grade, gastrin-positive, stage T2 duodenal NET. On routine follow-up over the next 2 years, clinical, radiographic, and endoscopic surveillance revealed no recurrent or metastatic gastric or duodenal disease. This first report of synchronous duodenal gastrinoma and gastric NET in the setting of autoimmune CAG can broaden our understanding of gastric NET pathophysiology.
C1 [Chen, William C.] Hosp Univ Penn, Dept Med, 3400 Spruce St, Philadelphia, PA 19104 USA.
   [Warner, Richard R. P.; Kim, Michelle Kang] Icahn Sch Med Mt Sinai, Dept Med, Div Gastroenterol, One Gustave L Levy Pl,Box 1069, New York, NY 10029 USA.
   [Harpaz, Noam; Zhu, Hongfa] Icahn Sch Med Mt Sinai, Dept Pathol, Div Gastrointestinal Pathol, New York, NY 10029 USA.
   [Roayaie, Sasan] White Plains Hosp, Dept Surg, White Plains, NY USA.
C3 University of Pennsylvania; Icahn School of Medicine at Mount Sinai;
   Icahn School of Medicine at Mount Sinai
RP Kim, MK (corresponding author), Icahn Sch Med Mt Sinai, Dept Med, Div Gastroenterol, One Gustave L Levy Pl,Box 1069, New York, NY 10029 USA.
EM michelle.kim@mssm.edu
RI Harpaz, Noam/L-3411-2017
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NR 36
TC 6
Z9 7
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD JAN
PY 2019
VL 48
IS 1
BP 131
EP 134
DI 10.1097/MPA.0000000000001204
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HF2XN
UT WOS:000454100100025
PM 30531243
DA 2025-06-01
ER

PT J
AU Ji, JG
   Sundquist, J
   Sundquist, K
AF Ji, Jianguang
   Sundquist, Jan
   Sundquist, Kristina
TI Family history of autoimmune diseases and risk of gastric cancer: a
   national cohort study
SO EUROPEAN JOURNAL OF CANCER PREVENTION
LA English
DT Article
DE autoimmune disease; familial risk; gastric cancer; incidence
ID HELICOBACTER-PYLORI INFECTION; LI-FRAUMENI SYNDROME; SWEDEN; TUMORS;
   ASSOCIATIONS; METAANALYSIS; MECHANISMS; DIAGNOSIS; HISTOLOGY
AB A personal history of autoimmune diseases is associated with an increased incidence of gastric cancer, but whether they share familial susceptibility is still unknown. The contribution of shared environmental or genetic factors toward the observed familial aggregation has not been determined. We used a few Swedish registers, including the Swedish Multigeneration Register and the Cancer Register, to examine the familial risk of gastric cancer among individuals with a family history of a set of autoimmune diseases. Standardized incidence ratios were used to calculate the relative risk. The overall risk of gastric cancer was 1.22 (95% confidence interval: 1.14-1.30) among individuals with a sibling affected with any of the 33 autoimmune diseases. For specific disease, siblings of individuals with Crohn's diseases, diabetes type 1, Graves'/hyperthyroidism, myasthenia gravis, psoriasis, rheumatoid arthritis, sarcoidosis, and uncreative colitis showed an association with an increased incidence of gastric cancer, with a standardized incidence ratio ranging between 1.17 and 1.64. Familial aggregation was found only for corpus cancer. No association was observed between spouses. Gastric cancer, mainly corpus cancer, shares familial susceptibility with a few autoimmune diseases, suggesting that shared genetic polymorphisms may contribute toward both Helicobacter pylori infection and autoimmune diseases. Copyright (c) 2018 Wolters Kluwer Health, Inc. All rights reserved.
C1 [Ji, Jianguang; Sundquist, Jan; Sundquist, Kristina] Lund Univ, Ctr Primary Healthcare Res, Dept Med, Lund, Sweden.
   [Sundquist, Jan; Sundquist, Kristina] Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA USA.
C3 Lund University; Stanford University
RP Ji, JG (corresponding author), Lund Univ, CRC, Ctr Primary Healthcare Res, Jan Waldenstroms Gata 35, S-20502 Malmo, Sweden.
EM Jianguang.ji@med.lu.se
RI Ji, Jianguang/E-9579-2011
OI Ji, Jianguang/0000-0003-0324-9496
FU Swedish Research Council [K2009-70X-15428-05-3, K2012-70X-15428-08-3];
   ALF funding from Region Skane
FX This work was supported by grants to Dr Kristina Sundquist from the
   Swedish Research Council (K2009-70X-15428-05-3; K2012-70X-15428-08-3),
   as well as ALF funding from Region Skane awarded to Jan Sundquist,
   Kristina Sundquist, and Jianguang Ji. The funding agencies played no
   role in the design and conduct of the study; in the collection,
   analysis, and interpretation of the data; or in the preparation, review,
   or approval of the manuscript.
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   Zentilin P, 2002, ALIMENT PHARM THERAP, V16, P1291, DOI 10.1046/j.1365-2036.2002.01284.x
NR 34
TC 5
Z9 5
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0959-8278
EI 1473-5709
J9 EUR J CANCER PREV
JI Eur. J. Cancer Prev.
PD MAY
PY 2018
VL 27
IS 3
BP 221
EP 226
DI 10.1097/CEJ.0000000000000420
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GB4EB
UT WOS:000429012200004
PM 29334503
DA 2025-06-01
ER

PT J
AU Arslan, Ç
   Kiliçkap, S
   Yalçin, S
AF Arslan, Cagatay
   Kilickap, Saadettin
   Yalcin, Suayib
TI Gastric cancer after cadaveric liver transplantation in a patient with
   autoimmune hepatitis: A case report and review of the literature
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Gastric cancer; autoimmune hepatitis; liver transplantation;
   immunosuppressive therapy
ID DE-NOVO NEOPLASIA; RISK-FACTORS; MALIGNANCIES; EXPERIENCE; KIDNEY
AB The risk of malignancy in transplant patients is higher than in the general population. The risk is increased mostly due to immune alteration and viral infections. While the most common cancers following liver transplantation include skin cancers, lymphoma and Kaposi's sarcoma, gastric cancer is uncommon. Herein, we report a case of gastric adenocarcinoma developing three years after cadaveric liver transplantation in a patient with autoimmune hepatitis. The patient was successfully operated. The patient did not receive any adjuvant therapy, and is free of disease at 9 months' follow-up.
C1 [Arslan, Cagatay; Kilickap, Saadettin; Yalcin, Suayib] Hacettepe Univ, Inst Oncol, Dept Med Oncol, TR-06100 Ankara, Turkey.
C3 Hacettepe University
RP Arslan, Ç (corresponding author), Hacettepe Univ, Inst Oncol, Dept Med Oncol, TR-06100 Ankara, Turkey.
EM arslancagatay@yahoo.com
RI Yalcin, Suayib/KWT-7106-2024; Aksoy, Sercan/S-2480-2019; Kilickap,
   Saadettin/AAP-3732-2021
OI Kilickap, Saadettin/0000-0003-1637-7390
CR Åberg F, 2008, LIVER TRANSPLANT, V14, P1428, DOI 10.1002/lt.21475
   Baccarani U, 2006, TRANSPLANT P, V38, P1135, DOI 10.1016/j.transproceed.2006.02.016
   Benlloch S, 2004, AM J TRANSPLANT, V4, P596, DOI 10.1111/j.1600-6143.2004.00380.x
   Buell JF, 2005, TRANSPLANTATION, V80, pS254, DOI 10.1097/01.tp.0000186382.81130.ba
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   Herrero JI, 2005, LIVER TRANSPLANT, V11, P89, DOI 10.1002/lt.20319
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   Mithoefer AB, 2002, LIVER TRANSPLANT, V8, P939, DOI 10.1053/jlts.2002.35551
   Nagata Y, 2007, GASTRIC CANCER, V10, P187, DOI 10.1007/s10120-007-0428-5
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   Sarkio S, 2001, NEPHROL DIAL TRANSPL, V16, P2053, DOI 10.1093/ndt/16.10.2053
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   Spadaro Michela, 2004, Novartis Found Symp, V256, P92
   Xiol X, 2001, LIVER TRANSPLANT, V7, P971, DOI 10.1053/jlts.2001.28744
NR 19
TC 4
Z9 6
U1 0
U2 0
PU TURKISH SOC GASTROENTEROLOGY
PI ABIDINPASA
PA GAZILER SOKAK 22-1, ABIDINPASA, ANKARA 06620, TURKEY
SN 1300-4948
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD FEB
PY 2011
VL 22
IS 1
BP 73
EP 76
DI 10.4318/tjg.2011.0160
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 752RJ
UT WOS:000289710100013
PM 21480115
DA 2025-06-01
ER

PT J
AU Kitamura, S
   Muguruma, N
   Okamoto, K
   Kagemoto, K
   Kida, Y
   Mitsui, Y
   Ueda, H
   Kawaguchi, T
   Miyamoto, H
   Sato, Y
   Aoki, R
   Shunto, J
   Bando, Y
   Takayama, T
AF Kitamura, Shinji
   Muguruma, Naoki
   Okamoto, Koichi
   Kagemoto, Kaizo
   Kida, Yoshifumi
   Mitsui, Yasuhiro
   Ueda, Hiroyuki
   Kawaguchi, Tomoyuki
   Miyamoto, Hiroshi
   Sato, Yasushi
   Aoki, Rika
   Shunto, Joji
   Bando, Yoshimi
   Takayama, Tetsuji
TI Clinicopathological characteristics of early gastric cancer associated
   with autoimmune gastritis
SO JGH OPEN
LA English
DT Article
DE endoscopy; gastric cancer; stomach
ID HELICOBACTER-PYLORI INFECTION; ATROPHIC GASTRITIS
AB Background: Autoimmune gastritis is known to be associated with neoplastic lesions but the relationship between autoimmunity and tumorigenesis have not been sufficiently clarified. The aim of this study is to assess the clinicopathological characteristics of gastric cancer cases associated with autoimmune gastritis.
   Methods: A total of 24 patients diagnosed as early gastric cancer with autoimmune gastritis were registered. Chart reviews with the data including age, gender, state of Helicobacter pylori infection, comorbidity, and concomitant gastric diseases were conducted. As for the characteristics of gastric cancer, location, size, morphological type, histopathology, invasion depth, and the presence of metachronous or simultaneous lesion were assessed. These data from autoimmune gastritis group were compared with those from 301 patients of early gastric cancer as a control group.
   Results: The gastric cancer associated with autoimmune gastritis was located in the upper, middle, and lower parts in 28.1%, 53.1%, and 18.8%, respectively. The morphological types are as follows: 0-I, 9.4%; 0-IIa, 28.1%; 0-IIb, 15.6%; 0-IIc, 46.9%; and 0-III, 0.0%. The mean tumor size was 21.8 mm. While 90.6% were confined to the mucosa, 9.4% showed submucosal invasion. The histological classifications are as follows: tub1, 50.0%; tub2, 15.6%; pap, 21.9%; sig, 9.4%; and por, 3.1%. More numbers of female, protruded types, larger tumor size, papillary tumor, and that in the upper location were observed in autoimmune gastritis group compared to control group.
   Conclusion: Early gastric cancer associated with autoimmune gastritis demonstrated different characteristics from those without autoimmune gastritis including variety of tumor morphologies and histological types with female dominancy.
C1 [Muguruma, Naoki; Okamoto, Koichi; Kagemoto, Kaizo; Kida, Yoshifumi; Mitsui, Yasuhiro; Ueda, Hiroyuki; Kawaguchi, Tomoyuki; Miyamoto, Hiroshi; Sato, Yasushi; Takayama, Tetsuji] Tokushima Univ, Dept Gastroenterol & Oncol, Grad Sch Biomed Sci, 3-18-15 Kuramoto Cho, Tokushima 7708503, Japan.
   [Aoki, Rika] Tokushima Hlth Screening Ctr, Tokushima, Japan.
   [Shunto, Joji] Shunto Clin, Tokushima, Japan.
   [Bando, Yoshimi] Tokushima Univ Hosp, Div Pathol, Tokushima, Japan.
C3 Tokushima University; Tokushima University
RP Kitamura, S (corresponding author), Tokushima Univ, Dept Gastroenterol & Oncol, Grad Sch Biomed Sci, 3-18-15 Kuramoto Cho, Tokushima 7708503, Japan.
EM shinji.kitamura@tokushima-u.ac.jp
RI Muguruma, Naoki/I-6494-2019; Mitsui, Yasuhiro/GNP-1434-2022; Sato,
   Yasushi/KWT-9473-2024; Sato, Yasushi/ADU-1226-2022
OI Sato, Yasushi/0000-0002-6776-4609; Muguruma, Naoki/0000-0002-4740-4809
CR Amedei A, 2003, J EXP MED, V198, P1147, DOI 10.1084/jem.20030530
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NR 25
TC 12
Z9 12
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2397-9070
J9 JGH OPEN
JI JGH Open
PD OCT
PY 2021
VL 5
IS 10
BP 1210
EP 1215
DI 10.1002/jgh3.12656
EA SEP 2021
PG 6
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA UZ6SI
UT WOS:000696173000001
PM 34622010
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Nova-Camacho, LM
   De Burgos, S
   Diaz, IR
   Collins, K
AF Nova-Camacho, Luiz M.
   De Burgos, Saul
   Diaz, Irune Ruiz
   Collins, Katrina
TI Comprehensive clinicopathologic features in autoimmune atrophic
   gastritis: Insights from a European cohort of 57 patients
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Article; Proceedings Paper
CT Annual Meeting of the United-States-and-Canadian-Academy-of-Pathology
   (USCAP)
CY MAR 11-16, 2023
CL New Orleans, LA
SP United States & Canadian Acad Pathol
DE Autoimmune gastritis; Atrophic gastritis; Metaplasia; Neuroendocrine;
   Carcinoid; Gastric; Tumors
ID HELICOBACTER-PYLORI; RISK; DIAGNOSIS; CANCER; OLGA
AB Context: Autoimmune atrophic gastritis (AAG) is a frequently underdiagnosed disease due to its broad-spectrum clinical presentation. The diagnosis is based on histological confirmation of corpus-restricted metaplastic chronic atrophic gastritis. Objective: To thoroughly describe the histological features of a European cohort of AAG patients. Design: Clinical and pathological data of 57 out of 676 patients diagnosed with AAG were reviewed. Results: Thirty-nine patients were female and eighteen were male. The mean age was 62 years. Antibodies were identified in 32/42 patients (76 %). Vitamin B12 levels were low (< 200 pg/mL) in 37/54 patients (69 %). Serum gastrin levels was elevated (> 115 pg/mL) in all cases tested. Associated autoimmune/inflammatory conditions were identified in 20/57 patients (35 %). Histologically, deep chronic inflammation was present in 46/57 (81 %) patients. Complete destruction of oxyntic glands was observed in 45/57 (79 %) patients. Pyloric metaplasia was present in 54/57 (95 %) patients, intestinal metaplasia in 51/57 (89 %) patients, and pancreatic metaplasia in 20/57 (35 %) patients. Among ECL cell proliferation, linear hyperplasia was present in all 57/57 patients, micronodular hyperplasia in 55/57 patients, and adenomatoid hyperplasia in 10/57 patients. ECL cell dysplasia was identified in 5/57 patients, and neuroendocrine microtumor in 4/57 patients. Conclusions: The diagnosing of AAG remains challenging due to the greater variability in symptoms than previously recognized. It is important to consider chronic AAG, especially with other concurrent autoimmune conditions. The importance of accurate diagnosis and surveillance is based on the potential development of type 1 gastric neuroendocrine tumor and increased risk of gastric adenocarcinoma.
C1 [Nova-Camacho, Luiz M.; De Burgos, Saul; Diaz, Irune Ruiz] Donostia Univ Hosp, Dept Pathol, San Sebastian 20014, Spain.
   [Nova-Camacho, Luiz M.] Univ Florida, Dept Pathol Immunol & Lab Med, 1600 SW Archer Rd, Gainesville, FL 32605 USA.
   [Collins, Katrina] Indiana Univ Sch Med, Dept Pathol, Indianapolis, IN 46202 USA.
C3 University Hospital Donostia; State University System of Florida;
   University of Florida; Indiana University System; Indiana University
   Bloomington
RP Nova-Camacho, LM (corresponding author), Univ Florida, Dept Pathol Immunol & Lab Med, 1600 SW Archer Rd, Gainesville, FL 32605 USA.
EM luismi_15_16@hotmail.com
CR Annibale B, 2001, HELICOBACTER, V6, P225, DOI 10.1046/j.1083-4389.2001.00032.x
   Bergman MP, 2005, INT REV IMMUNOL, V24, P63, DOI 10.1080/08830180590884648
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NR 21
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD NOV
PY 2024
VL 263
AR 155631
DI 10.1016/j.prp.2024.155631
EA OCT 2024
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Pathology
GA I5S6B
UT WOS:001330858800001
PM 39357180
DA 2025-06-01
ER

PT J
AU Lenti, MV
   Rugge, M
   Lahner, E
   Miceli, E
   Toh, BH
   Genta, RM
   De Block, C
   Hershko, C
   Di Sabatin, A
AF Lenti, Marco Vincenzo
   Rugge, Massimo
   Lahner, Edith
   Miceli, Emanuela
   Toh, Ban-Hock
   Genta, Robert M.
   De Block, Christophe
   Hershko, Chaim
   Di Sabatin, Antonio
TI Autoimmune gastritis
SO NATURE REVIEWS DISEASE PRIMERS
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; PARIETAL-CELL ANTIBODIES; ATROPHIC BODY
   GASTRITIS; IRON-DEFICIENCY ANEMIA; THYMIC STROMAL LYMPHOPOIETIN;
   PERNICIOUS-ANEMIA; INTRINSIC-FACTOR; CANCER-RISK; FOLLOW-UP; INTESTINAL
   METAPLASIA
AB Autoimmune gastritis (AIG) is a chronic, autoimmune disease characterized by atrophy of the oxyntic glands of the stomach. In this Primer, Di Sabatino and colleagues discuss the epidemiology, novel insights in AIG pathogenesis, diagnostic challenges and current therapeutic options.
   Autoimmune gastritis (AIG) is an increasingly prevalent, organ-specific, immune-mediated disorder characterized by the destruction of gastric parietal cells, leading to the loss of intrinsic factor and reduced acid output. These alterations result in malabsorption of iron, vitamin B-12(pernicious anaemia) and potentially other micronutrients. For several years, most studies have focused on pernicious anaemia only, generating confusion between the two entities. In AIG, the gastric proton pump, H+/K(+)ATPase, is the major autoantigen recognized by autoreactive T cells. The T cell-dependent activation of B cells stimulates the production of anti-parietal cell antibodies, the serological hallmark of AIG. The role ofHelicobacter pyloriinfection in activating or favouring the autoimmune process is still uncertain. Early histopathological alterations allowing a more precise and prompt recognition have recently been described. AIG is burdened by a substantial diagnostic delay as it can present with varied clinical signs including, among others, gastrointestinal symptoms and neuropsychiatric manifestations. In advanced stages, AIG might progress to neuroendocrine tumours and gastric adenocarcinoma. Management includes early detection through a proactive case-finding strategy, micronutrient supplementation and endoscopic surveillance. This Primer comprehensively describes the most important insights regarding the epidemiology, pathophysiology, diagnosis and management of AIG, focusing on the most controversial, outstanding issues and future directions.
C1 [Lenti, Marco Vincenzo; Miceli, Emanuela; Di Sabatin, Antonio] Univ Pavia, IRCCS San Matteo Hosp Fdn, Dept Internal Med, Pavia, Italy.
   [Rugge, Massimo] Univ Padua, Dept Med DIMED, Surg Pathol & Cytopathol Unit, Padua, Italy.
   [Lahner, Edith] Sapienza Univ Rome, St Andrea Hosp, Dept Surg Med Sci & Translat Med, Digest & Liver Dis Unit, Rome, Italy.
   [Toh, Ban-Hock] Monash Univ, Fac Med Nursing & Hlth Sci, Monash Hlth, Ctr Inflammatory Dis, Clayton, Vic, Australia.
   [Genta, Robert M.] Baylor Coll Med, Michael E DeBakey VA Med Ctr, Dept Med, Houston, TX 77030 USA.
   [De Block, Christophe] Antwerp Univ Hosp, Fac Med, Dept Endocrinol Diabetol & Metab, Antwerp, Belgium.
   [De Block, Christophe] Univ Antwerp, Antwerp, Belgium.
   [Hershko, Chaim] Hebrew Univ Jerusalem, Shaare Zedek Med Ctr, Dept Hematol, Jerusalem, Israel.
   [Hershko, Chaim] Clalit Hlth Serv, Hematol Clin, Jerusalem, Israel.
   [Hershko, Chaim] Clalit Hlth Serv, Cent Clin Labs, Jerusalem, Israel.
C3 University of Pavia; IRCCS Fondazione San Matteo; University of Padua;
   Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; Monash
   Health; Monash University; Baylor College of Medicine; Baylor College
   Medical Hospital; University of Antwerp; University of Antwerp; Hebrew
   University of Jerusalem; Shaare Zedek Medical Center; Clalit Health
   Services; Clalit Health Services
RP Di Sabatin, A (corresponding author), Univ Pavia, IRCCS San Matteo Hosp Fdn, Dept Internal Med, Pavia, Italy.
EM a.disabatino@smatteo.pv.it
RI Lahner, Edith/AAM-1039-2021; De+Block, Christophe/ABE-1600-2020; Lenti,
   Marco Vincenzo/F-9044-2018
OI De Block, Christophe/0000-0002-0679-3203; Lenti, Marco
   Vincenzo/0000-0002-6654-4911; RUGGE, MASSIMO/0000-0002-0679-0563
FU University of Pavia
FX M.V.L. thanks the University of Pavia for supporting his research
   projects. The authors thank A. Vanoli and F. Capuano (both at IRCCS San
   Matteo Hospital Foundation, University of Pavia) for providing
   histopathological images of the gastric neuroendocrine tumour.
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NR 222
TC 197
Z9 207
U1 13
U2 61
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2056-676X
J9 NAT REV DIS PRIMERS
JI Nat. Rev. Dis. Primers
PD JUL 9
PY 2020
VL 6
IS 1
AR 56
DI 10.1038/s41572-020-0187-8
PG 19
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA MP1NJ
UT WOS:000551977800001
PM 32647173
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Kamada, T
   Maruyama, Y
   Monobe, Y
   Haruma, K
AF Kamada, Tomoari
   Maruyama, Yasuhiko
   Monobe, Yasumasa
   Haruma, Ken
TI Endoscopic features and clinical importance of autoimmune gastritis
SO DIGESTIVE ENDOSCOPY
LA English
DT Review
DE autoimmune gastritis; autoimmune polyendocrine syndrome;
   corpus-predominant atrophy; gastric cancer; gastric neuroendocrine tumor
ID HELICOBACTER-PYLORI INFECTION; ATROPHIC BODY GASTRITIS; WHITE GLOBE
   APPEARANCE; PERNICIOUS-ANEMIA; FOLLOW-UP; RISK-FACTOR; INTESTINAL
   METAPLASIA; MOLECULAR MIMICRY; THYROID-DISEASE; PARIETAL-CELL
AB Autoimmune gastritis (AIG) is a special type of chronic gastritis characterized by autoimmune disorders caused by cellular immunity, resulting in the destruction of parietal cells and production of antiparietal cell antibodies. Endoscopic findings of AIG are mainly characterized by corpus-dominant advanced atrophy. The antral area is generally considered to have no or mild atrophy; however, there are cases wherein the gastric mucosa is red or faded due to past infection with Helicobacter pylori or bile reflux. Currently, there are no diagnostic criteria for AIG in Japan, and it is important to make a diagnosis based on the presence of gastric autoantibodies and characteristic endoscopic and histological findings. AIG is associated with gastric cancer, neuroendocrine tumors (NETs), and other autoimmune diseases, such as thyroid diseases, anemia, and neurological symptoms due to impaired absorption of iron and vitamin B-12, and thus requires systemic treatment. The significance of diagnosing AIG is to include patients as a high-risk group for the development of gastric cancer and gastric NETs, provide an opportunity to detect autoimmune endocrine diseases, and initiate therapeutic intervention before anemia and neurological symptoms develop. It is important to pay close attention to the occurrence of AIG comorbidities not only at the time of AIG diagnosis but also during follow-up after detection.
C1 [Kamada, Tomoari] Kawasaki Med Sch, Dept Hlth Care Med, Okayama, Japan.
   [Monobe, Yasumasa] Kawasaki Med Sch, Dept Pathol, Okayama, Japan.
   [Haruma, Ken] Kawasaki Med Sch, Dept Gen Internal Med 2, Okayama, Japan.
   [Maruyama, Yasuhiko] Fujieda Municipal Gen Hosp, Dept Gastroenterol, Shizuoka, Japan.
C3 Kawasaki Medical School; Kawasaki Medical School; Kawasaki Medical
   School
RP Kamada, T (corresponding author), Kawasaki Med Sch, Dept Hlth Care Med, Kita Ku, 2-6-1 Nakasange, Okayama, Okayama 7000821, Japan.
EM tkamada@med.kawasaki-m.ac.jp
OI KAMADA, TOMOARI/0000-0001-6195-2513
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NR 106
TC 39
Z9 45
U1 6
U2 33
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0915-5635
EI 1443-1661
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD MAY
PY 2022
VL 34
IS 4
BP 700
EP 713
DI 10.1111/den.14175
EA NOV 2021
PG 14
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 1A1UF
UT WOS:000716791900001
PM 34674318
OA Bronze
DA 2025-06-01
ER

PT J
AU Obata, Y
   Takahashi, T
   Sakamoto, J
   Tamaki, H
   Tominaga, S
   Hamajima, N
   Chen, YT
   Old, LJ
AF Obata, Y
   Takahashi, T
   Sakamoto, J
   Tamaki, H
   Tominaga, S
   Hamajima, N
   Chen, YT
   Old, LJ
TI SEREX analysis of gastric cancer antigens
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article; Proceedings Paper
CT 15thy Bristol-Myers Squibb Nagoya International Cancer Treatment
   Symposium
CY SEP 10-11, 1999
CL NAGOYA, JAPAN
DE cancer antigen; gastric cancer; autologous serum; expression cloning;
   SEREX
ID HUMAN TUMOR-ANTIGENS; IMMUNE-RESPONSE; HUMAN-MELANOMA; CANCER/TESTIS
   ANTIGENS; AUTOLOGOUS ANTIBODIES; MOLECULAR DEFINITION; METASTATIC
   MELANOMA; T-LYMPHOCYTES; GENE; IDENTIFICATION
AB Stomach cancer is the major malignancy in Japan and one of the most common cancers worldwide. To establish the basis for an immunotherapeutic approach to stomach cancer, we have initiated an analysis of stomach cancer antigens recognized by human immunoglobulin G (IgG) antibodies using SEREX, a powerful expression cloning method developed by Dr. M. Pfreundschuh's group. Five stomach cancer cDNA libraries have been screened with autologous patient sera: one moderately differentiated adenocarcinoma; two poorly differentiated adenocarcinomas; and two scirrhous-type poorly differentiated adenocarcinomas of Borrmann type 4, the most devastating form of stomach cancer. Based on the reactivities of clones with autologous IgG antibodies, an average of 50 independent clones from each library and a total of 297 clones were isolated. DNA sequencing revealed that these 297 clones were derived from 136 different genes. Comparison of the 136 genes to sequences in DNA databases showed that 95 are previously identified genes and 41 are newly identified in this study. The antigens are derived from various genes including a chimeric gene between E-cadherin and an unknown gene Y, AKT oncogene, genes overexpressed in stomach cancers, genes of which the transcripts are alternatively or aberrantly spliced, and genes known to be involved in autoimmune diseases. Thus stomach cancer patients can generate an immune response against a surprisingly diverse set of gene products. To identify antigens potentially useful in the diagnosis and therapy of gastric cancer, all 136 genes were tested for their reactivities with a panel of sera from 44 gastric cancer patients (17 women and 27 men, aged 35-81 years) and with a panel of sera from 100 control individuals with no previous history of cancer but some of whom had gastritis (55 women and 45 men, aged 30-69 years). Eleven antigens showed reactivity only with a certain proportion of cancer patient sera but not with any control sera. An additional 12 antigens elicited antibody production at a much higher frequency in cancer patients than in control individuals. To evaluate the clinical usefulness of these antigens we are now examining their expression in normal and malignant tissues.
C1 Aichi Canc Ctr, Res Inst, Immunol Lab, Chikusa Ku, Nagoya, Aichi 4648681, Japan.
   Aichi Canc Ctr Hosp, Dept Genet & Pathol, Chikusa Ku, Nagoya, Aichi 464, Japan.
   Aichi Prefectural Hosp, Okazaki, Aichi, Japan.
   Aichi Canc Ctr, Res Inst, Lab Epidemiol, Chikusa Ku, Nagoya, Aichi 464, Japan.
   Cornell Univ, Coll Med, Dept Pathol, New York, NY USA.
   Ludwig Inst Canc Res, New York, NY USA.
C3 Aichi Cancer Center; Aichi Cancer Center; Aichi Cancer Center; Cornell
   University; Ludwig Institute for Cancer Research
RP Obata, Y (corresponding author), Aichi Canc Ctr, Res Inst, Immunol Lab, Chikusa Ku, 1-1 Kanokoden, Nagoya, Aichi 4648681, Japan.
RI Hamajima, Nobuyuki/I-7237-2014; Obata, Yuichi/A-5300-2016
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NR 33
TC 20
Z9 24
U1 0
U2 2
PU SPRINGER-VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD JUN
PY 2000
VL 46
SU S
BP S37
EP S42
DI 10.1007/PL00014048
PG 6
WC Oncology; Pharmacology & Pharmacy
WE Conference Proceedings Citation Index - Science (CPCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA 340KY
UT WOS:000088532700009
PM 10950146
DA 2025-06-01
ER

PT J
AU Ahn, S
   Kim, TS
   Kushima, R
   Lee, JH
   Kim, KM
AF Ahn, Soomin
   Kim, Tae-Se
   Kushima, Ryoji
   Lee, Jun Haeng
   Kim, Kyoung-Mee
TI Autoimmune Gastritis in Korean Patients with Gastric Tumors:
   Clinicopathologic Correlations and Diagnostic Histological Features
SO GUT AND LIVER
LA English
DT Article
DE Stomach neoplasms; Autoimmune diseases; Gastritis; atrophic; Diagnosis
ID PARIETAL-CELL ANTIBODIES; ATROPHIC GASTRITIS; CLASSIFICATION
AB Background/Aims: Autoimmune gastritis (AIG) is a corpus-dominant atrophic gastritis in which patients are positive for antiparietal cell antibody (APCA) and/or anti-intrinsic factor antibody. The risk of developing gastric cancer in patients with AIG remains unclear, and reliable frequency data of AIG in patients with gastric cancer are lacking. Methods: We included 624 Korean patients with gastric tumors (612 gastric cancers and 12 neuroendocrine tumors) who had APCA results and were available for AIG evaluation. In patients with positive APCA results, endoscopy and histology findings were reviewed to diagnose AIG. Results: Of the 624 patients, 37 (5.9%) tested positive for APCA, and ultimately, 11 (1.8%) met the diagnostic criteria for AIG (5 both endoscopy and histology findings, 4 endoscopy-only findings, 2 histology-only findings). The frequency of AIG in patients with gastric cancer was 1.3% (8/612), and that in patients with neuroendocrine tumors was 25.0% (3/12). Of the 11 patients with AIG, serum Helicobacter pylori antibody was positive in six patients (54.5%), all of whom had gastric cancer. Histologically, three patients showed pure AIG, four patients exhibited concurrent AIG and H. pylori gastritis, and the findings for four were indefinite for AIG. The pepsinogen (PG) I levels and PG I/II ratio were significantly lower in patients with gastric cancer with AIG than in patients with gastric cancer without AIG (p=0.042 and p=0.016, respectively). Conclusions: The frequency of AIG in gastric cancer patients was very low compared to that in patients with neuroendocrine tumors. Rather, concurrent AIG and H. pylori gastritis was common in patients with AIG with gastric cancer. (Gut Liver 2025;19:177-188)
C1 [Ahn, Soomin; Kim, Kyoung-Mee] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Kim, Tae-Se; Lee, Jun Haeng] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Med, Seoul, South Korea.
   [Kushima, Ryoji] Shiga Univ Med Sci, Dept Pathol, Otsu, Japan.
C3 Sungkyunkwan University (SKKU); Samsung Medical Center; Sungkyunkwan
   University (SKKU); Samsung Medical Center; Shiga University of Medical
   Science
RP Kim, KM (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol & Translat Genom, Seoul, South Korea.; Lee, JH (corresponding author), Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Med, Seoul, South Korea.
EM stomachlee@gmail.com; kkmkys@skku.edu
OI Kim, Kyoung Mee/0000-0002-1162-9205; Ahn, Soo Min/0000-0002-2854-5032
FU Bio and Medical Tech-nology Development Program of the National Research
   Foundation (NRF) - Korean government (MSIT) [RS-2023-00222838]
FX This study was supported by the Bio and Medical Tech-nology Development
   Program of the National Research Foundation (NRF) , funded by the Korean
   government (MSIT) (No. RS-2023-00222838) to S.A.
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NR 38
TC 1
Z9 1
U1 1
U2 1
PU EDITORIAL OFFICE GUT & LIVER
PI SEOUL
PA 305 LOTTE GOLD ROSE II, 890-59, DAECHI 4-DONG, GANGNAM-GU, SEOUL,
   135-839, SOUTH KOREA
SN 1976-2283
EI 2005-1212
J9 GUT LIVER
JI Gut Liver
PD MAR
PY 2025
VL 19
IS 2
BP 177
EP 188
DI 10.5009/gnl240223
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 0HQ3N
UT WOS:001447591600001
PM 39506312
OA gold
DA 2025-06-01
ER

PT J
AU Gaur, K
   Saran, RK
   Batra, VV
   Sakhuja, P
   Mishra, PK
AF Gaur, Kavita
   Saran, Ravindra Kumar
   Batra, Vineeta Vijay
   Sakhuja, Puja
   Mishra, Pramod Kumar
TI Is thyrogastric disease a potential setting for oncogenesis? Gastric
   adenoneuroendocrine carcinoma arising from Helicobacter
   pylori-associated atrophic gastritis in a patient with autoimmune
   thyroiditis
SO ROMANIAN JOURNAL OF MORPHOLOGY AND EMBRYOLOGY
LA English
DT Article
DE carcinoma; neuroendocrine; Helicobacter pylori; gastritis; atrophic
ID INFECTION; STOMACH; ENTITY; LIPOPOLYSACCHARIDE; ADENOCARCINOMA;
   POPULATION; TUMOR
AB Gastric mixed adenoneuroendocrine carcinoma arising from Helicobacter pylori-associated multifocal atrophic gastritis is exceedingly rare. An added association with autoimmune thyroiditis in this case highlighted a complex interplay between Helicobacter, autoimmunity and gastric atrophy. A 55-year-old hypothyroid female presented with hematemesis and a large polypoidal mass in the gastric fundus, suggestive of gastrointestinal stromal tumor on imaging and endoscopy. Histopathology revealed a tumor comprised of nests of monomorphic cells immunopositive for synaptophysin and chromogranin A admixed with malignant glands. Follow-up imaging revealed a heterogeneously enhancing residual gastric body wall. A completion total gastrectomy was performed. Histopathology displayed multifocal atrophic gastritis, occasional Helicobacter and nests of neuroendocrine cells. The patient also had markedly elevated levels of anti-thyroid peroxidase and anti-thyroglobulin. To the best of our knowledge, this is the first case of gastric adenoneuroendocrine carcinoma arising from H. pylori associated atrophic gastritis, in a patient with autoimmune thyroiditis.
C1 [Gaur, Kavita; Saran, Ravindra Kumar; Batra, Vineeta Vijay; Sakhuja, Puja] Govind Ballabh Pant Inst Postgrad Med Educ & Res, Dept Pathol, 1 Jawaharlal Nehru Marg,Acad Block,Room 333, New Delhi 110002, India.
   [Mishra, Pramod Kumar] Govind Ballabh Pant Inst Postgrad Med Educ & Res, Dept Gastrointestinal Surg, New Delhi, India.
C3 Govind Ballabh Pant Institute of Postgraduate Medical Education &
   Research; Govind Ballabh Pant Institute of Postgraduate Medical
   Education & Research
RP Saran, RK (corresponding author), Govind Ballabh Pant Inst Postgrad Med Educ & Res, Dept Pathol, 1 Jawaharlal Nehru Marg,Acad Block,Room 333, New Delhi 110002, India.
EM ravindraksaran@hotmail.com
CR Adhikari D, 2002, ANN CLIN LAB SCI, V32, P422
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NR 25
TC 0
Z9 0
U1 0
U2 0
PU EDITURA ACAD ROMANE
PI BUCURESTI
PA CALEA 13 SEPTEMBRIE NR 13, SECTOR 5, BUCURESTI 050711, ROMANIA
SN 1220-0522
J9 ROM J MORPHOL EMBRYO
JI Rom. J. Morphol. Embryol.
PY 2017
VL 58
IS 4
BP 1491
EP 1496
PG 6
WC Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology
GA GA9KO
UT WOS:000428660300045
PM 29556646
DA 2025-06-01
ER

PT J
AU Liu, KT
   Chan, HM
   Lin, TJ
AF Liu, Kuan-Ting
   Chan, Hon-Man
   Lin, Tzeng-Jih
TI An unusual presentation of metastatic gastric adenocarcinoma - Acute
   onset of right neck swelling
SO JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
LA English
DT Article
DE central vein; gastric cancer; malignancy; thrombosis
ID JUGULAR-VEIN-THROMBOSIS
AB Central venous thrombosis is an uncommon problem associated with malignancy. We present here a 53-year-old male who visited the emergency room because of right neck swelling. Fluid accumulation over deep neck space led to the diagnosis of suspected hemorrhage, and central venous thrombosis was found by computed tomography. This patient had no other precipitating cause. Autoimmune disorders, hypercoagulation and malignancy surveys were performed during hospitalization. Elevated serum tissue polypeptide antigen and CA130 were noted, and multiple liver metastases were found by another computed tomography. Subsequently, gastric adenocarcinoma was confirmed after gastroendoscopy. Gastric adenocarcinoma with distal metastases was finally diagnosed. This case reminds us that central venous thrombosis is a sign of many diseases. Malignancy, including gastric adenocarcinoma, is one of the causes that should be considered.
C1 Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Emergency Med, Kaohsiung 807, Taiwan.
   Kaohsiung Med Univ, Coll Med, Fac Med, Kaohsiung, Taiwan.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Medical University
RP Lin, TJ (corresponding author), Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Emergency Med, 100 Shih Chuan 1st Rd, Kaohsiung 807, Taiwan.
EM ttiinngg@ms2.hinet.net
RI liu, kt/AFU-9413-2022; Lin, Tzeng-Jih/D-5026-2009
OI Liu, Kuan-Ting/0000-0002-1355-5019
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NR 9
TC 1
Z9 1
U1 0
U2 0
PU ELSEVIER TAIWAN
PI TAIPEI
PA RM N-412, 4F, CHIA HSIN BUILDING 11, NO 96, ZHONG SHAN N ROAD SEC 2,
   TAIPEI, 10449, TAIWAN
SN 0929-6646
EI 1876-0821
J9 J FORMOS MED ASSOC
JI J. Formos. Med. Assoc.
PD JUL
PY 2007
VL 106
IS 7
BP 589
EP 591
DI 10.1016/S0929-6646(07)60011-4
PG 3
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 197UT
UT WOS:000248582700011
PM 17660150
DA 2025-06-01
ER

PT J
AU Massironi, S
   Zilli, A
   Elvevi, A
   Invernizzi, P
AF Massironi, Sara
   Zilli, Alessandra
   Elvevi, Alessandra
   Invernizzi, Pietro
TI The changing face of chronic autoimmune atrophic gastritis: an updated
   comprehensive perspective
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Atrophic autoimmune gastritis; Pernicious anemia; Gastric carcinoids;
   Gastric neuroendocrine tumors; Gastric adenocarcinoma; OLGA; OLGIM
ID PARIETAL-CELL ANTIBODIES; PERNICIOUS-ANEMIA; FOLLOW-UP; COBALAMIN
   DEFICIENCY; HELICOBACTER-PYLORI; RISK-FACTORS; THYROID-DISEASE;
   IRON-DEFICIENCY; CHROMOGRANIN-A; BODY GASTRITIS
AB Chronic autoimmune atrophic gastritis (CAAG) is an organ-specific autoimmune disease, which affects the corpus fundus gastric mucosa. Although it has been described for several years, the real pathophysiological mechanisms, the natural history and the possible neoplastic complications are not completely known. Atrophy of the gastric mucosa is the endpoint of the chronic processes, with the loss of glandular cells and their replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. As a consequence, hydrochloric acid, pepsin and intrinsic-factor is impaired resulting in pernicious anemia. The exact causal agent is not yet known, but both genetic and environmental factors seem to play a decisive role.
   Moreover, the clinical onset may assume different characteristics; differently from what previously observed, recent evidence has reported the onset of CAAG at a younger age, frequently with iron deficiency anemia or upper gastro-intestinal symptoms.
   The diagnosis of CAAG might be challenging and usually requires the combination of clinical, serological and histopathologic data; moreover, CAAG patients are often misdiagnosed as refractory to HP eradication therapy, probably because achlorhydria might allow urease-positive bacteria other than H pylori to colonize the stomach, causing positive C-13-urea breath test results.
   However, biopsy is the most reliable method to evaluate the presence of metaplastic atrophic gastritis. In order to assess the severity of gastric atrophy and intestinal metaplasia, OLGA and OLGIM staging systems have been proposed and seem to correlate with the risk of developing gastric adenocarcinoma. Indeed, CAAG represents a pre-neoplastic condition, as patients with CAAG are very likely to develop either type-1 gastric neuroendocrine tumors and gastric adenocarcinomas, as well as several other neoplastic diseases. To date, the need, the intervals and cost-effectiveness of endoscopic/histological surveillance for patients with CAAG/pernicious anemia are yet to be established.
C1 [Massironi, Sara; Zilli, Alessandra] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, Via F Sforza 35, I-20122 Milan, Italy.
   [Elvevi, Alessandra; Invernizzi, Pietro] Univ Milano Bicocca, Dept Med & Surg, ASST San Gerardo Hosp, Div Gastroenterol, Monza, Italy.
   [Elvevi, Alessandra; Invernizzi, Pietro] Univ Milano Bicocca, Dept Med & Surg, ASST San Gerardo Hosp, Ctr Autoimmune Liver Dis, Monza, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of
   Milano-Bicocca; University of Milano-Bicocca
RP Massironi, S (corresponding author), Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, Via F Sforza 35, I-20122 Milan, Italy.
EM sara.massironi@libero.it
RI Invernizzi, Pietro/AAB-8367-2022; Massironi, Sara/X-2547-2019
OI Massironi, Sara/0000-0003-3214-8192
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NR 104
TC 102
Z9 120
U1 2
U2 39
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD MAR
PY 2019
VL 18
IS 3
BP 215
EP 222
DI 10.1016/j.autrev.2018.08.011
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA HO9EF
UT WOS:000461263500001
PM 30639639
DA 2025-06-01
ER

PT J
AU Chen, Y
   Ji, XW
   Zhao, WY
   Lin, J
   Xie, SY
   Xu, JH
   Mao, JS
AF Chen, Yu
   Ji, Xiaowei
   Zhao, Weiyi
   Lin, Jie
   Xie, Siyuan
   Xu, Jinghong
   Mao, Jianshan
TI A real-world study on the characteristics of autoimmune gastritis: A
   single-center retrospective cohort in China
SO CLINICS AND RESEARCH IN HEPATOLOGY AND GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune gastritis; Iron-deficiency anemia; Pernicious anemia; Gastric
   neuroendocrine tumors; Gastric adenocarcinoma
ID ATROPHIC GASTRITIS; DIAGNOSIS
AB Background and Aim: Autoimmune gastritis (AIG) was previously considered a rare disease in China, and its clinical characteristics were not fully understood. This study aimed to demonstrate the characteristics of AIG in China and evaluate gastric oxyntic mucosal atrophy using a modified AIG-atrophic staging. Methods: This was a single-center retrospective observational real-world study. The diagnosis of AIG was based on pathological results combined with parietal cell antibody (PCA) and intrinsic factor antibody (IFA) results, and endoscopic findings. Results: A total of 745 patients were enrolled, the median age at diagnosis was 58 years old, and 69.9 % were female. The symptoms of AIG patients were nonspecific, and about 2/5 of the cases were asymptomatic. The proportions of cases from modified AIG-atrophic stage 1 to 4 were 0.8 %, 14.1 %, 73.8 %, and 11.3 %, respectively. Approximately 1/5 had autoimmune thyroiditis (AITD). Near 1/2 had one or more comorbidities: iron-deficiency anemia (IDA), pernicious anemia (PA), neuropathy, gastric hyperplastic polyps (GHP), gastric intraepithelial neoplasia (GIN), type 1 gastric neuroendocrine tumors (g-NET), or gastric adenocarcinoma (GAC). There was a high risk of type 1 g-NET (7.0 %) and GAC (9.1 %) in AIG patients. Conclusions: AIG is not rare in China, and its early diagnosis is challenging, accompanied by a high risk of GAC. The modified four-stage AIG-atrophic staging can effectively represent the extent of oxyntic mucosal atrophy and the progression in AIG.
C1 [Chen, Yu; Ji, Xiaowei; Lin, Jie; Xie, Siyuan; Mao, Jianshan] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Gastroenterol, Hangzhou, Peoples R China.
   [Zhao, Weiyi; Xu, Jinghong] Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Pathol, Hangzhou, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP Mao, JS (corresponding author), Zhejiang Univ, Affiliated Hosp 2, Sch Med, Dept Gastroenterol, Hangzhou, Peoples R China.
EM jshmao@zju.edu.cn
RI Xie, Siyuan/LFV-4129-2024; Zhao, Weiyi/LUY-3083-2024; Xu,
   Jinghong/JPK-2139-2023
FU National Nature Science Fund from National Nature Science Foundation of
   China [81372348]
FX This work was supported by National Nature Science Fund from National
   Nature Science Foundation of China (81372348) .
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NR 38
TC 0
Z9 0
U1 2
U2 2
PU ELSEVIER MASSON, CORP OFF
PI PARIS
PA 65 CAMILLE DESMOULINS CS50083 ISSY-LES-MOULINEAUX, 92442 PARIS, FRANCE
SN 2210-7401
EI 2210-741X
J9 CLIN RES HEPATOL GAS
JI Clin. Res. Hepatol. Gastroenterol.
PD APR
PY 2025
VL 49
IS 4
AR 102556
DI 10.1016/j.clinre.2025.102556
EA FEB 2025
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA Y2J6W
UT WOS:001430457200001
PM 39961485
DA 2025-06-01
ER

PT J
AU Kawai, H
   Sarai, M
   Toyama, H
   Izawa, H
AF Kawai, Hideki
   Sarai, Masayoshi
   Toyama, Hiroshi
   Izawa, Hideo
TI Activation of cardiac sarcoidosis associated with development of gastric
   cancer: a case report
SO EUROPEAN HEART JOURNAL-CASE REPORTS
LA English
DT Article
DE Case report; Cardiac sarcoidosis; PET-CT; F-18-FDG; Malignant tumour
ID POSITRON-EMISSION-TOMOGRAPHY; SERIAL FDG-PET
AB Background The high F-18-fluorodeoxyglucose (FDG) uptake in sarcoidosis lesions reflects infiltration of inflammatory cells such as macrophages. An increased incidence of cancer in patients with sarcoidosis has been suggested, and some combination of the following mechanisms has been proposed: chronic inflammation, immune dysfunction, shared aetiologic agents, and genetic susceptibility to both cancer and autoimmune diseases.
   Case summary A 73-year-old man was admitted to our hospital due to effort dyspnoea. Initial investigations showed complete atrioventricular block on electrocardiography, basal thinning of the interventricular septum, and preserved left ventricular (LV) systolic function on echocardiography, and late gadolinium enhancement (LGE) in all layers of the basal interventricular septum on cardiac magnetic resonance imaging. FDG positron emission tomography/computerized tomography (FDG-PET/CT) showed no abnormal uptake in the whole-body including myocardium. After discussion, corticosteroid was not initiated then. One year later, he developed stomach adenocarcinoma. Repeated investigations demonstrated enlargement of the LV (LV diastolic diameter 63 mm) and diffuse systolic impairment of LV function (LV ejection fraction 31%) on echocardiography, and abnormal focal uptake at the lateral walls of LV and hilar lymph nodes on FDG-PET/CT imaging. One more year after the surgery for gastric cancer and corticosteroid initiation, echocardiography showed recovery of systolic function and FDG-PET/CT showed no uptake in either the myocardium or hilar lymph nodes.
   Discussion In the present case, it is speculated that the first inflammation which left scarred areas showing LGE was already completed before the first FDG-PET/CT. The development of gastric cancer may be associated with the reactivation of cardiac sarcoidosis.
C1 [Kawai, Hideki; Sarai, Masayoshi; Izawa, Hideo] Fujita Hlth Univ, Dept Cardiol, 1-98 Dengakugakubo, Toyoake, Aichi, Japan.
   [Toyama, Hiroshi] Fujita Hlth Univ, Dept Radiol, 1-98 Dengakugakubo, Toyoake, Aichi, Japan.
C3 Fujita Health University; Fujita Health University
RP Kawai, H (corresponding author), Fujita Hlth Univ, Dept Cardiol, 1-98 Dengakugakubo, Toyoake, Aichi, Japan.
EM hkawai@fujita-hu.ac.jp
RI Kawai, Hideki/HJI-7311-2023
OI Sarai, Masayoshi/0000-0001-6621-4325; Kawai, Hideki/0000-0003-2924-3615;
   Izawa, Hideo/0000-0003-2136-2855
CR Bennett MK, 2013, CIRC-HEART FAIL, V6, P676, DOI 10.1161/CIRCHEARTFAILURE.112.000087
   Bonifazi M, 2015, CHEST, V147, P778, DOI 10.1378/chest.14-1475
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NR 10
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
EI 2514-2119
J9 EUR HEART J-CASE REP
JI Eur. Heart J.-Case Rep.
PD FEB
PY 2021
VL 5
IS 2
DI 10.1093/ehjcr/ytaa558
EA JAN 2021
PG 5
WC Cardiac & Cardiovascular Systems
WE Emerging Sources Citation Index (ESCI)
SC Cardiovascular System & Cardiology
GA RV8HH
UT WOS:000646067400054
PM 33738412
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Miyatani, K
   Saito, H
   Murakami, Y
   Watanabe, J
   Kuroda, H
   Matsunaga, T
   Fukumoto, Y
   Osaki, T
   Nakayama, Y
   Umekita, Y
   Ikeguchi, M
AF Miyatani, Kozo
   Saito, Hiroaki
   Murakami, Yuki
   Watanabe, Joji
   Kuroda, Hirohiko
   Matsunaga, Tomoyuki
   Fukumoto, Yoji
   Osaki, Tomohiro
   Nakayama, Yuji
   Umekita, Yoshihisa
   Ikeguchi, Masahide
TI A high number of IgG4-positive cells in gastric cancer tissue is
   associated with tumor progression and poor prognosis
SO VIRCHOWS ARCHIV
LA English
DT Article
DE B cell; Gastric cancer; IgG4; prognosis
ID REGULATORY T-CELLS; AUTOIMMUNE PANCREATITIS; HELICOBACTER-PYLORI; IGG4
   PRODUCTION; MECHANISMS; EXPRESSION; IDENTIFICATION; RECRUITMENT;
   TOLERANCE; NIVOLUMAB
AB IgG4-related disease is a newly defined disease characterized by elevated serum IgG4 levels and infiltration of affected organs by IgG4-positive plasma cells. Recently, increased IgG4 levels were reported to be closely related with malignancy. To assess the relationship between IgG4 and the progression of gastric cancer, we immunohistochemically stained in this study gastric cancer tissue samples for IgG4-positive cells using an anti-IgG4 antibody. In addition, pre- and postoperative serum concentrations of IgG4 were measured, using an enzyme-linked immunosorbent assay. In gastric cancer samples, the number of CD138-positive plasma cells was significantly lower and the number of IgG4-positive cells significantly higher than in non-cancerous gastric mucosa. The number of IgG4-positive cells was significantly correlated with gross tumor appearance, tumor depth, lymph node metastasis, venous invasion, and lymphatic invasion. Prognosis was significantly poorer in patients with a high number of IgG4-positive cells than in those with a low number. Multivariate analysis indicated that both the number of IgG4-positive cells and the depth of tumor invasion were independently prognostic of survival. In conclusion, in gastric cancer, the number of IgG4-positive cells is increased and this is closely associated with gastric cancer progression.
C1 [Miyatani, Kozo; Saito, Hiroaki; Murakami, Yuki; Watanabe, Joji; Kuroda, Hirohiko; Matsunaga, Tomoyuki; Fukumoto, Yoji; Osaki, Tomohiro; Ikeguchi, Masahide] Tottori Univ, Dept Surg, Div Surg Oncol, Sch Med, 36-1 Nishi Cho, Yonago, Tottori 6838504, Japan.
   [Nakayama, Yuji] Tottori Univ, Div Funct Genom, Res Ctr Biosci & Technol, Yonago, Tottori 6838503, Japan.
   [Umekita, Yoshihisa] Tottori Univ, Div Organ Pathol, Dept Pathol, Sch Med, Yonago, Tottori 6838503, Japan.
C3 Tottori University; Tottori University; Tottori University
RP Saito, H (corresponding author), Tottori Univ, Dept Surg, Div Surg Oncol, Sch Med, 36-1 Nishi Cho, Yonago, Tottori 6838504, Japan.
EM kozo0427@med.tottori-u.ac.jp; sai10@med.tottori-u.ac.jp;
   ymurakami@med.tottori-u.ac.jp; watanabe.j@med.tottori-u.ac.jp;
   kurodahmt@med.tottori-u.ac.jp; matut0m0@med.tottori-u.ac.jp;
   y-fukumoto@med.tottori-u.ac.jp; t-osaki@med.tottori-u.ac.jp;
   yujin@med.tottori-u.ac.jp; yume@med.tottori-u.ac.jp;
   ikeguchim@pref.tottori.jp
OI Miyatani, Kozo/0000-0003-3040-7576
FU Grants-in-Aid for Scientific Research [15K06896] Funding Source: KAKEN
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NR 43
TC 26
Z9 30
U1 0
U2 9
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0945-6317
EI 1432-2307
J9 VIRCHOWS ARCH
JI Virchows Arch.
PD MAY
PY 2016
VL 468
IS 5
BP 549
EP 557
DI 10.1007/s00428-016-1914-0
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DL5ZX
UT WOS:000375717200004
PM 26951261
DA 2025-06-01
ER

PT J
AU Gladdy, RA
   Strong, VE
   Coit, D
   Allen, PJ
   Gerdes, H
   Shia, J
   Klimstra, DS
   Brennan, MF
   Tang, LH
AF Gladdy, Rebecca A.
   Strong, Vivian E.
   Coit, Daniel
   Allen, Peter J.
   Gerdes, Hans
   Shia, Jinru
   Klimstra, David S.
   Brennan, Murray F.
   Tang, Laura H.
TI Defining Surgical Indications for Type I Gastric Carcinoid Tumor
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID PRECURSOR LESIONS; PERNICIOUS-ANEMIA; CELL TUMOR; MANAGEMENT; RESECTION;
   STOMACH; ANTRECTOMY
AB Most gastric carcinoid tumors (GC) (type I) occur in association with achlorhydria, hypergastrinemia, atrophic gastritis and exhibit low-grade histopathology. The management of this indolent disease is controversial. The aim of this study was to evaluate endoscopic surveillance (ES) compare with surgical resection (SR) for type I GC.
   Between 1985 and 2007, 65 patients with type I GC were identified. Data analysis included: demographics, biochemical and endoscopic assessment, type of operation performed, and pathologic evaluation. The primary endpoints were disease-specific survival (DSS) in both groups and recurrence-free survival (RFS) in SR patients.
   Median follow-up was 30 months (range 1-176 months); most patients were female (83%) with median age of 58 years (range 29-91 years). Type I GC was diagnosed by evidence of hypergastrinemia and/or positive autoimmune antibodies with histopathologic confirmation. Patients underwent ES with polypectomy (n = 46) or gastric resection (n = 19). SR was performed with larger tumor size, increased depth of invasion, and solitary tumors. Although the 5-year RFS in SR patients was 75%, the DSS in both groups was 100%. However, concomitant adenocarcinoma was identified in 4/19 resected cases; 2/4 were detected on preoperative biopsies. All cases with coexisting gastric adenocarcinoma had larger carcinoid tumors and more advanced carcinoid disease.
   The DSS is excellent for type I GC patients treated with either ES or SR. SR should be considered with more advanced carcinoid disease given its association with an increased risk of adenocarcinoma. ES is appropriate to assess both the status of carcinoid disease and dysplasia or adenocarcinoma that can develop in association with type I GC.
C1 [Shia, Jinru; Klimstra, David S.; Tang, Laura H.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
   [Gladdy, Rebecca A.; Strong, Vivian E.; Coit, Daniel; Allen, Peter J.; Brennan, Murray F.] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA.
   [Gerdes, Hans] Mem Sloan Kettering Canc Ctr, Dept Gastroenterol, New York, NY 10021 USA.
C3 Memorial Sloan Kettering Cancer Center; Memorial Sloan Kettering Cancer
   Center; Memorial Sloan Kettering Cancer Center
RP Tang, LH (corresponding author), Mem Sloan Kettering Canc Ctr, Dept Pathol, 1275 York Ave, New York, NY 10021 USA.
EM tangl@mskcc.org
RI ; Gladdy, Rebecca/A-2516-2013
OI Shia, Jinru/0000-0002-4351-2511; Gladdy, Rebecca/0000-0003-4143-6620;
   Brennan, Murray/0000-0003-2358-4371
FU Raymond and Beverley Sackler Foundation
FX This work was partially supported by Raymond and Beverley Sackler
   Foundation.
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NR 36
TC 69
Z9 72
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1068-9265
EI 1534-4681
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD NOV
PY 2009
VL 16
IS 11
BP 3154
EP 3160
DI 10.1245/s10434-009-0687-y
PG 7
WC Oncology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Surgery
GA 510LE
UT WOS:000271089200025
PM 19727959
DA 2025-06-01
ER

PT J
AU Zhang, B
   Rong, GH
   Wei, HF
   Zhang, M
   Bi, JW
   Ma, LY
   Xue, XC
   Wei, G
   Liu, XK
   Fang, GE
AF Zhang, Bin
   Rong, Guanghua
   Wei, Huafeng
   Zhang, Meng
   Bi, Jianwei
   Ma, Liye
   Xue, Xuchao
   Wei, Guo
   Liu, Xiaokang
   Fang, Guoen
TI The prevalence of Th17 cells in patients with gastric cancer
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE Th17 cells; IL-17; IL-23; RORC; gastric cancer
ID GROWTH-FACTOR-BETA; REGULATORY T-CELLS; INFILTRATING LYMPHOCYTES; T-H-17
   CELLS; LUNG-CANCER; IL-17; RECEPTOR; DIFFERENTIATION; EXPRESSION; T(H)17
AB Th17 cells have emerged as an important mediator in inflammatory and autoimmune diseases. However, recent studies Suggest a potential impact of Th17 cells on tuition The current study was designed to investigate the possible involvement of Th17 cells in gastric cancer. Compared with healthy Volunteers, patients with gastric cancer had a higher proportion of Th17 cells in peripheral blood. Notably, the increased prevalence of Th17 cells was associated with clinical stage. In addition, increased populations of Th17 cells were present in tumor-draining lymph nodes with advanced disease. Furthermore the, mRNA expression levels of Th17-related factors (IL-17, IL-23p19, and RORC) in tumor tissues and the serum concentrations of IL-17 and IL-23 cytokines were significantly increased in patients with advanced gastric cancer. The results indicate that Th17 cells may contribute to gastric cancer pathogenesis. (C) 2008 Elsevier Inc. All rights reserved.
C1 [Zhang, Bin; Bi, Jianwei; Ma, Liye; Xue, Xuchao; Wei, Guo; Liu, Xiaokang; Fang, Guoen] Second Mil Med Univ, Changhai Hosp, Dept Gen Surg, Shanghai 200433, Peoples R China.
   [Rong, Guanghua] Second Mil Med Univ, Changzheng Hosp, Dept Lab Med, Shanghai 200003, Peoples R China.
   [Wei, Huafeng] Second Mil Med Univ, Int Joint Canc Inst, Shanghai 200433, Peoples R China.
   [Zhang, Meng] Second Artillary Gen Hosp, Dept Lab Med, Beijing 100088, Peoples R China.
C3 Naval Medical University; Naval Medical University; Naval Medical
   University
RP Fang, GE (corresponding author), Second Mil Med Univ, Changhai Hosp, Dept Gen Surg, 168 Changhai Rd, Shanghai 200433, Peoples R China.
EM thalarus@126.com
RI zhang, Bin/JJD-2446-2023; Guo, Wei/KJM-4941-2024
OI Wei, Huafeng/0000-0003-2491-7510
CR Bettelli E, 2007, NAT IMMUNOL, V8, P345, DOI 10.1038/ni0407-345
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NR 32
TC 220
Z9 308
U1 0
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
EI 1090-2104
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD SEP 26
PY 2008
VL 374
IS 3
BP 533
EP 537
DI 10.1016/j.bbrc.2008.07.060
PG 5
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 346ZT
UT WOS:000259108800025
PM 18655770
DA 2025-06-01
ER

PT J
AU Al-Zahawi, S
   Sadeghi, Y
   Azhari, V
   Mahmoudi, H
   Daneshpazhooh, M
AF Al-Zahawi, Saman
   Sadeghi, Yasaman
   Azhari, Vahidesadat
   Mahmoudi, Hamidreza
   Daneshpazhooh, Maryam
TI Bullous pemphigoid, malignant acanthosis nigricans, and erysipeloid
   carcinoma in a woman with gastric adenocarcinoma
SO CLINICAL CASE REPORTS
LA English
DT Article
DE bullous pemphigoid; erysipeloid carcinoma; gastric adenocarcinoma;
   malignant acanthosis nigricans
ID ASSOCIATION; BLADDER; CANCER
AB Key Clinical MessageBullous pemphigoid did not follow the course of Gastric Carcinoma relapse and remisson, unlike the malignant acanthosis nigricans which was in alignment with the paraneoplastic effect of the Gastric Carcinoma.AbstractAcanthosis nigricans (AN) is a dermatosis characterized by the presence of hyperpigmented, velvety cutaneous thickening in the flexural areas, posterior neck, and occasionally the extensor surfaces of hand, face, and oral mucosa. AN is commonly associated with insulin resistance, drugs, and rarely internal malignancy (malignant AN). Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by tense blisters involving the skin of mainly elderly patients. The association of BP and malignancy is not well established and the co-existence of BP with AN has not been reported. Here we report a 58-year-old, event-free gastric adenocarcinoma with three types of skin findings with different pathogenesis- BP, malignant AN, and erysipelas-like metastasis.
   image
C1 [Al-Zahawi, Saman; Sadeghi, Yasaman; Mahmoudi, Hamidreza; Daneshpazhooh, Maryam] Univ Tehran Med Sci, Razi Hosp, Dept Dermatol, Vahdat E Eeslami Sq, Tehran 11996, Iran.
   [Azhari, Vahidesadat] Univ Tehran Med Sci, Razi Hosp, Dept Dermatopathol, Tehran, Iran.
   [Mahmoudi, Hamidreza; Daneshpazhooh, Maryam] Univ Tehran Med Sci, Razi Hosp, Autoimmune Bullous Dis Res Ctr, Tehran, Iran.
C3 Tehran University of Medical Sciences; Razi Hospital; Tehran University
   of Medical Sciences; Razi Hospital; Tehran University of Medical
   Sciences; Razi Hospital
RP Daneshpazhooh, M (corresponding author), Univ Tehran Med Sci, Razi Hosp, Dept Dermatol, Vahdat E Eeslami Sq, Tehran 11996, Iran.
EM maryamdanesh.pj@gmail.com
RI Mahmoudi, Hamidreza/AAA-2594-2019; Daneshpazhooh, Maryam/B-9512-2018
OI Al Zahawi, Saman/0009-0003-7324-0347
FU Tehran University of Medical Sciences
FX The authors are grateful of the Tehran University of Medical Sciences.
CR Brady MF., 2017, Acanthosis nigricans
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NR 14
TC 2
Z9 2
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2050-0904
J9 CLIN CASE REP
JI Clin. Case Rep.
PD JAN
PY 2024
VL 12
IS 1
AR e8351
DI 10.1002/ccr3.8351
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA DV1G4
UT WOS:001134759700001
PM 38173884
OA gold
DA 2025-06-01
ER

PT J
AU Lenti, MV
   Miceli, E
   Lahner, E
   Natalello, G
   Massironi, S
   Schiepatti, A
   Zingone, F
   Sciola, V
   Rossi, RE
   Cannizzaro, R
   De Giorgi, EM
   Gregorio, V
   Fazzino, E
   Gentile, A
   Petrucci, C
   Dilaghi, E
   Pivetta, G
   Vanoli, A
   Luinetti, O
   Paulli, M
   Anderloni, A
   Vecchi, M
   Biagi, F
   Repici, A
   Savarino, EV
   Joudaki, S
   Delliponti, M
   Pasini, A
   Facciotti, F
   Farinati, F
   D'Elios, MM
   Della Bella, C
   Annibale, B
   Klersy, C
   Corazza, GR
   Di Sabatino, A
AF Lenti, Marco Vincenzo
   Miceli, Emanuela
   Lahner, Edith
   Natalello, Gabriele
   Massironi, Sara
   Schiepatti, Annalisa
   Zingone, Fabiana
   Sciola, Valentina
   Rossi, Roberta Elisa
   Cannizzaro, Renato
   De Giorgi, Elena Maria
   Gregorio, Virginia
   Fazzino, Erica
   Gentile, Antonella
   Petrucci, Clarissa
   Dilaghi, Emanuele
   Pivetta, Giulia
   Vanoli, Alessandro
   Luinetti, Ombretta
   Paulli, Marco
   Anderloni, Andrea
   Vecchi, Maurizio
   Biagi, Federico
   Repici, Alessandro
   Savarino, Edoardo Vincenzo
   Joudaki, Shamim
   Delliponti, Mariangela
   Pasini, Alessandra
   Facciotti, Federica
   Farinati, Fabio
   D'Elios, Mario Milco
   Della Bella, Chiara
   Annibale, Bruno
   Klersy, Catherine
   Corazza, Gino Roberto
   Di Sabatino, Antonio
TI Distinguishing Features of Autoimmune Gastritis Depending on Previous
   Helicobacter pylori Infection or Positivity to Anti-Parietal Cell
   Antibodies: Results From the Autoimmune gastRitis Italian netwOrk Study
   grOup (ARIOSO)
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE anemia; gastric atrophy; gastric adenocarcinoma; gastric autoimmunity;
   Helicobacter pylori; neuroendocrine neoplasm; vitamin B12
ID ATROPHIC GASTRITIS; SOCIOECONOMIC-FACTORS; PREVALENCE; RISK
AB INTRODUCTION:To describe the clinical features and the risk of developing gastric tumors in patients with autoimmune gastritis (AIG). METHODS:This was a retrospective, longitudinal, multicenter study conducted at 8 Italian tertiary referral centers. We retrieved clinical data from all histologically proven patients with AIG. Differences between Helicobacter pylori-exposed vs H. pylori-naive and anti-parietal cell antibody (PCA)-positive vs PCA-negative patients were investigated. The rate of gastric adenocarcinoma and type 1 gastric neuroendocrine neoplasm (gNEN) was assessed. A multivariable model for factors associated with gNEN was fitted. RESULTS:A total of 1,598 patients with AIG (median age 58 years, interquartile range 46-68; F:M ratio 2.7:1) were included. H. pylori-naive patients were more likely to have a first-degree family history of AIG (14.7% vs 8.9%; P = 0.012), type 1 diabetes mellitus (4.9% vs 2.3%; P = 0.025), and pernicious anemia (30.9% vs 21.1%; P = 0.003). PCA-positive patients had significantly more associated autoimmune diseases (59.0% vs 42.9%; P < 0.001) and were more likely to have been diagnosed by a case-finding strategy (15.3% vs 2.6%; P < 0.001). Overall, 15 cases (0.9%) of gastric adenocarcinoma and 153 cases (9.6%) of gNEN occurred, with a global rate of 0.12 (95% confidence interval [CI] 0.07-0.20) and 1.22 (95% CI 1.03-1.42) per 100 person/year, respectively. Having a vitamin B12/iron deficiency manifestation at AIG diagnosis was associated with a 16.44 (95% CI 9.94-27.20 P < 0.001) hazard ratio of gNEN. DISCUSSION:The "pure" AIG pattern has typical features of an autoimmune disease and seems to be unrelated to H. pylori. In a tertiary referral setting, the risk of developing overt gastric adenocarcinoma is low, while patients with vitamin B12 deficiency complications at onset may benefit from a more intense endoscopic follow-up for early gNEN detection.
C1 [Lenti, Marco Vincenzo; Miceli, Emanuela; Natalello, Gabriele; Schiepatti, Annalisa; De Giorgi, Elena Maria; Gregorio, Virginia; Fazzino, Erica; Gentile, Antonella; Petrucci, Clarissa; Biagi, Federico; Joudaki, Shamim; Corazza, Gino Roberto; Di Sabatino, Antonio] Univ Pavia, Dept Internal Med & Med Therapeut, Pavia, Italy.
   [Lenti, Marco Vincenzo; Natalello, Gabriele; Joudaki, Shamim; Delliponti, Mariangela; Pasini, Alessandra; Corazza, Gino Roberto; Di Sabatino, Antonio] Fdn IRCCS Policlin San Matteo, Dept Internal Med 1, Pavia, Italy.
   [Lahner, Edith; Dilaghi, Emanuele; Pivetta, Giulia; Annibale, Bruno] Sapienza Univ Rome, St Andrea Hosp, Dept Med Surg Sci & Translat Med, Rome, Italy.
   [Massironi, Sara] Fdn IRCCS San Gerardo Tintori, Div Gastroenterol, Monza, Italy.
   [Massironi, Sara] Fdn IRCCS San Gerardo Tintori, Ctr Autoimmune Liver Dis, Dept Med & Surg, Monza, Italy.
   [Massironi, Sara] Univ Milano Bicocca, Monza, Italy.
   [Schiepatti, Annalisa; Biagi, Federico] Ist Clin Sci Maugeri IRCCS, Pavia Inst, Gastroenterol Unit, Pavia, Italy.
   [Zingone, Fabiana; Savarino, Edoardo Vincenzo; Farinati, Fabio] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
   [Zingone, Fabiana; Savarino, Edoardo Vincenzo; Farinati, Fabio] Univ Padua, Azienda Osped, Gastroenterol Unit, Padua, Italy.
   [Sciola, Valentina; Vecchi, Maurizio] Fdn IRCCS Ca Granda Osped Maggiore Policlin Milano, Osped Maggiore Policlin Milano, Milan, Italy.
   [Rossi, Roberta Elisa; Repici, Alessandro] IRCCS, Human Res Hosp, Milan, Italy.
   [Cannizzaro, Renato] IRCCS, Ctr Riferimento Oncol Aviano CRO, Oncol Gastroenterol, Trieste, Italy.
   [Cannizzaro, Renato] Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
   [Vanoli, Alessandro; Luinetti, Ombretta; Paulli, Marco] Univ Pavia, Dept Mol Med, Unit Anat Pathol, Pavia, Italy.
   [Vanoli, Alessandro; Luinetti, Ombretta; Paulli, Marco] IRCCS San Matteo Hosp Fdn, Pavia, Italy.
   [Anderloni, Andrea] Fdn IRCCS Policlin San Matteo, Gastroenterol & Digest Endoscopy Unit, Pavia, Italy.
   [Repici, Alessandro] Humanitas Univ, Dept Biomed Sci, Milan, Pieve Emanuele, Italy.
   [Facciotti, Federica] European Inst Oncol IRCCS, Dept Expt Oncol, IEO, Milan, Italy.
   [Facciotti, Federica] Univ Milano Bicocca, Dept Biotechnol & Biosci, Milan, Italy.
   [D'Elios, Mario Milco; Della Bella, Chiara] Univ Siena, Dept Mol & Dev Med, Siena, Italy.
   [Klersy, Catherine] Fdn IRCCS Policlin San Matteo, Biostat & Clin Trial Ctr, Pavia, Italy.
C3 University of Pavia; IRCCS Fondazione San Matteo; Sapienza University
   Rome; Azienda Ospedaliera Sant'Andrea; Fondazione IRCCS San Gerardo dei
   Tintori; Fondazione IRCCS San Gerardo dei Tintori; University of
   Milano-Bicocca; University of Padua; University of Padua; Azienda
   Ospedaliera - Universita di Padova; IRCCS Ca Granda Ospedale Maggiore
   Policlinico; University of Trieste; University of Pavia; IRCCS
   Fondazione San Matteo; IRCCS Fondazione San Matteo; Humanitas
   University; IRCCS European Institute of Oncology (IEO); University of
   Milano-Bicocca; University of Siena; IRCCS Fondazione San Matteo
RP Di Sabatino, A (corresponding author), Univ Pavia, Dept Internal Med & Med Therapeut, Pavia, Italy.; Di Sabatino, A (corresponding author), Fdn IRCCS Policlin San Matteo, Dept Internal Med 1, Pavia, Italy.
EM marco.lenti@unipv.it; e.miceli@smatteo.pv.it; edith.lahner@uniroma1.it;
   gabriele.natalello01@universitadipavia.it;
   sara.massironi@irccs-sangerardo.it; annalisa.schiepatti@unipv.it;
   fabiana.zingone@unipd.it; valentinasciola@libero.it;
   robertaelisa.rossi@gmail.com; rcannizzaro@cro.it;
   elenamaria.degiorgi01@universitadipavia.it;
   virginia.gregorio01@universitadipavia.it;
   erica.fazzino01@universitadipavia.it;
   antonella.gentile01@universitadipavia.it;
   clarissa.petrucci01@universitadipavia.it; emanuele.dilaghi@uniroma1.it;
   pivetta.1697847@studenti.uniroma1.it; alessandro.vanoli@unipv.it;
   o.luinetti@smatteo.pv.it; markus198690@gmail.com;
   a.anderloni@smatteo.pv.it; markus1986@hotmail.it;
   federico.biagi@icsmaugeri.it; catapresan@icloud.com;
   edoardo.savarino@unipd.it; shamim.joudakidinarva01@universitadipavia.it;
   m.delliponti@smatteo.pv.it; a.pasini@smatteo.pv.it;
   federica.facciotti@unimib.it; fabio.farinati@unipd.it; delios@unisi.it;
   chiara.dellabella@unifi.it; bruno.annibale@uniroma1.it;
   klersy@smatteo.pv.it; gr.corazza@smatteo.pv.it;
   a.disabatino@smatteo.pv.it
RI Pasini, Alessandra/AAP-8573-2021; Savarino, Edoardo/AAC-7510-2022;
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NR 51
TC 5
Z9 5
U1 2
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD DEC
PY 2024
VL 119
IS 12
BP 2408
EP 2417
DI 10.14309/ajg.0000000000002948
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA O6Z4G
UT WOS:001372581700031
PM 38976374
DA 2025-06-01
ER

PT J
AU Li, QX
   Li, QJ
   Chen, JX
   Liu, Y
   Zhao, XF
   Tan, BB
   Ai, J
   Zhang, ZP
   Song, JJ
   Shan, BE
AF Li, Qiaoxia
   Li, Qingjing
   Chen, Jinxia
   Liu, Yu
   Zhao, Xuefeng
   Tan, Bibo
   Ai, Jun
   Zhang, Zhiping
   Song, Jingjing
   Shan, Baoen
TI Prevalence of Th17 and Treg cells in gastric cancer patients and its
   correlation with clinical parameters
SO ONCOLOGY REPORTS
LA English
DT Article
DE gastric cancer; Th17; regulatory T cells; TGF-beta; interleukin-6;
   interleukin-17
ID REGULATORY T-CELLS; GROWTH-FACTOR-BETA; TUMOR-INFILTRATING LYMPHOCYTES;
   UTERINE CERVICAL-CANCER; ROR-GAMMA-T; PERIPHERAL-BLOOD; OVARIAN-CANCER;
   HELPER-CELLS; TGF-BETA; DIFFERENTIATION
AB Th17 cells and CD4(+)CD25(+) regulatory T (Treg) cells have been reported to share reciprocal developmental pathways but exhibit opposite effects, and the balance between them controls inflammation and autoimmune diseases. However, information regarding Th17/Treg cells in cancer-bearing hosts is still limited. In the present study, we investigated the distribution of Th17 cells in relation to Treg cells in gastric cancer patients, and evaluated how the imbalance in Th17/Treg cells in gastric cancer correlates with clinical and pathological parameters. We observed that the accumulation of Th17 and Treg cells in the tumor microenvironment was gradually increased according to disease progression, leading to an imbalance in Th17/Treg cells in gastric cancer patients. TGF-beta and interleukin (IL)-6 present in the gastric cancer microenvironment promoted the differentiation and expansion of Th17 cells, and increased numbers of Th17 cells promoted tumor progression through promotion of inflammation by secretion of IL-17. Treg cells promoted tumor progression by helping cancer cells escape from host immunosurveillance by secreting TGF-beta, and a high level of TGF-beta in the tumor microenvironment promoted differentiation and expansion of Treg cells. In conclusion, the imbalance in Th17/Treg cells was involved in the development and progression of gastric cancer. A better understanding of the nature, regulation, and function of Th17 and Treg cells in tumor immunity may aid in the development of novel and effective immunotherapy for gastric cancer.
C1 [Li, Qiaoxia; Li, Qingjing; Chen, Jinxia; Ai, Jun; Zhang, Zhiping; Song, Jingjing; Shan, Baoen] Hebei Med Univ, Hosp 4, Res Ctr, Shijiazhuang 050011, Hebei, Peoples R China.
   [Liu, Yu; Zhao, Xuefeng; Tan, Bibo] Hebei Med Univ, Hosp 4, Dept Surg, Shijiazhuang 050011, Hebei, Peoples R China.
C3 Hebei Medical University; Hebei Medical University
RP Shan, BE (corresponding author), Hebei Med Univ, Hosp 4, Res Ctr, Jiankang Rd 12, Shijiazhuang 050011, Hebei, Peoples R China.
EM hbydsysbe@yahoo.com.cn
RI Liu, Lu/AAM-4152-2020; Song, Jing/HRC-8045-2023; Li,
   Qiaoxia/AAT-9590-2021
FU Natural Science Foundation of Hebei Province [C2011206086]; Key Science
   and Technology Project of the Health Department of Hebei Province
   [20110456]
FX The present study was supported by grants from the Natural Science
   Foundation of Hebei Province (no. C2011206086); Key Science and
   Technology Project of the Health Department of Hebei Province (no.
   20110456).
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NR 35
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Z9 77
U1 0
U2 21
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
J9 ONCOL REP
JI Oncol. Rep.
PD SEP
PY 2013
VL 30
IS 3
BP 1215
EP 1222
DI 10.3892/or.2013.2570
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 191AJ
UT WOS:000322384700027
PM 23807713
DA 2025-06-01
ER

PT J
AU Waldum, HL
   Rehfeld, JF
AF Waldum, Helge L.
   Rehfeld, Jens F.
TI Gastric cancer and gastrin: on the interaction of Helicobacter pylori
   gastritis and acid inhibitory induced hypergastrinemia
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Classification of gastric cancer; ECL cell; gastric cancer; gastrin;
   gastritis; Helicobacter pylori; inhibitors of gastric acid secretion;
   proton pump inhibitors
ID ANTAGONIST NETAZEPIDE YF476; PROTON PUMP INHIBITORS; ECL-CELL
   CARCINOIDS; PERNICIOUS-ANEMIA; INTESTINAL METAPLASIA; ATROPHIC
   GASTRITIS; SERUM GASTRIN; NEUROENDOCRINE DIFFERENTIATION; AUTOIMMUNE
   GASTRITIS; HISTAMINE-RELEASE
AB Gastric cancer, a disease with a reduced frequency for decades, now appears to be on the rise again in young Americans. The epidemiology of gastric cancer differs between tumors in the cardia and those of the more distal parts of the stomach. The tumors are divided into the intestinal type showing glandular growth pattern and the diffuse type with a different pattern. The latter often expresses neuroendocrine and more specifically ECL-cell markers suggesting that they originate from the ECL cell, the target cell for the antral hormone, gastrin. Helicobacter pylori gastritis is accepted as the major cause of gastric cancer, but only after having induced oxyntic atrophy which reduces gastric acid secretion and thus induces hypoacidity leading to hypergastrinemia. Long-term hypergastrinemia is known to induce malignant neoplasia in the stomach of animals as well as man. Recently treatment with proton pump inhibitor after Helicobacter pylori eradication in patients with gastroesophageal reflux disease, has been reported to predispose to gastric cancer. Since profound acid inhibition is a well-known cause of gastric neoplasia, it is to be expected that Helicobacter pylori infection and profound acid inhibition has an additive or possibly potentiating effect on the development of gastric cancer.
C1 [Waldum, Helge L.] Norwegian Univ Sci & Technol, Dept Clin & Mol Med, Fac Med & Hlth Sci, Trondheim, Norway.
   [Rehfeld, Jens F.] Rigshosp, Dept Clin Biochem, Copenhagen, Denmark.
C3 Norwegian University of Science & Technology (NTNU); University of
   Copenhagen; Copenhagen University Hospital; Rigshospitalet
RP Waldum, HL (corresponding author), St Olavs Hosp, Dept Gastroenteroy, Jakobstien 4, N-7021 Trondheim, Norway.
EM helge.waldum@ntnu.no
OI Waldum, Helge/0000-0002-3137-0843
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NR 90
TC 26
Z9 30
U1 0
U2 17
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD SEP 2
PY 2019
VL 54
IS 9
BP 1118
EP 1123
DI 10.1080/00365521.2019.1663446
EA SEP 2019
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JB9EW
UT WOS:000486558000001
PM 31524029
DA 2025-06-01
ER

PT J
AU Castoro, C
   Le Moli, R
   Arpi, ML
   Tavarelli, M
   Sapuppo, G
   Frittitta, L
   Squatrito, S
   Pellegriti, G
AF Castoro, C.
   Le Moli, R.
   Arpi, M. L.
   Tavarelli, M.
   Sapuppo, G.
   Frittitta, L.
   Squatrito, S.
   Pellegriti, G.
TI Association of autoimmune thyroid diseases, chronic atrophic gastritis
   and gastric carcinoid: experience from a single institution
SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
LA English
DT Article
DE Autoimmune disease; Thyroid disease; Autoimmune gastritis; Carcinoid;
   Graves' disease
ID PERNICIOUS-ANEMIA; FOLLOW-UP; NEUROENDOCRINE TUMORS;
   HELICOBACTER-PYLORI; BODY GASTRITIS; CLASSIFICATION; AUTOANTIBODIES;
   PREVALENCE; GUIDELINES; ANTIBODIES
AB Purpose Autoimmune polyendocrine syndromes (APS) type III are characterized by the association of autoimmune thyroid disease (ATD) with other autoimmune diseases such as diabetes, alopecia, pernicious anemia, vitiligo and chronic atrophic gastritis. A strong association between ATD and atrophic gastritis (AG) has been demonstrated. Moreover 10 % of patients affected by AG have a predisposition to develop gastric carcinoid and adenocarcinoma as a result of chronic hypergastrinemia caused by achlorhydria and subsequent ELC cells neoplastic transformation.
   Methods The aim of the study is to evaluate, in a consecutive series of patients followed for ATD in our outpatients clinic, the prevalence of AG. In the period 2004-2014, 242 patients with ATD underwent a screening performing APCA, Vitamin B12, ferritin, iron, and hemoglobin and red cells count measurements with subsequent gastroscopy in case of APCA positivity.
   Results We found 57/242 (23.5 %) patients with APCA positivity. Of these patients 33/57 (57.8 %), 31 F and 2 M, were affected by Graves disease; 24/57 (42.1 %) 21 F and 3 M by Hashimoto thyroiditis; 10/57 (17.5 %) presented with anemia, 14/57 (24.5 %) with vitamin B12 deficiency, 9/57 (15.7 %) with iron deficiency. In 2/57 a gastric carcinoid was found.
   Conclusions Our data confirm the high association rate of AG in ATD which frequently is not an isolated disease but configure the picture of APS type III and need to be followed accordingly. An early diagnosis may be useful for diagnosis of gastric carcinoids and to explain and treat a gastric related l-thyroxine malabsorption and presence of chronic unexplained anemia.
C1 [Castoro, C.; Le Moli, R.; Tavarelli, M.; Sapuppo, G.; Frittitta, L.; Squatrito, S.] Univ Catania, Dept Clin & Expt Med, Catania, Italy.
   [Arpi, M. L.; Pellegriti, G.] Garibaldi Nesima Hosp, Endocrinol, Via Palermo 636, I-95126 Catania, Italy.
C3 University of Catania; Presidio Ospedaliero Garibaldi-Nesima
RP Pellegriti, G (corresponding author), Garibaldi Nesima Hosp, Endocrinol, Via Palermo 636, I-95126 Catania, Italy.
EM g.pellegriti@unict.it
RI LEMOLI, ROBERTO/AAC-2370-2022; Castoro, Carlo/GNM-8249-2022; frittitta,
   lucia/J-2334-2012; Pellegriti, Gabriella/J-7923-2012; Sapuppo,
   Giulia/J-1386-2018
OI Pellegriti, Gabriella/0000-0001-6102-379X; LE MOLI,
   Rosario/0000-0002-1398-9271; Sapuppo, Giulia/0000-0002-8471-7310;
   FRITTITTA, Lucia/0000-0002-7941-5828
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NR 31
TC 24
Z9 24
U1 0
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1720-8386
J9 J ENDOCRINOL INVEST
JI J. Endocrinol. Invest.
PD JUL
PY 2016
VL 39
IS 7
BP 779
EP 784
DI 10.1007/s40618-016-0445-5
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA DO7BQ
UT WOS:000377937600009
PM 26928404
DA 2025-06-01
ER

PT J
AU Wang, MH
   Xie, C
AF Wang, Menghui
   Xie, Chuan
TI DNA Damage Repair and Current Therapeutic Approaches in Gastric Cancer:
   A Comprehensive Review
SO FRONTIERS IN GENETICS
LA English
DT Review
DE DNA damage repair; Helicobacter pylori; therapeutic approaches; gastric
   cancer; PARP inhibitors
ID CHROMOSOMAL INSTABILITY; EXPRESSION; INHIBITION; MECHANISMS; CROSSTALK;
   VARIANTS; PATHWAY; RISK; PKCS
AB DNA in cells is frequently damaged by endogenous and exogenous agents. However, comprehensive mechanisms to combat and repair DNA damage have evolved to ensure genomic stability and integrity. Improper DNA damage repair may result in various diseases, including some types of tumors and autoimmune diseases. Therefore, DNA damage repair mechanisms have been proposed as novel antitumor drug targets. To date, numerous drugs targeting DNA damage mechanisms have been developed. For example, PARP inhibitors that elicit synthetic lethality are widely used in individualized cancer therapies. In this review, we describe the latent DNA damage repair mechanisms in gastric cancer, the types of DNA damage that can contribute to the development of gastric cancer, and new therapeutic approaches for gastric cancer that target DNA damage repair pathways.
C1 [Wang, Menghui; Xie, Chuan] Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanchang, Peoples R China.
C3 Nanchang University
RP Xie, C (corresponding author), Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanchang, Peoples R China.
EM xcsghhz@ncu.edu.cn
RI wang, menghui/JWA-4356-2024; XIE, CHUAN/GRX-3320-2022
FU National Natural Science Foundation of China [82100599, 81960112];
   Jiangxi Provincial Department of Science and Technology
   [20212ACB216003]; Young Talents Project of Jiangxi Provincial Academic
   and Technical Leaders Training Program for Major Disciplines
   [20204BCJ23022]
FX This work was supported by the National Natural Science Foundation of
   China (82100599 and 81960112), the Jiangxi Provincial Department of
   Science and Technology (20212ACB216003), and The Young Talents Project
   of Jiangxi Provincial Academic and Technical Leaders Training Program
   for Major Disciplines (20204BCJ23022).
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NR 102
TC 11
Z9 11
U1 6
U2 23
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD AUG 12
PY 2022
VL 13
AR 931866
DI 10.3389/fgene.2022.931866
PG 11
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA 4A2WR
UT WOS:000844968800001
PM 36035159
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Vavallo, M
   Cingolani, S
   Cozza, G
   Schiavone, FP
   Dottori, L
   Palumbo, C
   Lahner, E
AF Vavallo, Marica
   Cingolani, Sophia
   Cozza, Giulio
   Schiavone, Francesco P.
   Dottori, Ludovica
   Palumbo, Carla
   Lahner, Edith
TI Autoimmune Gastritis and Hypochlorhydria: Known Concepts from a New
   Perspective
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE autoimmune gastritis; cobalamin (vitamin B12) deficiency; gastric
   cancer; gastric microbiota; gastrin; iron deficiency anemia; pernicious
   anemia; type 1 gastric neuroendocrine tumors
ID ATROPHIC BODY GASTRITIS; HELICOBACTER-PYLORI INFECTION; PARIETAL-CELL
   AUTOANTIBODIES; PERNICIOUS-ANEMIA; IRON-DEFICIENCY; H+,K+-ADENOSINE
   TRIPHOSPHATASE; VITAMIN-B-12 DEFICIENCY; INTESTINAL METAPLASIA; MUCOSAL
   ATROPHY; ALPHA-SUBUNIT
AB Autoimmune atrophic gastritis is an immune-mediated disease resulting in autoimmune destruction of the specialized acid-producing gastric parietal cells. As a consequence, in autoimmune atrophic gastritis, gastric acid secretion is irreversibly impaired, and the resulting hypochlorhydria leads to the main clinical manifestations and is linked, directly or indirectly, to the long-term neoplastic complications of this disease. In the last few years, autoimmune atrophic gastritis has gained growing interest leading to the acquisition of new knowledge on different aspects of this disorder. Although reliable serological biomarkers are available and gastrointestinal endoscopy techniques have substantially evolved, the diagnosis of autoimmune atrophic gastritis is still affected by a considerable delay and relies on histopathological assessment of gastric biopsies. One of the reasons for the diagnostic delay is that the clinical presentations of autoimmune atrophic gastritis giving rise to clinical suspicion are very different, ranging from hematological to neurological-psychiatric up to gastrointestinal and less commonly to gynecological-obstetric symptoms or signs. Therefore, patients with autoimmune atrophic gastritis often seek advice from physicians of other medical specialties than gastroenterologists, thus underlining the need for increased awareness of this disease in a broad medical and scientific community.
C1 [Vavallo, Marica; Cingolani, Sophia; Cozza, Giulio; Schiavone, Francesco P.; Dottori, Ludovica; Palumbo, Carla; Lahner, Edith] Sapienza Univ Rome, St Andrea Univ Hosp, Dept Med Surg Sci & Translat Med, Gastroenterol Unit, I-00189 Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea
RP Lahner, E (corresponding author), Sapienza Univ Rome, St Andrea Univ Hosp, Dept Med Surg Sci & Translat Med, Gastroenterol Unit, I-00189 Rome, Italy.
EM giulio.cozza@uniroma1.it; schiavone.1794884@studenti.uniroma1.it;
   edith.lahner@uniroma1.it
RI Schiavone, Francesco/M-7460-2017; Lahner, Edith/AAM-1039-2021
OI Cozza, Giulio/0009-0008-8123-6416; LAHNER, EDITH/0000-0002-9503-8639;
   Dottori, Ludovica/0009-0008-8178-2273
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NR 127
TC 0
Z9 0
U1 7
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUL
PY 2024
VL 25
IS 13
AR 6818
DI 10.3390/ijms25136818
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA YJ1G6
UT WOS:001268025500001
PM 38999928
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Probst, A
   Schaller, T
   Sommer, F
   Geissler, B
   Agaimy, A
   Messmann, H
   Märkl, B
AF Probst, Andreas
   Schaller, Tina
   Sommer, Florian
   Geissler, Bernd
   Agaimy, Abbas
   Messmann, Helmut
   Maerkl, Bruno
TI Immunoglobulin G4 (IgG4)-related disease of the stomach - a challenging
   differential diagnosis in suspected gastric cancer
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Article
DE gastric ulcer; IgG4; IgG4-related disease
ID G4-RELATED INFLAMMATORY PSEUDOTUMOR; AUTOIMMUNE PANCREATITIS; LESION;
   MANIFESTATION; STATEMENT; ULCER; MASS
AB Background Immunoglobulin G4-related disease (IgG4-RD) can involve different organs and is diagnosed by a combination of clinicopathological features, including storiform fibrosclerosis infiltrated by numerous IgG4-positive plasma cells that frequently forms tumor-like lesions with or without associated obliterative phlebitis. Involvement of the stomach is rare and can occur as part of a multiorgan involvement of IgG4-RD or as isolated gastric involvement. Case report We report 2 female patients with therapy-refractory gastric ulcers associated with gastric wall thickening and lymphadenopathy that were highly suggestive of gastric cancer or lymphoma. Biopsies failed to confirm a diagnosis, and IgG4-RD was diagnosed only after surgical resection in both patients. The previous literature on gastric IgG4-RD is summarized and shows different characteristics in patients with multiorgan IgG4-RD and isolated gastric IgG4-RD. As reported for autoimmune pancreatitis type 1, patients with multiorgan IgG4-RD are mainly elderly men with frequently elevated serum IgG4 concentrations. In contrast, isolated gastric IgG4-RD predominantly affects female patients with normal serum IgG4 levels. Surgical resection is commonly performed due to the clinical suspicion of malignancy and the absence of findings indicative of IgG4-RD on biopsy. Today, diagnosis is confirmed histopathologically only after resection. Conclusion IgG4-RD should be taken into account when gastric malignancy is suspected endoscopically or radiologically and biopsies fail to confirm the presence of a malignancy (especially subepithelial tumors or refractory gastric ulcers). Serum IgG4 concentrations are insufficient to confirm localized gastric IgG4-RD. Diagnostic workups need to be improved to avoid unnecessary surgical resections with the attendant potential morbidity and mortality.
C1 [Probst, Andreas; Messmann, Helmut] Univ Klinikum Augsburg, Dept Gastroenterol, Augsburg, Germany.
   [Schaller, Tina; Maerkl, Bruno] Univ Klinikum Augsburg, Inst Pathol, Augsburg, Germany.
   [Sommer, Florian; Geissler, Bernd] Univ Klinikum Augsburg, Dept Gen Visceral & Transplantat Surg, Augsburg, Germany.
   [Agaimy, Abbas] Univ Klinikum Erlangen, Inst Pathol, Erlangen, Germany.
C3 University of Erlangen Nuremberg
RP Probst, A (corresponding author), Klinikum Augsburg, Med Klin 3, Stenglinstr 2, D-86156 Augsburg, Germany.
EM andreas.probst@uk-augsburg.de
RI Messmann, Helmut/AAB-6758-2020; Maerkl, Bruno/H-6832-2019; Sommer,
   Florian/LTZ-7825-2024
OI Messmann, Helmut/0000-0002-4026-6837
CR [Anonymous], ISRN GASTROENTEROL
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NR 28
TC 5
Z9 5
U1 0
U2 2
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD NOV
PY 2019
VL 57
IS 11
BP 1298
EP 1303
DI 10.1055/a-1013-4437
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JO7AH
UT WOS:000497727800018
PM 31739375
DA 2025-06-01
ER

PT J
AU Li, WD
   Huang, XD
   Han, XW
   Zhang, JY
   Gao, L
   Chen, H
AF Li, Weidong
   Huang, Xiaodong
   Han, Xiaowen
   Zhang, Jiayi
   Gao, Lei
   Chen, Hao
TI IL-17A in gastric carcinogenesis: good or bad?
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE gastric cancer; IL-17; tumor microenvironment; Helicobacter
   pylori; immunotherapy
ID EPITHELIAL-MESENCHYMAL TRANSITION; STEM-CELLS; CANCER; TH17;
   INTERLEUKIN-17; EXPRESSION; CONTRIBUTE; SURVIVAL; LINK
AB Cytokines, which are important to the tumor microenvironment (TME), play critical roles in tumor development, metastasis, and immune responses. Interleukin-17(IL-17) has emerged as a key biomarker in many malignancies; however, its precise involvement in gastric cancer is less fully understood. Elevated levels of IL-17 have been observed in stomach diseases such as Helicobacter pylori infection and autoimmune gastritis, indicating that a sustained Th17 response may precede the development of gastric cancer. While IL-17 is related to inflammatory processes that may lead to cancer, its specific influence on gastric cancer development and therapy needs to be completely understood. Specifically, the release of IL-17A by diverse immune cells has been associated with both tumor development and inhibition in gastric cancer. It may impact tumor development through mechanisms such as boosting cell proliferation, inducing angiogenesis, and enabling immune cell recruitment or, conversely, suppressing tumor growth via the activation of anti-tumor immune responses. The dual role of IL-17 in cancer, along with its various effects depending on the TME and immune cell composition, highlights the complexity of its activity. Current research reveals that although IL-17 might serve as a target for immunotherapy, its therapeutic potential is hindered by its various activities. Some studies have shown that anti-IL-17 drugs may be helpful, especially when paired with immune checkpoint inhibitors, whereas others point to concerns about the validity of IL-17 in gastric cancer therapy. The lack of clinical trials and the heterogeneity of human tumors underscore the necessity for individualized treatment approaches. Further studies are needed to identify the specific mechanisms of IL-17 in gastric cancer and to design targeted therapeutics appropriately.
C1 [Li, Weidong; Huang, Xiaodong; Han, Xiaowen; Zhang, Jiayi; Gao, Lei; Chen, Hao] Lanzhou Univ Second Hosp, Dept Surg Oncol, Lanzhou, Peoples R China.
   [Chen, Hao] Lanzhou Univ Second Hosp, Key Lab Environm Oncol Gansu Prov, Lanzhou, Peoples R China.
RP Chen, H (corresponding author), Lanzhou Univ Second Hosp, Dept Surg Oncol, Lanzhou, Peoples R China.; Chen, H (corresponding author), Lanzhou Univ Second Hosp, Key Lab Environm Oncol Gansu Prov, Lanzhou, Peoples R China.
EM ery_chenh@lzu.edu.cn
RI Huang, Xiaodong/J-1217-2019; Li, Wei-Dong/KFQ-2581-2024; Zhang,
   Jiayi/AAJ-6276-2021
FU National Natural Science Foundation of China [8247104651, 82160129]; Key
   Project of Science and Technology in Gansu province [22ZD6FA054]; Key
   Talents Project of Gansu Province [2019RCXM020]; General Project of
   Gansu Province Joint Research Fund [24JRRA92]; National Natural Science
   Foundation of China [8247104651, 82160129]; Research Fund [24JRRA929];
   Science and Technology Project of Chengguan District of Lanzhou City
   [2020SHFZ0039, 2020JSCX0073]; Cuiying Scientific and Technological
   Innovation Program of Lanzhou and Technological Innovation Program of
   Lanzhou University Second Hospital [CY2017-ZD01]; Medical Research
   Innovation Ability Improvement Project of Lanzhou University
   [lzuyxcx-2022-160]; Excellent Textbook Cultivation Project of Lanzhou
   University [lzuyxcx-2022-45]; English Curriculum Construction and
   Cultivation Project of Lanzhou University [lzuyxcx-2022-45]; Gansu
   Province Innovation Driven Assistance Project [GXH20230817-14]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This research was
   supported by National Natural Science Foundation of China (8247104651,
   82160129), Key Project of Science and Technology in Gansu province
   (22ZD6FA054), Key Talents Project of Gansu Province (2019RCXM020),
   General Project of Gansu Province Joint Research Fund (24JRRA92), and
   the National Natural Science Foundation of China (8247104651, 82160129).
   Research Fund (24JRRA929), Science and Technology Project of Chengguan
   District of Lanzhou City (2020SHFZ0039, 2020JSCX0073), Cuiying
   Scientific and Technological Innovation Program of Lanzhou and
   Technological Innovation Program of Lanzhou University Second Hospital
   (CY2017-ZD01), Medical Research Innovation Ability Improvement Project
   of Lanzhou University (lzuyxcx-2022-160), Excellent Textbook Cultivation
   Project of Lanzhou University (lzuyxcx-2022-45), English Curriculum
   Construction and Cultivation Project of Lanzhou University
   (lzuyxcx-2022-45); Gansu Province Innovation Driven Assistance Project
   (GXH20230817-14).
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NR 81
TC 1
Z9 1
U1 5
U2 5
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD NOV 29
PY 2024
VL 15
AR 1501293
DI 10.3389/fimmu.2024.1501293
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA P1X0L
UT WOS:001375912500001
PM 39676857
OA gold
DA 2025-06-01
ER

PT J
AU McColl, KEL
AF McColl, Kenneth E. L.
TI Cancer of the gastric cardia
SO BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE gastric cancer; cardia; H. pylori; carditis; atrophy
ID HELICOBACTER-PYLORI INFECTION; N-NITROSO COMPOUNDS; GASTROESOPHAGEAL
   JUNCTION; DIETARY NITRATE; NITRIC-OXIDE; ESOPHAGUS; ADENOCARCINOMA;
   CARCINOMA; ETIOLOGY; STOMACH
AB Current evidence indicates that cardia cancers are of at least two distinct and disparate aetiologies. One type resembles cancer of the more distal stomach (Type A), being a consequence of atrophic gastritis due to Helicobacter pylori infection or more rarely autoimmune atrophic gastritis. Another type (Type B) resembles oesophageal adenocarcinoma and is likely to be a consequence of short-segment gastro-oesophageal reflux disease. The two cancers are themselves indistinguishable but examination of the gastric phenotype indicates the aetiology: Type A occurring in patients with evidence of atrophic gastritis whereas Type B occurs in subjects with healthy acid secreting stomachs. In subjects with healthy acid secreting stomachs the cardia has a specific luminal chemistry remaining highly acidic and unbuffered following a meal and having very active nitrosative chemistry due to the acidification of nitrite in saliva. This luminal chemistry may contribute to the high incidence of metaplasia and neoplasia at this anatomical site.
C1 Univ Glasgow, Western Infirm, Gardiner Inst, Med Sect, Glasgow G11 6NT, Lanark, Scotland.
C3 University of Glasgow
RP McColl, KEL (corresponding author), Univ Glasgow, Western Infirm, Gardiner Inst, Med Sect, Glasgow G11 6NT, Lanark, Scotland.
EM k.e.l.mccoll@clinmed.gla.ac.uk
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NR 52
TC 42
Z9 49
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PY 2006
VL 20
IS 4
BP 687
EP 696
DI 10.1016/j.bpg.2006.03.005
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 095BN
UT WOS:000241283300005
PM 16997153
DA 2025-06-01
ER

PT J
AU Tüzün, A
   Keskin, O
   Yakut, M
   Kalkan, C
   Soykan, I
AF Tuzun, Ali
   Keskin, Onur
   Yakut, Mustafa
   Kalkan, Cagdas
   Soykan, Irfan
TI The predictive value of mean platelet volume, plateletcrit and red cell
   distribution width in the differentiation of autoimmune gastritis
   patients with and without type I gastric carcinoid tumors
SO PLATELETS
LA English
DT Article
DE Autoimmune gastritis; mean platelet volume; plateletcrit; red cell
   distribution width
ID C-REACTIVE PROTEIN; CIRCULATING LEVELS; HEART-FAILURE; INTERLEUKIN-6;
   MARKER; INFLAMMATION; PARAMETERS; RELEVANCE; FEATURES; DISEASE
AB Autoimmune gastritis is an autoimmune and inflammatory condition that may predispose to gastric carcinoid tumors or adenocarcinomas. The early diagnosis of these tumors is important in order to decrease morbidity and mortality. Platelet indices such as mean platelet volume and plateletcrit levels increase in inflammatory, infectious and malign conditions. The primary aim of this study was to explore wheter platelet indices and red cell distribution width have any predictive role in the discrimination of autoimmune gastritis patients with and without gastric carcinoid tumors. Also secondary aim of this study was to investigate whether any changes exist betwenn autoimmune gastritis and functional dyspepsia patients by means of platelet indices. Plateletcrit (0.22 +/- 0.06 vs. 0.20 +/- 0.03%, p<0.001) and red cell distribution width (16.11 +/- 3.04 vs. 13.41 +/- 0.95%, p<0.001) were significantly higher in autoimmune gastritis patients compared to control group. Receiver operating curve analysis suggested that optimum plateletcrit cut-off point was 0.20% (AUC: 0.646), and 13.95% as the cut off value for red cell distribution width (AUC: 0.860). Although plateletcrit (0.22 +/- 0.06 vs. 0.21 +/- 0.04%, p = 0.220) and mean platelet volume (8.94 +/- 1.44 vs. 8.68 +/- 0.89 fl, p = 0.265) were higher in autoimmune gastritis patients without carcinoid tumor compared to patients with carcinoid tumors, these parameters were not statistically significant. Changes in plateletcrit and red cell distribution width values may be used as a marker in the discrimination of autoimmune gastritis and fucntional dyspepsia patients but not useful in patients with gastric carcinoid tumor type I.
C1 [Tuzun, Ali; Keskin, Onur; Yakut, Mustafa; Kalkan, Cagdas; Soykan, Irfan] Ankara Univ, Fac Med, Ibni Sina Hosp, Div Gastroenterol, TR-06100 Ankara, Turkey.
C3 Ankara University
RP Soykan, I (corresponding author), Ankara Univ, Fac Med, Ibni Sina Hosp, Div Gastroenterol, TR-06100 Ankara, Turkey.
EM isoykan@medicine.ankara.edu.tr
RI soykan, irfan/KMD-7090-2024; Kalkan, Cagdas/AAD-7481-2020; Keskin,
   Onur/P-2213-2015
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NR 37
TC 11
Z9 12
U1 0
U2 4
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0953-7104
EI 1369-1635
J9 PLATELETS
JI Platelets
PY 2014
VL 25
IS 5
BP 363
EP 366
DI 10.3109/09537104.2013.821607
PG 4
WC Cell Biology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Hematology
GA AM0UY
UT WOS:000339563700009
PM 24175991
DA 2025-06-01
ER

PT J
AU Waldum, H
   Modlin, I
AF Waldum, Helge
   Modlin, Irvin
TI The central role of gastrin in Helicobacter pylori gastric
   carcinogenesis
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review; Early Access
DE Atrophic gastritis; autoimmune gastritis;
   enterochromaffin-like(ECL)cell; gastric cancer; gastrin; Helicobacter
   pylori; neuroendocrine tumour (NET); trophic effect
ID PROTON PUMP INHIBITORS; ENTEROCHROMAFFIN-LIKE CELL;
   UPPER-GASTROINTESTINAL-TRACT; LONG-TERM TREATMENT; ACID-SECRETION;
   PERNICIOUS-ANEMIA; ENDOSCOPIC RESECTION; NEUROENDOCRINE CELLS; ATROPHIC
   GASTRITIS; ENDOCRINE-CELLS
AB Gastric cancer is still a prevalent and lethal cancer. Gastric hypoacidity and gastritis have long been recognized in the pathogenesis. The identification of Helicobacter(H.) pylori as the main cause of gastritis leading to peptic ulcer disease and gastric cancer was a breakthrough. H. pylori was the first bacterium accepted as a carcinogen. The mechanism was not found before H. pylori was shown to predispose to cancer only after having induced oxyntic atrophy incriminating reduced killing of microorganisms and/or secondary hypergastrinemia. H. pylori has an uncertain carcinogenic role in cardia cancer, making microbes more unlikely. Gastrin has a trophic effect on the oxyntic mucosa, particularly on the enterochromaffin like cell carrying the gastrin receptor. Every condition with long-term hypergastrinemia in whatever species predisposes to gastric neoplasia. All observations on gastric neoplasia connected to H. pylori gastritis (the protective effect of duodenal ulcer, increased risk with oxyntic atrophy and preserved risk after loss of H. pylori in complete oxyntic atrophy) may be explained by gastrin. The role of gastrin in gastric carcinogenesis is also reflected by autoimmune gastritis and profound long-term gastric acid inhibition.
C1 [Waldum, Helge] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, Trondheim, Norway.
   [Modlin, Irvin] FCS RSA Emeritus Prof Yale Univ, Sch Med, New Haven, CT USA.
C3 Norwegian University of Science & Technology (NTNU)
RP Waldum, H (corresponding author), Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, Trondheim, Norway.
EM helge.waldum@ntnu.no
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NR 121
TC 0
Z9 0
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD 2025 MAY 24
PY 2025
DI 10.1080/00365521.2025.2509094
EA MAY 2025
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 2YF6L
UT WOS:001494156400001
PM 40411354
DA 2025-06-01
ER

PT J
AU Haam, K
   Kim, HJ
   Lee, KT
   Kim, JH
   Kim, M
   Kim, SY
   Noh, SM
   Song, KS
   Kim, YS
AF Haam, Keeok
   Kim, Hee-Jin
   Lee, Kyung-Tae
   Kim, Jeong-Hwan
   Kim, Mirang
   Kim, Seon-Young
   Noh, Seung-Moo
   Song, Kyu-Sang
   Kim, Yong Sung
TI Epigenetic silencing of BTB and CNC homology 2 and concerted promoter
   CpG methylation in gastric cancer
SO CANCER LETTERS
LA English
DT Article
DE Gastric cancer; RLGS; BACH2; Concerted methylation
ID GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; REPRESSOR BACH2;
   CELL-MIGRATION; RISK LOCI; GENE; HYPERMETHYLATION; ACTIVATION;
   CARCINOMA; PROTEIN
AB BTB and CNC homology 2 (BACH2) is a lymphoid-specific transcription factor with a prominent role in B-cell development. Genetic polymorphisms within a single locus encoding BACH2 are associated with various autoimmune diseases and allergies. In this study, restriction landmark genomic scanning revealed methylation at a NotI site in a CpG island covering the BACH2 promoter in gastric cancer cell lines and primary gastric tumors. Increased methylation of the BACH2 promoter was observed in 52% (43/83) of primary gastric tumors, and BACH2 hypermethylation was significantly associated with decreased gene expression. Treatment with 5-aza-2'-deoxycytidine and/or trichostatin. A restored BACH2 expression in BACH2-silenced gastric cancer cell lines, and knockdown of BACH2 using short hairpin RNA (i.e. RNA interference) increased cell proliferation in gastric cancer cells. Clinicopathologic data showed that decreased BACH2 expression occurred significantly more frequently in intestinal-type (27/44, 61%) compared with diffuse-type (13/50, 26%) gastric cancers (P < 0.001). Furthermore, BACH2 promoter methylation paralleled that of previously identified targets, such as LRRC3B, LIMS2, PRKD1 and POPDC3, in a given set of gastric tumors. We propose that concerted methylation in many promoters plays a role in accelerating gastric tumor formation and that methylated promoter loci may be targets for therapeutic treatment, such as the recently introduced technique of epigenetic editing. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
C1 [Haam, Keeok; Kim, Hee-Jin; Lee, Kyung-Tae; Kim, Jeong-Hwan; Kim, Mirang; Kim, Seon-Young; Kim, Yong Sung] Korea Res Inst Biosci & Biotechnol, Med Genom Res Ctr, Taejon 305806, South Korea.
   [Haam, Keeok; Kim, Hee-Jin; Kim, Mirang; Kim, Seon-Young; Kim, Yong Sung] Korea Univ Sci & Technol, Dept Funct Genom, Taejon 305806, South Korea.
   [Noh, Seung-Moo; Song, Kyu-Sang] Chungnam Natl Univ, Coll Med, Taejon 301747, South Korea.
C3 Korea Research Institute of Bioscience & Biotechnology (KRIBB); Chungnam
   National University
RP Kim, YS (corresponding author), Korea Res Inst Biosci & Biotechnol, Med Genom Res Ctr, 125 Gwahak Ro, Taejon 305806, South Korea.
EM yongsung@kribb.re.kr
RI KIM, SEON HAHN/JTU-1415-2023; Kim, Mirang/KSL-4408-2024; Kim,
   Heejin/HII-8568-2022
OI Haam, Keeok/0000-0002-9933-7433; Kim, Mirang/0000-0001-7415-0077
FU National Research Foundation of Korea (NRF) - Korea government (MSIP)
   [2011-0030049, 2011-0015710]; A3 Foresight Program; KRIBB Research
   Initiative Grant
FX This work was supported by the National Research Foundation of Korea
   (NRF) Grants funded by the Korea government (MSIP) (Nos. 2011-0030049
   and 2011-0015710), the A3 Foresight Program and a KRIBB Research
   Initiative Grant.
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PU ELSEVIER IRELAND LTD
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PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3835
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WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AM9SR
UT WOS:000340221800004
PM 24858026
DA 2025-06-01
ER

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   Rugge, Massimo
   Martini, Chiara
   Zorzetto, Valerio
   Maddalo, Gemma
   Cazzagon, Nora
   Nitti, Donato
   Farinati, Fabio
TI Gastric type I carcinoid: a pilot study with human G17DT immunogen
   vaccination
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Gastric carcinoid; Cancer vaccine; Gastrin; G17; Autoimmune gastritis;
   ECL hyperplasia
ID NEUROENDOCRINE TUMORS; ENDOCRINE TUMORS; CELL CARCINOIDS;
   CLASSIFICATION; PATHOGENESIS; MANAGEMENT; STOMACH
AB Context Gastric type I carcinoid is a rare neoplasm, deriving from enterochromaffin-like cells (ECL), mainly affecting women with autoimmune gastritis. The approach to treatment, either endoscopic, medical or surgical, is not well defined, particularly in multifocal tumours or carcinoids with rapid growth/frequent recurrence.
   Objective To determine whether an anti-G17 vaccination might interfere on the natural history of gastric type I carcinoid.
   Setting Padua teaching Hospital, outpatient clinic.
   Design and patients Three patients with type I gastric carcinoid in autoimmune gastritis were administered, after informed consent and ethic committee approval, with a vaccine against gastrin 17 (G17), a synthetic peptide that stimulates specific and high-affinity anti-G17 antibodies, and followed up endoscopically and clinically for a mean of 36 months.
   Main outcome measures Gastric histology and specifically carcinoid growth/recurrence and trend in time in gastrin, G17, pepsinogens, chromogranin A and clinical parameters.
   Results Following vaccination, carcinoid regression was observed in 2/3 patients and, in one of the patients, even the disappearance of ECL hyperplasia, with a reduced ECL cells stimulation, confirmed by a significant reduction in chromogranin A levels. Regression was observed in the two patients that showed a more clear local response to the vaccine. Increased autoantibody titre was observed, but no appearance of new autoimmune diseases.
   Conclusions Anti-G17 vaccination induced regression of type I gastric carcinoid and could be considered for the treatment of this tumour, when endoscopic removal is not indicated.
C1 [Tieppo, Chiara; Zorzetto, Valerio; Maddalo, Gemma; Farinati, Fabio] Univ Padua Polyclin, Dept Surg & Gastroenterol Sci, I-35128 Padua, Italy.
   [Betterle, Corrado; Martini, Chiara] Univ Padua Polyclin, Dept Med & Surg Sci, I-35128 Padua, Italy.
   [Basso, Daniela] Univ Padua Polyclin, Dept Lab Med, I-35128 Padua, Italy.
   [Mescoli, Claudia; Rugge, Massimo] Univ Padua Polyclin, Dept Med Diagnost Sci & Special Therapies, Pathol Unit, I-35128 Padua, Italy.
   [Cazzagon, Nora] Univ Padua Polyclin, IOV Venetian Inst Oncol, IRCCS, I-35128 Padua, Italy.
   [Nitti, Donato] Univ Padua Polyclin, Dept Oncol & Surg Sci, I-35128 Padua, Italy.
C3 University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua; Azienda Ospedaliera - Universita di Padova;
   University of Padua; Azienda Ospedaliera - Universita di Padova; IRCCS
   Istituto Oncologico Veneto (IOV)
RP Farinati, F (corresponding author), Univ Padua Polyclin, Dept Surg & Gastroenterol Sci, Via Giustiniani 2, I-35128 Padua, Italy.
EM fabio.farinati@unipd.it
RI Farinati, Fabio/A-8267-2012; Rugge, Massimo/K-7525-2016; Martini,
   Chiara/M-3546-2016; Basso, Daniela/J-7855-2016
OI FARINATI, FABIO/0000-0002-2944-1374; Martini,
   Chiara/0000-0002-0877-4954; Cazzagon, Nora/0000-0002-6937-8664; Basso,
   Daniela/0000-0001-8745-6171
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NR 20
TC 9
Z9 12
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD JUL
PY 2011
VL 60
IS 7
BP 1057
EP 1060
DI 10.1007/s00262-011-1031-5
PG 4
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA 780TZ
UT WOS:000291883500015
PM 21590490
OA Green Published
DA 2025-06-01
ER

PT J
AU Waldum, H
   Fossmark, R
AF Waldum, Helge
   Fossmark, Reidar
TI Gastritis, Gastric Polyps and Gastric Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE ECL cell; gastrin; gastric cancer; gastric polyps; gastritis
ID FUNDIC GLAND POLYPS; HELICOBACTER-PYLORI INFECTION; PROTON PUMP
   INHIBITOR; LONG-TERM USE; MULTIPLE HYPERPLASTIC POLYPS;
   ENTEROCHROMAFFIN-LIKE CELL; MALIGNANT-TRANSFORMATION; ADENOMATOUS
   POLYPOSIS; RECEPTOR ANTAGONIST; PROXIMAL POLYPOSIS
AB Gastric cancer is still an important disease causing many deaths worldwide, although there has been a marked reduction in prevalence during the last few decades. The decline in gastric cancer prevalence is due to a reduction in Helicobacter pylori infection which has occurred for at least 50 years. The most probable mechanism for the carcinogenic effect of H. pylori is hypergastrinemia since H. pylori infected individuals do not have increased risk of gastric cancer before the development of oxyntic atrophy. When atrophy has developed, the carcinogenic process continues independent of H. pylori. Autoimmune gastritis also induces oxyntic atrophy leading to marked hypergastrinemia and development of ECL cell neoplasia as well as adenocarcinoma. Similarly, long-term treatment with efficient inhibitors of acid secretion like the proton pump inhibitors (PPIs) predisposes to ECL cell neoplasia of a different degree of malignancy. Contrasting the colon where most cancers develop from polyps, most polyps in the stomach have a low malignant potential. Nevertheless, gastric polyps may also give rise to cancer and have some risk factors and mechanisms in common with gastric cancer. In this overview the most common gastric polyps, i.e., hyperplastic polyps, adenomatous polyps and fundic gland polyps will be discussed with respect to etiology and particularly use of PPIs and relation to gastric carcinogenesis.
C1 [Waldum, Helge; Fossmark, Reidar] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
   [Fossmark, Reidar] Trondheim Reg & Univ Hosp, Dept Gastroenterol & Hepatol, St Olavs Hosp, N-7006 Trondheim, Norway.
C3 Norwegian University of Science & Technology (NTNU); Norwegian
   University of Science & Technology (NTNU)
RP Waldum, H (corresponding author), Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
EM helge.waldum@ntnu.no; Reidar.fossmark@ntnu.no
RI Fossmark, Reidar/AAP-6442-2021
OI Waldum, Helge/0000-0002-3137-0843
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NR 135
TC 85
Z9 95
U1 7
U2 53
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUN
PY 2021
VL 22
IS 12
AR 6548
DI 10.3390/ijms22126548
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA SZ2SX
UT WOS:000666422700001
PM 34207192
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Saito, S
   Kasai, Y
   Nomoto, S
   Fujiwara, M
   Akiyama, S
   Ito, K
   Nakao, A
AF Saito, S
   Kasai, Y
   Nomoto, S
   Fujiwara, M
   Akiyama, S
   Ito, K
   Nakao, A
TI Polymorphism of tumor necrosis factor in esophageal, gastric or
   colorectal carcinoma
SO HEPATO-GASTROENTEROLOGY
LA English
DT Article
DE polymorphism; tumor necrosis factor (a,d); esophageal carcinoma; gastric
   carcinoma; colorectal carcinoma
ID DEPENDENT DIABETES-MELLITUS; FACTOR MICROSATELLITE POLYMORPHISMS;
   FACTOR-BETA-GENE; CANCER PATIENTS; FACTOR-ALPHA; FACTOR TNF; ALLELES;
   REGION; ASSOCIATION; SUSCEPTIBILITY
AB Background/Aims: Several microsatellite polymorphisms located in the tumor necrosis factor locus on the chromosomal region 6p21.3 in the major histocompatibility complex region have been associated with malignant neoplasms and autoimmune diseases. In this study, we focused on the polymorphisms of tumor necrosis factor a and d from gastrointestinal carcinoma patients to ascertain whether they can be useful to predict these neoplasms.
   Methodology: We examined esophageal, gastric, and colorectal cancers (47, 53, 77 patients, respectively), and 213 normal controls. To compare the microsatellite polymorphisms of tumor necrosis factor a, d in Japanese individuals, dioxyribonucleic acids were extracted from normal mucosa (cancer patients) and from peripheral blood monocytes (the normal controls) by polymerase chain reaction.
   Results: The frequency of tumor necrosis factor a3 allele was significantly higher in gastric cancer (P=0.012 and that of tumor necrosis factor d7 allele was significantly higher in the colorectal cancer than the normal controls (P=0.037). That of tumor necrosis factor a10 was significantly lower in the gastric cancer than the normal controls (P=0.008).
   Conclusions: Microsatellite polymorphisms of tumor necrosis factor a and d might be significantly correlated with carcinogenesis of specific neoplasms, and may be useful for predicting these cancers.
C1 Nagoya Univ, Sch Med, Dept Surg 2, Showa Ku, Nagoya, Aichi 4668550, Japan.
C3 Nagoya University
RP Saito, S (corresponding author), Nagoya Univ, Sch Med, Dept Surg 2, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan.
RI Fujiwara, Michitaka/AAV-9715-2021
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NR 24
TC 14
Z9 14
U1 0
U2 3
PU H G E UPDATE MEDICAL PUBL LTD.
PI ATHENS
PA PO BOX 17160, ATHENS GR-10024, GREECE
SN 0172-6390
J9 HEPATO-GASTROENTEROL
JI Hepato-Gastroenterol.
PD MAR-APR
PY 2001
VL 48
IS 38
BP 468
EP 470
PG 3
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 425QU
UT WOS:000168303500041
PM 11379335
DA 2025-06-01
ER

PT J
AU Jing, YM
   Xu, FM
   Liang, WQ
   Liu, J
   Zhang, L
AF Jing, Yuanming
   Xu, Fangming
   Liang, Wenqing
   Liu, Jian
   Zhang, Lin
TI Role of regulatory B cells in gastric cancer: Latest evidence and
   therapeutics strategies
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE Gastric cancer; Regulatory B cells; Immune modulation; Tumor
   microenvironment; Tumor progression
ID TUMOR-INFILTRATING LYMPHOCYTES; HELICOBACTER-PYLORI INFECTION; CD8(+)
   T-CELLS; PERIPHERAL-BLOOD; GROWTH-FACTOR; AUTOIMMUNE; EXPRESSION;
   INFLAMMATION; PHENOTYPE; SURVIVAL
AB Gastric cancer (GC) is the second most common cancer globally and kills about 700,000 people annually. Today's knowledge clearly shows a close and complicated relationship between the tumor microenvironment (TME) and the immune system. The immune system components can both stimulate tumor growth and inhibit tumor cells. However, numerous of these mechanisms are not yet fully understood. As an essential immune cell in humoral immunity, B lymphocytes can play a dual role during various pathologic states, including infections, autoimmune diseases, and cancer, depending on their phenotype and environmental signals. Inherently, B cells can inhibit tumor growth by producing antibodies as well as the presentation of tumor antigens. However, evidence suggests that a subset of these cells termed regulatory B cells (Bregs) with an inhibitory phenotype can suppress antitumor responses and support the tumor growth by producing anti-inflammatory cytokines and the expression of inhibitory molecules. Therefore, in this review, the role of Bregs in the microenvironment of GC and treatment strategies based on targeting this subset of B cells have been investigated.
C1 [Jing, Yuanming] Shaoxing Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Shaoxing Peoples Hosp,Shaoxing Hosp, Shaoxing 312000, Zhejiang, Peoples R China.
   [Xu, Fangming; Liang, Wenqing] Zhejiang Chinese Med Univ, Zhoushan Hosp Tradit Chinese Med, Dept Orthoped, 355 Xinqiao Rd, Zhoushan 316000, Zhejiang, Peoples R China.
   [Liu, Jian] Shanghai Oriental Hepatobiliary Hosp, Dept Hepatobiliary Surg, Shanghai 200438, Peoples R China.
   [Zhang, Lin] Shaoxing Univ, Affiliated Hosp 1, Shaoxing Hosp, Dept Pharm,Shaoxing Peoples Hosp, Shaoxing 312000, Zhejiang, Peoples R China.
C3 Shaoxing University; Zhejiang Chinese Medical University; Shaoxing
   University
RP Jing, YM (corresponding author), Shaoxing Univ, Affiliated Hosp 1, Dept Gastrointestinal Surg, Shaoxing Peoples Hosp,Shaoxing Hosp, Shaoxing 312000, Zhejiang, Peoples R China.; Zhang, L (corresponding author), Shaoxing Univ, Affiliated Hosp 1, Shaoxing Hosp, Dept Pharm,Shaoxing Peoples Hosp, Shaoxing 312000, Zhejiang, Peoples R China.
EM amaeba@usx.edu.cn; zhanglinfudan@zju.edu.cn
OI Zhang, Lin/0000-0002-3767-0249
FU Project of Health and Family Planning Commission of Zhejiang province
   [2021KY1139, 2018KY831]; Shaoxing Medical and Health Science and
   Technology Plan Project [2020A13026]; Project of Shaoxing Medical Key
   Discipline Construction Plan [2019SZD06]
FX This research work was supported by the Project of Health and Family
   Planning Commission of Zhejiang province (2021KY1139, 2018KY831) ,
   Shaoxing Medical and Health Science and Technology Plan Project
   (2020A13026) and the Project of Shaoxing Medical Key Discipline
   Construction Plan (2019SZD06) .
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NR 118
TC 14
Z9 14
U1 0
U2 14
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JUL
PY 2021
VL 96
AR 107581
DI 10.1016/j.intimp.2021.107581
EA MAR 2021
PG 8
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA SV8QB
UT WOS:000664081300008
PM 33812259
DA 2025-06-01
ER

PT J
AU Boyce, M
   Thomsen, L
AF Boyce, Malcolm
   Thomsen, Liv
TI Gastric neuroendocrine tumors: prevalence in Europe, USA, and Japan, and
   rationale for treatment with a gastrin/CCK2 receptor
   antagonist
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE autoimmune chronic atrophic gastritis; gastric carcinoids; gastrin/CCK2
   receptor antagonist; hypergastrinemia; netazepide; pernicious anemia
ID ZOLLINGER-ELLISON-SYNDROME; LONG-TERM TREATMENT; PERNICIOUS-ANEMIA;
   HELICOBACTER-PYLORI; NETAZEPIDE YF476; CARCINOID-TUMORS;
   GASTROINTESTINAL-TRACT; ATROPHIC GASTRITIS; FOLLOW-UP; OMEPRAZOLE
AB Objective. Gastric carcinoids (neuroendocrine tumors) arise from enterochromaffin-like cells in the gastric mucosa. Most are caused by hypergastrinemia. The objectives were to determine if their prevalence in Europe, USA and Japan meets the criteria for an orphan disease and to justify treatment with a gastrin/CCK2 receptor antagonist. Methods. We obtained data from European and USA cancer registries, and searched PubMed. Results. Prevalence per 10,000 population obtained from cancer registries was: median 0.32 (range 0.09-0.92) for Europe; and 0.17 for the USA, equivalent to 4812 for the whole population. A PubMed search for gastric carcinoids yielded prevalence for Japan only, which was 0.05 per 10,000 population, equivalent to 665 for the entire population. A further search for gastric carcinoids in patients with pernicious anemia (PA) or autoimmune chronic atrophic gastritis (CAG), two presentations of about 80% of gastric carcinoids, produced prevalence rates of 5.2-11%. Prevalence of PA itself was 0.12-1.9%. Data on CAG epidemiology were sparse. Conclusion. Prevalence of gastric carcinoids varied widely. All sources probably underestimate prevalence. However, prevalence was below the limits required for recognition by drug regulatory authorities as an orphan disease: 5 per 10,000 population of Europe; 200,000 for the whole population of the USA; and 50,000 for the whole population of Japan. Because gastric carcinoids are an orphan disease, and nonclinical and healthy volunteer studies support treatment with netazepide, a gastrin/CCK2 antagonist, netazepide has been designated an orphan medicinal product in Europe and the USA for development as targeted treatment for gastric carcinoids.
C1 [Boyce, Malcolm] Cent Middlesex Hosp, Hammersmith Med Res, London NW10 7NS, England.
   [Boyce, Malcolm; Thomsen, Liv] Hammersmith Med Res, London NW10 7EW, England.
C3 Imperial College London
RP Boyce, M (corresponding author), Hammersmith Med Res, Cumberland Ave, London NW10 7EW, England.
EM mboyce@hmrlondon.com
OI Boyce, Malcolm/0000-0001-8807-612X
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NR 84
TC 27
Z9 34
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD MAY
PY 2015
VL 50
IS 5
BP 550
EP 559
DI 10.3109/00365521.2015.1009941
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CD9VQ
UT WOS:000351448100007
PM 25665655
DA 2025-06-01
ER

PT J
AU Sato, R
   Matsumoto, K
   Kanzaki, H
   Matsumi, A
   Miyamoto, K
   Morimoto, K
   Terasawa, H
   Fujii, Y
   Yamazaki, T
   Uchida, D
   Tsutsumi, K
   Horiguchi, S
   Kato, H
AF Sato, Ryosuke
   Matsumoto, Kazuyuki
   Kanzaki, Hiromitsu
   Matsumi, Akihiro
   Miyamoto, Kazuya
   Morimoto, Kosaku
   Terasawa, Hiroyuki
   Fujii, Yuki
   Yamazaki, Tatsuhiro
   Uchida, Daisuke
   Tsutsumi, Koichiro
   Horiguchi, Shigeru
   Kato, Hironari
TI Gastric linitis plastica with autoimmune pancreatitis diagnosed by an
   endoscopic ultrasonography-guided fine-needle biopsy: A case report
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Endoscopic ultrasound-guided fine needle aspiration; Linitis plastica;
   Autoimmune pancreatitis; Paraneoplastic syndromes; Case report
ID CANCER
AB BACKGROUND Gastric linitis plastica (GLP) is a subset of gastric cancer with a poor prognosis. It is difficult to obtain a definitive diagnosis by endoscopic mucosal biopsies, and the usefulness of an endoscopic ultrasonography-guided fine-needle biopsy (EUS-FNB) for GLP has been recently reported. Meanwhile, autoimmune diseases are occasionally known to coexist with malignant tumors as paraneoplastic syndrome. We herein report the usefulness of an EUS-FNB for detecting GLP and the possibility of paraneoplastic syndrome coexisting with GLP. CASE SUMMARY An 81-year-old man was admitted to our hospital for a 1-mo history of epigastric pain that increased after eating. His laboratory data revealed high levels of serum carbohydrate antigen 19-9 and immunoglobulin-G4. Endoscopic examinations showed giant gastric folds and reddish mucosa; however, no epithelial changes were observed. The gastric lumen was not distensible by air inflation, suggesting GLP. Computed tomography showed the thickened gastric wall, the diffuse enlargement of the pancreas, and the peripancreatic rim, which suggested autoimmune pancreatitis (AIP) coexisting with GLP. Because the pathological findings of the endoscopic biopsy showed no malignancy, he underwent an EUS-FNB and was diagnosed with GLP. He received chemotherapy for unresectable gastric cancer due to peritoneal metastasis, after which both the gastric wall thickening and diffuse enlargement of the pancreas were improved. CONCLUSION An EUS-FNB for GLP with a negative endoscopic biopsy is useful, and AIP may develop as a paraneoplastic syndrome.
C1 [Sato, Ryosuke; Matsumoto, Kazuyuki; Kanzaki, Hiromitsu; Matsumi, Akihiro; Miyamoto, Kazuya; Morimoto, Kosaku; Terasawa, Hiroyuki; Fujii, Yuki; Yamazaki, Tatsuhiro; Uchida, Daisuke; Tsutsumi, Koichiro; Horiguchi, Shigeru; Kato, Hironari] Okayama Univ Hosp, Gastroenterol & Hepatol, Okayama 7008558, Japan.
   [Matsumoto, Kazuyuki] Okayama Univ Hosp, Gastroenterol & Hepatol, 2-5-1 Shikata cho,Kita ku, Okayama 7008558, Japan.
C3 Okayama University; Okayama University
RP Matsumoto, K (corresponding author), Okayama Univ Hosp, Gastroenterol & Hepatol, 2-5-1 Shikata cho,Kita ku, Okayama 7008558, Japan.
EM matsumoto.k@okayama-u.ac.jp
OI Sato, Ryosuke/0000-0002-5368-6347
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NR 26
TC 2
Z9 2
U1 0
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD NOV 6
PY 2022
VL 10
IS 31
BP 11607
EP 11616
DI 10.12998/wjcc.v10.i31.11607
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 6H2DB
UT WOS:000885256200043
PM 36387831
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Foo, VHX
   Mehta, J
   Chan, ASY
   Ong, HS
AF Foo, Valencia Hui Xian
   Mehta, Jodhbir
   Chan, Anita Sook Yee
   Ong, Hon Shing
TI Case Report: Peripheral Ulcerative Keratitis in Systemic Solid Tumour
   Malignancies
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE malignancy; paraneoplastic; corneal; inflammation; peripheral ulcerative
   keratitis
ID GRANULOMATOSIS; ASSOCIATION; SCLERITIS
AB PurposeTo describe a case series of peripheral ulcerative keratitis (PUK) as a paraneoplastic condition in three patients with known underlying systemic solid tumor malignancies. ObservationsThree patients with different systemic malignancies (1 recurrent breast cancer, 1 metastatic thyroid cancer, and 1 metastatic gastric adenocarcinoma) were identified to have PUK with significant corneal stromal melt. Autoimmune and infective work up for other etiologies were all negative. They all responded well to topical steroids and intravenous methylprednisolone. One patient had recurrences of her PUK and required repeated amniotic grafts and tectonic keratoplasties before her corneal condition stabilized. Conclusions and ImportancePUK can be a rare manifestation of systemic solid tumor malignancies. Although PUK may not be an indicator of progression of the underlying malignancy, it can be sight-threatening. This case series highlights the necessity for clinicians to refer patients with systemic malignancies presenting with inflamed eyes for an early ophthalmological review. This facilitates the detection of this blinding disease, allowing for early therapeutic interventions and potentially better visual outcomes for these patients.
C1 [Foo, Valencia Hui Xian; Mehta, Jodhbir; Chan, Anita Sook Yee; Ong, Hon Shing] Singapore Natl Eye Ctr, Singapore, Singapore.
   [Foo, Valencia Hui Xian; Mehta, Jodhbir; Chan, Anita Sook Yee; Ong, Hon Shing] Singapore Eye Res Inst, Singapore, Singapore.
   [Mehta, Jodhbir; Chan, Anita Sook Yee; Ong, Hon Shing] Duke Natl Univ Singapore, Med Sch, Ophthalmol & Visual Sci Acad Clin Res Program, Singapore, Singapore.
C3 Singapore National Eye Center; National University of Singapore;
   Singapore National Eye Center; National University of Singapore
RP Ong, HS (corresponding author), Singapore Natl Eye Ctr, Singapore, Singapore.; Ong, HS (corresponding author), Singapore Eye Res Inst, Singapore, Singapore.; Ong, HS (corresponding author), Duke Natl Univ Singapore, Med Sch, Ophthalmol & Visual Sci Acad Clin Res Program, Singapore, Singapore.
EM honshing@gmail.com
RI Ong, Shing/AAH-7512-2019
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NR 21
TC 0
Z9 0
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD MAY 31
PY 2022
VL 9
AR 907285
DI 10.3389/fmed.2022.907285
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 2C6CY
UT WOS:000810955300001
PM 35712100
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Panozzo, MP
   Antico, A
   Bizzaro, N
AF Panozzo, Maria Piera
   Antico, Antonio
   Bizzaro, Nicola
TI Monitoring the follow-up of autoimmune chronic atrophic gastritis using
   parietal cell antibodies and markers of gastric function
SO JOURNAL OF TRANSLATIONAL AUTOIMMUNITY
LA English
DT Article
DE Parietal cell autoantibodies; Intrinsic factor autoantibodies;
   Autoimmune chronic atrophic gastritis; Neuroendocrine tumors;
   Pepsinogens; Gastrin 17
ID IRON-DEFICIENCY ANEMIA; INTRINSIC-FACTOR; BODY GASTRITIS;
   AUTOANTIBODIES; PREVALENCE; DIAGNOSIS; DISEASES; AGE; CLASSIFICATION;
   PATHOGENESIS
AB Increased interest in the pathogenesis and the evolution of autoimmune chronic atrophic gastritis (A-CAG) has led to the search for serological markers that can be used to detect changes in the gastric mucosa at an early stage and to monitor the course of the disease. Parietal cell autoantibodies have been proposed as suitable immunological markers of atrophic damage, as they can be detected in the serum when symptoms of gastritis are not yet present. However, the utility of measuring only the level of parietal cell autoantibodies in the follow-up of A-CAG does not appear to suffice. Recent evidence has suggested that, in monitoring A-CAG, parietal cell antibodies should be associated with an evaluation of gastric function through biochemical and hormonal tests, such as pepsinogens and gastrin 17. This integrated approach will allow for the more effective real-time monitoring of the state of the gastric mucosa. As A-CAG is a progressive disorder associated with an increased risk of gastric cancer and neuroendocrine tumors, the precise follow-up of patients with gastric atrophy needs to be better defined. Further longitudinal studies in large cohorts must be performed with long-term follow-up.
C1 [Panozzo, Maria Piera] AULSS7 Pedemontana, Dept Lab Med, Santorso, Italy.
   [Antico, Antonio] AULSS2 Marca Trevigiana, Dept Lab Med, Treviso, Italy.
   [Bizzaro, Nicola] Azienda Sanit Univ Integrata, Lab Clin Pathol, Udine, Italy.
C3 ULSS 2 Marca TV; Ospedale Ca' Foncello Treviso
RP Bizzaro, N (corresponding author), Azienda Sanit Univ Integrata, Lab Clin Pathol, Udine, Italy.
EM nic.bizzaro@gmail.com
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NR 85
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2589-9090
J9 J TRANSL AUTOIMMUN
JI J. Transl. Autoimmun.
PD JUN
PY 2025
VL 10
AR 100273
DI 10.1016/j.jtauto.2025.100273
EA JAN 2025
PG 8
WC Immunology
WE Emerging Sources Citation Index (ESCI)
SC Immunology
GA U4M4R
UT WOS:001411554300001
PM 39917315
DA 2025-06-01
ER

PT J
AU Livzan, MA
   Gaus, OV
   Mozgovoi, SI
   Bordin, DS
AF Livzan, Maria A.
   Gaus, Olga V.
   Mozgovoi, Sergei I.
   Bordin, Dmitry S.
TI Chronic Autoimmune Gastritis: Modern Diagnostic Principles
SO DIAGNOSTICS
LA English
DT Review
DE chronic autoimmune gastritis; atrophic gastritis; nutritional status;
   vitamin B12 deficiency; megaloblastic anemia; neuroendocrine tumors;
   gastric adenocarcinoma
ID CHRONIC ATROPHIC GASTRITIS; CHROMOGRANIN-A; INTESTINAL METAPLASIA;
   HELICOBACTER-PYLORI; NEUROENDOCRINE NEOPLASMS; FOLLOW-UP;
   CLASSIFICATION; PREVALENCE; COBALAMIN; GASTROPANEL
AB This article summarizes and systematizes the available data from the literature on chronic autoimmune gastritis (CAG) in order to increase the awareness of specialists about the modern possibilities for diagnosing the disease, including its early stages. The clinical manifestation of the disease includes possible variants such as gastrointestinal, hematological (first of all, the formation of iron deficiency and B12-deficiency anemia), and neurological variants. Patients with chronic autoimmune gastritis are characterized by comorbidity with other autoimmune diseases. In this paper, data on the most informative serological markers for the diagnosis of CAG, as well as laboratory tests to detect micronutrient deficiencies, information on the characteristic changes in the gastric mucosa, and the prognosis of the disease, are presented. The diagnosis of CAG should be based on a multidisciplinary approach that combines a thorough analysis of a patient's complaints with a mandatory assessment of nutritional status, as well as the results of serological, endoscopic, and histological research methods.
C1 [Livzan, Maria A.; Gaus, Olga V.; Mozgovoi, Sergei I.] Omsk Sate Med Univ, Omsk 644099, Russia.
   [Bordin, Dmitry S.] AS Loginov Moscow Clin Sci Ctr, Moscow 111123, Russia.
   [Bordin, Dmitry S.] AI Yevdokimov Moscow State Univ Med & Dent, Moscow 127473, Russia.
   [Bordin, Dmitry S.] Tver State Med Univ, Tver 170100, Russia.
C3 Moscow State University of Medicine & Dentistry
RP Bordin, DS (corresponding author), AS Loginov Moscow Clin Sci Ctr, Moscow 111123, Russia.; Bordin, DS (corresponding author), AI Yevdokimov Moscow State Univ Med & Dent, Moscow 127473, Russia.; Bordin, DS (corresponding author), Tver State Med Univ, Tver 170100, Russia.
EM mlivzan@yandex.ru; gaus_olga@bk.ru; simozgovoy@yandex.com;
   d.bordin@mknc.ru
RI Mozgovoi, Sergei/M-6121-2016; Livzan, Maria/AAA-1409-2019; Gaus,
   Olga/AAB-1979-2019; Bordin, Dmitry/M-4708-2017
OI Mozgovoi, Sergei/0000-0001-7200-7082; Gaus, Ol'ga/0000-0001-9370-4768;
   Livzan, Maria/0000-0002-6581-7017; Bordin, Dmitry/0000-0003-2815-3992
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NR 60
TC 15
Z9 16
U1 1
U2 30
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD NOV
PY 2021
VL 11
IS 11
AR 2113
DI 10.3390/diagnostics11112113
PG 15
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XH1UG
UT WOS:000725226600001
PM 34829460
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Iida, T
   Iwahashi, M
   Katsuda, M
   Ishida, K
   Nakamori, M
   Nakamura, M
   Naka, T
   Ojima, T
   Ueda, K
   Hayata, K
   Nakamura, Y
   Yamaue, H
AF Iida, Takeshi
   Iwahashi, Makoto
   Katsuda, Masahiro
   Ishida, Koichiro
   Nakamori, Mikihito
   Nakamura, Masaki
   Naka, Teiji
   Ojima, Toshiyasu
   Ueda, Kentaro
   Hayata, Keiji
   Nakamura, Yasushi
   Yamaue, Hiroki
TI Tumor-infiltrating CD4<SUP>+</SUP> Th17 cells produce IL-17 in tumor
   microenvironment and promote tumor progression in human gastric cancer
SO ONCOLOGY REPORTS
LA English
DT Article
DE Th17; IL-17; IL-21; gastric cancer; angiogenesis; inflammation
ID T-CELLS; HELICOBACTER-PYLORI; OVARIAN-CANCER; T(H)17 CELLS; TGF-BETA;
   INTERLEUKIN-17; GROWTH; ANGIOGENESIS; INFLAMMATION; DIFFERENTIATION
AB Recently, a subset of IL-17 producing T cells distinct from Th1 or Th2 cells has been described as key players in inflammation and autoimmune diseases as well as cancer development. In this study, we investigated the expression level of IL-17 and T helper 17 (Th17)-related cytokines in gastric cancer tissues and assessed the association of their expression with angiogenesis and their clinicopathological parameters. Tumor and adjacent normal tissues were obtained from 82 patients with gastric cancer. IL-17, IL-21 and IL-23 mRNA expression levels were quantified by real-time RT-PCR. Th17 infiltration, microvessel density and neutrophil infiltration in tumor tissues were examined by immunohistochemistry and double immunofluorescence histochemistry. Expression of IL-17, IL-21 and IL-23 mRNA was found to be significantly up-regulated in tumor tissues compared with adjacent normal tissues. The expression level of IL-17 mRNA strongly and positively correlated with that of IL-21 mRNA in tumor tissue. The number of vascular endothelial cells and infiltrating neutrophils was significantly larger in tumors expressing a high level of IL-17 mRNA than in tumors expressing a low level of IL-17 mRNA. In tumor tissues most CD4(+) cells were stained with anti-IL-17 antibody. The expression level of IL-17 mRNA in gastric tumors was associated with the depth of the tumors, lymph-vascular invasion and lymph node involvement, suggesting that IL-17 obviously was related to tumor progression. IL-17 and IL-21, which regulates IL-17, would be potential therapeutic targets for the treatment of gastric cancer.
C1 [Iida, Takeshi; Iwahashi, Makoto; Katsuda, Masahiro; Ishida, Koichiro; Nakamori, Mikihito; Nakamura, Masaki; Naka, Teiji; Ojima, Toshiyasu; Ueda, Kentaro; Hayata, Keiji; Yamaue, Hiroki] Wakayama Med Univ, Sch Med, Dept Surg 2, Wakayama 6418510, Japan.
   [Nakamura, Yasushi] Wakayama Med Univ, Sch Med, Div Pathol, Dept Clin Lab Med, Wakayama 6418510, Japan.
C3 Wakayama Medical University; Wakayama Medical University
RP Iwahashi, M (corresponding author), Wakayama Med Univ, Sch Med, Dept Surg 2, 811-1 Kimiidera, Wakayama 6418510, Japan.
EM makoto@wakayama-med.ac.jp
RI Nakamura, Yasushi/J-5143-2014
FU Grants-in-Aid for Scientific Research [23791492, 22791296] Funding
   Source: KAKEN
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NR 30
TC 128
Z9 145
U1 0
U2 16
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1021-335X
EI 1791-2431
J9 ONCOL REP
JI Oncol. Rep.
PD MAY
PY 2011
VL 25
IS 5
BP 1271
EP 1277
DI 10.3892/or.2011.1201
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 753YS
UT WOS:000289817300010
PM 21369705
OA Bronze
DA 2025-06-01
ER

PT J
AU Wang, ZX
   Zhu, JL
   Gu, HD
   Yuan, YA
   Zhang, B
   Zhu, DM
   Zhou, JA
   Zhu, YB
   Chen, WC
AF Wang, Zhenxin
   Zhu, Jinlian
   Gu, Haidi
   Yuan, Yuan
   Zhang, Bin
   Zhu, Dongming
   Zhou, Jian
   Zhu, Yibei
   Chen, Weichang
TI The Clinical Significance of Abnormal Tim-3 Expression on NK Cells from
   Patients with Gastric Cancer
SO IMMUNOLOGICAL INVESTIGATIONS
LA English
DT Article
DE gastric cancer; natural killer cells; T-bet; Tim-3; tumor progression
ID ANTITUMOR IMMUNITY; DISEASE; EXHAUSTION; GALECTIN-9; AUTOIMMUNE;
   PROMOTION; LYMPHOMA; RECEPTOR
AB Aim: To investigate the clinical significance of Tim-3 (T-cell immunoglobulin-and mucin-domain-containing molecule 3) expression in natural killer (NK) cells from patients with gastric cancer.
   Materials and methods: Sixty-two patients with gastric cancer and 32 healthy controls were recruited for this study. Tim-3 expression in peripheral blood samples was analyzed using flow cytometry. The expression pattern of Tim-3 on NK cells was also confirmed using a gastric cancer-bearing mouse model. To further investigate the mechanisms that regulate Tim-3 expression, T-bet(-/-), Eomes(-/-), and Eomes/T-bet double knockout mice were utilized. Additionally, we statistically analyzed the clinical significance of Tim-3 expression on NK cells.
   Results: We found that the levels of Tim-3 in NK cells obtained from patients with gastric cancer were significantly higher than the levels in healthy controls. Clinical analyses showed that Tim-3 levels on NK cells were associated with advanced tumor stage. In a tumor-bearing mouse model, Tim-3 levels in NK cells increased with tumor growth, indicating that tumor progression could induce Tim-3 expression in NK cells. Finally, we report that T-bet is a key factor involved in regulating Tim-3 expression.
   Conclusion: Our data indicate that Tim-3 expression on NK cells is regulated by T-bet, and that Tim-3 levels correlate with advanced stages of gastric cancer.
C1 [Wang, Zhenxin; Zhu, Jinlian; Gu, Haidi] Soochow Univ, Affiliated Hosp 1, Dept Med Oncol, Suzhou 215006, Peoples R China.
   [Wang, Zhenxin; Chen, Weichang] Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Suzhou 215006, Peoples R China.
   [Yuan, Yuan] Hebei United Univ, Jitang Coll, Dept Teaching Serv, Tangshan, Peoples R China.
   [Zhang, Bin] Soochow Univ, Affiliated Hosp 1, Dept Nucl Med, Suzhou 215006, Peoples R China.
   [Zhu, Dongming; Zhou, Jian] Soochow Univ, Affiliated Hosp 1, Dept Gen Surg, Suzhou 215006, Peoples R China.
   [Zhu, Yibei; Chen, Weichang] Soochow Univ, Affiliated Hosp 1, Clin Immunol Jiangsu Prov, Suzhou 215006, Peoples R China.
C3 Soochow University - China; Soochow University - China; North China
   University of Science & Technology; Soochow University - China; Soochow
   University - China; Soochow University - China
RP Chen, WC (corresponding author), Soochow Univ, Affiliated Hosp 1, Dept Gastroenterol, Suzhou 215006, Peoples R China.
EM weichangchen@126.com
RI Wang, Zongrui/AAB-2799-2020
OI wang, zhen xin/0000-0002-1908-9848; Chen, Wei-Chang/0000-0001-8849-6204
FU National Natural Science Foundation of China [NO81272737, NO31170866]
FX This work was supported in part by the National Natural Science
   Foundation of China (NO81272737 and NO31170866).
CR Anderson AC, 2007, SCIENCE, V318, P1141, DOI 10.1126/science.1148536
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NR 22
TC 65
Z9 75
U1 0
U2 17
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0882-0139
EI 1532-4311
J9 IMMUNOL INVEST
JI Immunol. Invest.
PY 2015
VL 44
IS 6
BP 578
EP 589
DI 10.3109/08820139.2015.1052145
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CP6HK
UT WOS:000359986700005
PM 26214042
DA 2025-06-01
ER

PT J
AU Deswaerte, V
   Nguyen, P
   West, A
   Browning, AF
   Yu, L
   Ruwanpura, SM
   Balic, J
   Livis, T
   Girard, C
   Preaudet, A
   Oshima, H
   Fung, KY
   Tye, H
   Najdovska, M
   Ernst, M
   Oshima, M
   Gabay, C
   Putoczki, T
   Jenkins, BJ
AF Deswaerte, Virginie
   Nguyen, Paul
   West, Alison
   Browning, Alison F.
   Yu, Liang
   Ruwanpura, Saleela M.
   Balic, Jesse
   Livis, Thaleia
   Girard, Charlotte
   Preaudet, Adele
   Oshima, Hiroko
   Fung, Ka Yee
   Tye, Hazel
   Najdovska, Meri
   Ernst, Matthias
   Oshima, Masanobu
   Gabay, Cem
   Putoczki, Tracy
   Jenkins, Brendan J.
TI Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by
   an IL18-Mediated Inflammation-Independent Mechanism
SO CANCER RESEARCH
LA English
DT Article
ID INCREASED RISK; INTERLEUKIN-18; TUMORIGENESIS; PROMOTES; NLRP3;
   ACTIVATION; METHYLATION; SECRETION; ASC/TMS1; COLITIS
AB Inflammasomes are key regulators of innate immunity in chronic inflammatory disorders and autoimmune diseases, but their role in inflammation-associated tumorigenesis remains ill-defined. Here we reveal a protumorigenic role in gastric cancer for the key inflammasome adaptor apoptosis-related speck-like protein containing a CARD (ASC) and its effector cytokine IL18. Genetic ablation of ASC in the gp130(F/F) spontaneous mouse model of intestinal-type gastric cancer suppressed tumorigenesis by augmenting caspase-8-like apoptosis in the gastric epithelium, independently from effects on myeloid cells and mucosal inflammation. This phenotype was characterized by reduced activation of caspase-1 and NF-kappa B activation and reduced expression of mature IL18, but not IL1 beta, in gastric tumors. Genetic ablation of IL18 in the same model also suppressed gastric tumorigenesis, whereas blockade of IL1 beta and IL1 alpha activity upon genetic ablation of the IL1 receptor had no effect. The specific protumorigenic role for IL18 was associated with high IL18 gene expression in the gastric tumor epithelium compared with IL1 beta, which was preferentially expressed in immune cells. Supporting an epithelial-specific role for IL18, we found it to be highly secreted from human gastric cancer cell lines. Moreover, IL18 blockade either by a neutralizing anti-IL18 antibody or by CRISPR/Cas9-driven deletion of ASC augmented apoptosis in human gastric cancer cells. In clinical specimens of human gastric cancer tumors, we observed a significant positive correlation between elevated mature IL18 protein and ASC mRNA levels. Collectively, our findings reveal the ASC/IL18 signaling axis as a candidate therapeutic target in gastric cancer.
   Significance: Inflammasome activation that elevates IL18 helps drive gastric cancer by protecting cancer cells against apoptosis, with potential implications for new therapeutic strategies in this setting. (C) 2017 AACR.
C1 [Deswaerte, Virginie; West, Alison; Browning, Alison F.; Yu, Liang; Ruwanpura, Saleela M.; Balic, Jesse; Livis, Thaleia; Tye, Hazel; Najdovska, Meri; Jenkins, Brendan J.] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
   [Deswaerte, Virginie; West, Alison; Browning, Alison F.; Yu, Liang; Ruwanpura, Saleela M.; Balic, Jesse; Livis, Thaleia; Tye, Hazel; Najdovska, Meri; Jenkins, Brendan J.] Monash Univ, Sch Clin Sci, Dept Mol Translat Sci, Clayton, Vic, Australia.
   [Nguyen, Paul; Preaudet, Adele; Fung, Ka Yee; Putoczki, Tracy] Walter & Eliza Hall Inst Med Res, Inflammat Div, Parkville, Vic, Australia.
   [Nguyen, Paul; Preaudet, Adele; Fung, Ka Yee; Putoczki, Tracy] Univ Melbourne, Dept Med Biol, Parkville, Vic, Australia.
   [Girard, Charlotte; Gabay, Cem] Univ Hosp Geneva, Div Rheumatol, Geneva, Switzerland.
   [Girard, Charlotte; Gabay, Cem] Univ Geneva, Dept Pathol & Immunol, Sch Med, Geneva, Switzerland.
   [Oshima, Hiroko; Oshima, Masanobu] Kanazawa Univ, Canc Res Inst, Div Genet, Kanazawa, Ishikawa, Japan.
   [Ernst, Matthias] La Trobe Univ, Sch Canc Med, Olivia Newton John Canc Res Inst, Heidelberg, Vic, Australia.
C3 Hudson Institute of Medical Research; Monash University; Walter & Eliza
   Hall Institute; University of Melbourne; University of Geneva;
   University of Geneva; Kanazawa University; La Trobe University; Olivia
   Newton-John Cancer Research Institute
RP Jenkins, BJ (corresponding author), Hudson Inst Med Res, 27-31 Wright St, Clayton, Vic 3168, Australia.
EM brendan.jenkins@hudson.org.au
RI jenkins, brendan/J-7854-2012; Girard, Charlotte/IWU-5167-2023; Gabay,
   Cem/LJM-4539-2024; Oshima, Masanobu/F-9958-2014; Ernst,
   Matthias/D-5111-2012
OI BROWNING, Alison/0000-0002-0400-9921; Girard-Guyonvarc'h,
   Charlotte/0000-0002-4901-2059; Nguyen, Paul/0000-0003-1490-5401; Balic,
   Jesse/0000-0002-9681-6834; Oshima, Masanobu/0000-0002-3304-0004; Ernst,
   Matthias/0000-0002-6399-1177; Ruwanpura, saleela/0000-0002-4074-2012;
   Jenkins, Brendan/0000-0002-7552-4656
FU National Health and Medical Research Council (NHMRC) of Australia;
   Operational Infrastructure Support Program by the Victorian Government
   of Australia; Australian Postgraduate Awards from the Australian
   Government; NHMRC Early Career Fellowship; Victorian Cancer Agency
   Mid-Career Fellowship; NHMRC Senior Medical Research Fellowship
FX We thank R. Smith and P. Bouillet for comments, K. Fitzgerald
   (University of Massachusetts Medical School, Worcester, MA) for
   providing Asc<SUP>-/-</SUP> mice, and C. Nold (Hudson Institute of
   Medical Research, Melbourne, Australia) for providing anakinra. This
   work was funded by the National Health and Medical Research Council
   (NHMRC) of Australia (to B. Jenkins), and the Operational Infrastructure
   Support Program by the Victorian Government of Australia. P. Nguyen, A.
   Browning, and J. Balic were supported by Australian Postgraduate Awards
   from the Australian Government, and A. West was supported by an NHMRC
   Early Career Fellowship. T. Putoczki was supported by a Victorian Cancer
   Agency Mid-Career Fellowship. B. Jenkins was supported by an NHMRC
   Senior Medical Research Fellowship.
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NR 50
TC 64
Z9 72
U1 1
U2 27
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD MAR 1
PY 2018
VL 78
IS 5
BP 1293
EP 1307
DI 10.1158/0008-5472.CAN-17-1887
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA FY6UQ
UT WOS:000426998800013
PM 29282220
OA Green Submitted
DA 2025-06-01
ER

PT J
AU Monari, M
   Foschi, J
   Calabrese, C
   Liguori, G
   Di Febo, G
   Rizzello, F
   Gionchetti, P
   Trinchero, A
   Serrazanetti, GP
AF Monari, M.
   Foschi, J.
   Calabrese, C.
   Liguori, G.
   Di Febo, G.
   Rizzello, F.
   Gionchetti, P.
   Trinchero, A.
   Serrazanetti, G. P.
TI Implications of antioxidant enzymes in human gastric neoplasms
SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
LA English
DT Article
DE catalase; Cu/ZnSOD; gastric neoplasms; MnSOD; oxidative stress
ID HELICOBACTER-PYLORI; SUPEROXIDE-DISMUTASE; LIPID-PEROXIDATION; OXIDATIVE
   STRESS; DNA; CANCER; MNSOD; ASSOCIATION; EXPRESSION; DAMAGE
AB The present study is the first to evaluate the expression and activity of MnSOD, Cu/ZnSOD and catalase in human gastric samples, since ROS play a significant role in the pathogenesis of different forms of malignancy inducing mutations and various diseases such as gastric cancer. Biopsies and surgical samples from 53 patients (male/female 22/31, mean age 56.5 +/- 15.8 years) consisted of 15 healthy, 12 autoimmune atrophic gastritis, 10 Helicobacter pylori (HP) infection, 8 HP-negative chronic gastritis (CG) and 8 adenocarcinoma cases. Enzyme activity and expression were evaluated by spectrophotometry and immunoblotting after specific extraction in phosphate buffer. We found that MnSOD activity was increased in adenocarcinoma, CG and HP tissues (p<0.05-0.001), while Cu/ZnSOD was significantly lower in adenocarcinoma and HP tissues (p<0.001) when compared to the healthy control. MnSOD and Cu/ZnSOD were expressed to a significantly higher degree in adenocarcinoma and HP tissues (p<0.05 and <0.001 respectively) and to a significantly lower degree in CG tissues with respect to the healthy patients (p<0.05 and <0.001). A significant decrease in CAT activity in adenocarcinoma and HP tissues was observed (p<0.01 and <0.05). Gastric human neoplasms showed significant changes in antioxidant enzymes, that represent the first line in antioxidant protection against radical attack. The difficulties in correlating the antioxidant enzyme with the neoplasms was related to the complexity of the biochemical pathways that regulate the cellular redox balance. Our results are important in enhancing the understanding of the role that these enzymes play in the promotion/suppression of the carcinogenesis cascade in human gastric mucosa.
C1 [Monari, M.; Foschi, J.; Trinchero, A.; Serrazanetti, G. P.] Univ Bologna, Dipartimento Biochim G Moruzzi, Fac Med Vet, I-40064 Ozzano Dell Emilia, Italy.
   [Calabrese, C.; Liguori, G.; Di Febo, G.; Rizzello, F.; Gionchetti, P.] Univ Bologna, Fac Med & Chirurg, Dipartimento Med Clin, I-40139 Bologna, Italy.
C3 University of Bologna; University of Bologna
RP Monari, M (corresponding author), Univ Bologna, Dipartimento Biochim G Moruzzi, Fac Med Vet, Via Tolara Sopra 50, I-40064 Ozzano Dell Emilia, Italy.
EM marta.monari@unibo.it
RI Calabrese, Carlo/HLQ-6495-2023; monari, marta noemi/LXA-0099-2024
OI GIONCHETTI, PAOLO/0000-0001-9479-5307; Rizzello,
   Fernando/0000-0002-7949-5362; Calabrese, Carlo/0000-0003-3657-4463
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Z9 31
U1 0
U2 4
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1107-3756
EI 1791-244X
J9 INT J MOL MED
JI Int. J. Mol. Med.
PD NOV
PY 2009
VL 24
IS 5
BP 693
EP 700
DI 10.3892/ijmm_00000281
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 502YP
UT WOS:000270497400013
PM 19787204
OA Bronze
DA 2025-06-01
ER

PT J
AU Cao, BW
   Zhu, LZ
   Zhu, ST
   Li, DP
   Zhang, CZ
   Xu, CQ
   Zhang, ST
AF Cao, Bangwei
   Zhu, Linzhong
   Zhu, Shengtao
   Li, Danping
   Zhang, Chuanzhen
   Xu, Changqing
   Zhang, Shutian
TI Genetic variations and haplotypes in TIM-3 gene and the risk of gastric
   cancer
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE TIM-3 gene; Susceptibility; Gastric cancer
ID T-CELL IMMUNOGLOBULIN; POLYMORPHISMS; ASSOCIATION; AUTOIMMUNE;
   TOLERANCE; RESPONSES; IMMUNITY; DISEASE
AB T cell immunoglobulin and mucin domain-containing molecule 3 (TIM-3) could weaken the Th1-mediated anti-tumor responses and accelerate the tumor cell proliferation by inhabiting the production of IL-2 or IFN-gamma. This study was to assess the association between TIM-3 genetic variations and the development of gastric cancer.
   Five polymorphisms located in the promoter or encoding region of TIM-3 gene were genotyped in 212 gastric cancer patients and 252 controls who matched with the patients on the frequency of age, gender, smoking, and drinking. Logistic regression was used to determine whether the inherited variations within TIM-3 gene were associated with gastric cancer risk. Linkage disequilibrium and Haplotype analyses were performed by using SHEsis program.
   By the individual genotype analysis, three polymorphisms (-574G/T, -882C/T, and -1516G/T) within TIM-3 gene were significantly associated with gastric cancer in the study population [ORs (95% CIs): 2.74 (1.21-6.20), 3.19 (1.29-7.91), and 2.03 (1.15-3.59); respectively]. Among the gastric cancer patients, the relationship between the -1516 polymorphic genotype and the distant metastasis of tumor was found (OR = 2.21, 95% CI = 1.05-4.63). Under the analysis of haplotypes, an even stronger association with haplotype TTGCT was observed in gastric cancer risk (OR = 5.57, 95% CI: 1.04-29.80, P = 0.024).
   These results indicated that the three genetic variations within the TIM-3 gene promoter may be associated with the increased susceptibility to gastric cancer, especially among the haplotypes with the risk.
C1 [Zhu, Shengtao; Zhang, Shutian] Capital Med Univ, Dept Gastroenterol, Beijing Friendship Hosp, Beijing Digest Dis Ctr, Beijing 100050, Peoples R China.
   [Cao, Bangwei] Capital Med Univ, Beijing Friendship Hosp, Dept Oncol, Beijing 100050, Peoples R China.
   [Zhu, Linzhong] Peking Univ, Sch Oncol, Dept Intervent Therapy, Beijing Canc Hosp & Inst, Beijing 100142, Peoples R China.
   [Li, Danping; Zhang, Chuanzhen; Xu, Changqing] Qianfoshan Hosp, Dept Gastroenterol, Jinan 250014, Shandong, Peoples R China.
C3 Capital Medical University; Capital Medical University; Peking
   University; Shandong First Medical University & Shandong Academy of
   Medical Sciences
RP Zhang, ST (corresponding author), Capital Med Univ, Dept Gastroenterol, Beijing Friendship Hosp, Beijing Digest Dis Ctr, 95 Yong An Rd, Beijing 100050, Peoples R China.
EM shutianzhangbj@126.com
RI Zhuang, Peiyu/HII-5769-2022
FU National High Technology Research and Development Program of China
   [2007AA02Z4Z4]; Beijing Municipal Natural Science Foundation [7092103]
FX This study was supported by grants from the National High Technology
   Research and Development Program of China (2007AA02Z4Z4 to Shutian
   Zhang) and the Beijing Municipal Natural Science Foundation (7092103 to
   Bangwei Cao).
CR Anderson AC, 2007, SCIENCE, V318, P1141, DOI 10.1126/science.1148536
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NR 22
TC 34
Z9 45
U1 1
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD DEC
PY 2010
VL 59
IS 12
BP 1851
EP 1857
DI 10.1007/s00262-010-0910-5
PG 7
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA 654RC
UT WOS:000282184700009
PM 20811886
OA Green Published
DA 2025-06-01
ER

PT J
AU Zhang, HJ
   Jin, Z
   Cui, RL
   Ding, SG
   Huang, YH
   Zhou, LY
AF Zhang, Hejun
   Jin, Zhu
   Cui, Rongli
   Ding, Shigang
   Huang, Yonghui
   Zhou, Liya
TI Autoimmune metaplastic atrophic gastritis in chinese: a study of 320
   patients at a large tertiary medical center
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Adenocarcinoma; autoimmune metaplastic atrophic gastritis; carcinoid;
   hyperplastic polyp
ID PRIMARY BILIARY-CIRRHOSIS; PERNICIOUS-ANEMIA; LESIONS; CLASSIFICATION;
   MANAGEMENT; DIAGNOSIS; FEATURES; STOMACH; DISEASE; MUCOSA
AB Objectives: Autoimmune metaplastic atrophic gastritis (AMAG) is an uncommon disease worldwide and may predispose to gastric carcinoid tumors or adenocarcinomas. The aims of this study were to outline the clinical characteristics of Chinese AMAG patients, including demographic pattern, hematologic features, and gastroscopic and histopathologic findings.
   Patients and methods: A total of 320 Chinese patients with AMAG, from January 2007 to December 2014, were reviewed in a regional hospital of China.
   Results: Of the 320 AMAG patients, the mean age was 60.6 +/- 12.3 years [range 26-86; 206 (64.4%) women]. The coarse annual detection rate was 0.9%. Anemia was present in only 19.3% patients (53/275) and 3.5% (11/315) AMAG patients also had primary biliary cirrhosis. One hundred and thirty-six had endoscopically identifiable lesions. These lesions consisted of 130 polypoid lesions (63 hyperplastic polyps, 2 oxyntic mucosa pseudopolyps, 2 intestinal-type gastric adenomas, 2 fundic gland polyps, 5 concurrent polyps, 14 well-differentiated neuroendocrine neoplasms, 7 submucosal tumors and 35 chronic gastritis), 6 adenocarcinomas. The detection rate of atrophy and intestinal metaplasia in antral mucosa were 47.2 and 37.5%, respectively.
   Conclusions: AMAG is more frequent than expected in China and display a female predominance, accompanied with other autoimmune disorders. AMAG should be paid more attention by clinicians through a multidisciplinary team approach.
C1 [Zhang, Hejun; Jin, Zhu; Cui, Rongli; Ding, Shigang; Huang, Yonghui; Zhou, Liya] Peking Univ, Hosp 3, Beijing Key Lab Helicobacter Pylori Infect & Uppe, Pathol Lab,Dept Gastroenterol, Beijing, Peoples R China.
C3 Peking University
RP Jin, Z (corresponding author), 49 Rd Huayuan North, Beijing 100191, Peoples R China.
EM Jin-8993@163.com
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NR 30
TC 40
Z9 54
U1 1
U2 13
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PY 2017
VL 52
IS 2
BP 150
EP 156
DI 10.1080/00365521.2016.1236397
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA EI4UD
UT WOS:000392488000006
PM 27652682
DA 2025-06-01
ER

PT J
AU Bie, QL
   Jin, CQ
   Zhang, B
   Dong, HX
AF Bie, Qingli
   Jin, Chengqiang
   Zhang, Bin
   Dong, Haixin
TI IL-17B: A new area of study in the IL-17 family
SO MOLECULAR IMMUNOLOGY
LA English
DT Review
DE Cancer; Chemokines; Inflammation; Tumour immunology; Stem cells
ID MARIE-TOOTH DISEASE; CYTOKINE FAMILY; INTERLEUKIN-17 FAMILY;
   GASTRIC-CANCER; TNF-ALPHA; STEM-CELLS; RECEPTOR; EXPRESSION; MEMBERS;
   LIGAND
AB The interleukin (IL)-17 superfamily, a relatively new family of cytokines, consists of six ligands (from IL-17A to IL-17F), which bind to five receptor subtypes (fromIL-17RA toIL-17RE) and induce downstream signaling. IL-17A, a prototype member of this family, has been reported to be involved in the pathogenesis of allergies, autoimmune diseases, allograft transplantations, and malignancies. Unlike IL-17A, which is mainly produced by T helper 17 cells, IL-17B is widely expressed in various tissues. Recently, the biological function of IL-17B in diseases, particularly tumors, has attracted the attention of researchers. We previously reported that the expression ofIL-17RB increased in gastric cancer tissues and demonstrated that IL-17B/IL-17RB signaling plays a critical role in gastric tumor progression. However, studies on IL-17B are scant. In this review, we detail the structural characteristics, expression patterns, and biological activities of IL-17B and its potential role in the pathogenesis of diseases.
C1 [Bie, Qingli; Jin, Chengqiang; Zhang, Bin; Dong, Haixin] Jining Med Univ, Affiliated Hosp, Dept Lab Med, 89 Guhuai Rd, Jining 272000, Shandong, Peoples R China.
   [Bie, Qingli; Zhang, Bin] Jiangsu Univ, Sch Med, Key Lab Lab Med Jiangsu Prov, Zhenjiang, Jiangsu, Peoples R China.
C3 Jining Medical University; Jiangsu University
RP Dong, HX (corresponding author), Jining Med Univ, Affiliated Hosp, Dept Lab Med, 89 Guhuai Rd, Jining 272000, Shandong, Peoples R China.; Zhang, B (corresponding author), Jiangsu Univ, Sch Med, 301 Xuefu Rd, Zhenjiang 212013, Peoples R China.
EM zhb861109@163.com; donghaixin2011@126.com
RI B, Zhang/R-4316-2019
FU China Postdoctoral Science Foundation Funded Project [2016M600383];
   Special Funded Projects of National Postdoctoral Fund [2017T100337];
   project of science and technology development research center of
   ministry of health [28-10-2]; Natural Science Foundation of Shandong
   Province [ZR2010HL038]; Jining Municipal Science and Technology
   development projects [2012jnjc16, 2014jnnk23]; Shandong provincial
   medical and health science and technology development project
   [2013WS033]; Shandong Province Traditional Chinese medicine science and
   technology development project [2015-244]; Project of Shandong Province
   Higher Educational Science and Technology Program [J15LL11]
FX This work was supported by China Postdoctoral Science Foundation Funded
   Project (grant number 2016M600383), the Special Funded Projects of
   National Postdoctoral Fund (grant number 2017T100337), the project of
   science and technology development research center of ministry of health
   (grant number 28-10-2), the Natural Science Foundation of Shandong
   Province (grant number ZR2010HL038), Jining Municipal Science and
   Technology development projects (grant number 2012jnjc16 & 2014jnnk23),
   Shandong provincial medical and health science and technology
   development project (grant number 2013WS033), Shandong Province
   Traditional Chinese medicine science and technology development project
   (grant number 2015-244), and the Project of Shandong Province Higher
   Educational Science and Technology Program (grant number J15LL11).
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NR 47
TC 60
Z9 64
U1 3
U2 18
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0161-5890
J9 MOL IMMUNOL
JI Mol. Immunol.
PD OCT
PY 2017
VL 90
BP 50
EP 56
DI 10.1016/j.molimm.2017.07.004
PG 7
WC Biochemistry & Molecular Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Immunology
GA FK3JO
UT WOS:000413381600007
PM 28704706
OA hybrid
DA 2025-06-01
ER

PT J
AU Miskovic, R
   Miljanovic, D
   Cumic, MD
   Lazarevic, I
   Banko, A
AF Miskovic, Rada
   Miljanovic, Danijela
   Dimic Cumic, Maja
   Lazarevic, Ivana
   Banko, Ana
TI Epstein-Barr virus positive gastric adenocarcinoma with systemic EBV
   reactivation in a patient with persistently active systemic lupus
   erythematosus
SO ONCOLOGIE
LA English
DT Article
DE Epstein-Barr virus (EBV); gastric carcinoma; herpes viruses; systemic
   lupus erythematosus (SLE)
ID CANCER
AB Objectives: Epstein-Barr virus (EBV) has been associated with several types of cancers, most often with nasopharyngeal carcinomas and hematological malignancies. It is also suggested that EBV has significant role in the pathogenesis of different types of autoimmune diseases including systemic lupus erythematosus (SEL). The exact mechanisms behind these processes are not elucidated.Case presentation: We present a case of a 52-years old female patients with moderately active SLE presenting with severe fatigue, purpuric lesions, alopecia, polyarthritis, mucosal ulcerations, and progressive thrombocytopenia over a period of 10 months. During the work-up, the patient was evaluated for several viral infections. Serology testing showed elevation of anti-EBV, anti-CMV and anti-HSV1/2 IgM antibodies with the presence of IgG antibodies against all mentioned viruses except HSV2. Corticosteroid therapy was escalated, and azathioprine was introduced. Due to the persistence of significant thrombocytopenia and monoclonal IgG sternal puncture was performed. Morphological and immunohistochemical analysis of bone marrow specimen presented infiltration with metastatic deposits of adenocarcinoma and monoclonal plasmacytosis. Esophagogastroduodenoscopy showed multiple prepyloric erosions of gastric mucosa, which were biopsied. Pathohistological analysis demonstrated infiltration of gastric mucosa with diffuse type adenocarcinoma. Further PCR testing of biopsied gastric adenocarcinoma revealed the presence of EBV DNA in carcinoma tissue. The patient was sent to the oncologist for further evaluation.Conclusions: Assessment of SLE patients with persistently active disease should include the analysis of the herpesvirus infection status. Reactivations of EBV may be considered as possible trigger for lupus flares and the factor for increased risk of developing malignancies.
C1 [Miskovic, Rada] Univ Belgrade, Univ Clin Ctr Serbia, Fac Med, Clin Allergy & Immunol, Belgrade 11000, Serbia.
   [Miljanovic, Danijela; Lazarevic, Ivana; Banko, Ana] Univ Belgrade, Inst Microbiol & Immunol, Fac Med, Belgrade, Serbia.
   [Dimic Cumic, Maja] Univ Clin Ctr Serbia, Dept Pathol, Belgrade, Serbia.
C3 Clinical Centre of Serbia; University of Belgrade; University of
   Belgrade; Clinical Centre of Serbia
RP Miskovic, R (corresponding author), Univ Belgrade, Univ Clin Ctr Serbia, Fac Med, Clin Allergy & Immunol, Belgrade 11000, Serbia.
EM rada_delic@hotmail.com
RI Miskovic, Rada/AAK-6822-2020; Banko, Ana/GQQ-2011-2022; Lazarevic,
   Ivana/AEY-3871-2022
OI Miljanovic, Danijela/0000-0001-9446-8701; Lazarevic,
   Ivana/0000-0001-6795-1378; Banko, Ana/0000-0002-6829-096X
FU Science Fund of the Republic of Serbia, PROMIS [6060866]
FX The work was supported by the Science Fund of the Republic of Serbia,
   PROMIS, grant number 6060866, ROLERS.
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   Zádori N, 2021, FRONT IMMUNOL, V12, DOI 10.3389/fimmu.2021.750533
NR 21
TC 1
Z9 2
U1 0
U2 6
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1292-3818
EI 1765-2839
J9 ONCOLOGIE
JI Oncologie
PD MAR 16
PY 2023
VL 25
IS 1
BP 93
EP 97
DI 10.1515/oncologie-2022-1010
EA FEB 2023
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA A6UG9
UT WOS:000952572900001
OA hybrid
DA 2025-06-01
ER

PT J
AU Sun, XF
   Gao, XD
   Shen, KT
AF Sun, Xiang-Fei
   Gao, Xiao-Dong
   Shen, Kun-Tang
TI Treatment of gastric cancer with dermatomyositis as the initial symptom:
   Two case reports and review of literature
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Gastric cancer; Dermatomyositis; Treatment; Literature review; Rash;
   Case report
ID ANTIBODY-POSITIVE DERMATOMYOSITIS; POLYMYOSITIS; PATIENT; DIAGNOSIS;
   MUSCLE
AB BACKGROUND Dermatomyositis ( DM) is a rare autoimmune disease involving the connective tissue. The association between DM and gastric cancer remains unclear. Patients with DM have an increased risk of cancer and higher mortality. It requires immunosuppressive therapy, heightened surveillance, and immunologic response to internal malignancy. CASE SUMMARY Two cases of gastric cancer with DM as the first symptom in Zhongshan Hospital, Fudan University (Shanghai, China) were reported. Two patients had a typical skin rash. The rash in the first patient involved mainly bilateral upper limbs and neck, while the second patient manifested rash associated mainly with the face, neck, and back. Both manifested muscle weakness in the extremities and elevated serum creatine kinase. Radical resection of the tumor dramatically improved DMrelated symptoms in the two patients. The literature review showed that gastric cancer is more commonly associated with DM in middle- aged and older male populations. CONCLUSION The findings suggest the need for comprehensive screening for malignant tumors in patients with DM refractory to long-term pharmacotherapy or hormone manipulation.
C1 [Sun, Xiang-Fei; Gao, Xiao-Dong; Shen, Kun-Tang] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Sch Med, Shanghai 200032, Peoples R China.
C3 Fudan University
RP Shen, KT (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Sch Med, 180 Fenglin Rd, Shanghai 200032, Peoples R China.
EM shen.kuntang@zs-hospital.sh.cn
RI Sun, Xiangfei/HGE-9599-2022
FU National Natural Science Foundation of China [81773080]
FX Supported by the National Natural Science Foundation of China, No.
   81773080.
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NR 30
TC 0
Z9 1
U1 1
U2 4
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD SEP 26
PY 2022
VL 10
IS 27
BP 9727
EP 9733
DI 10.12998/wjcc.v10.i27.9727
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 6R2JS
UT WOS:000892134800017
PM 36186186
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Tajima, S
   Koda, K
AF Tajima, Shogo
   Koda, Kenji
TI Type 1 autoimmune pancreatitis may develop in gastric-type intraductal
   papillary mucinous neoplasm
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE Autoimmune pancreatitis; intraductal papillary mucinous neoplasm; mural
   nodule; pancreatoduodenectomy; type 1
ID OF-THE-LITERATURE; DUCTAL ADENOCARCINOMA; ASSOCIATION; DISEASE; LESIONS;
   CANCER
AB A subtype of autoimmune pancreatitis (AIP) is associated with increased serum IgG4, and IgE levels and steroid responsiveness, suggesting abnormal immunity, including allergy or autoimmunity. This subtype also exhibits dense infiltration of IgG4-positive plasma cells, storiform fibrosis, and obliterative phlebitis. Recognized as lymphoplasmacytic sclerosing pancreatitis (LPSP; type 1 AIP), this is a pancreatic manifestation of IgG4-related diseases (IgG4-RD). IgG4-RD can occur simultaneously with malignancies, which might also be applicable to AIP. However, the relationship between AIP and pancreatic carcinoma needs to be clarified. Recently, there are 4 reported cases of the coexistence of intraductal papillary mucinous neoplasm (IPMN) and AIP. We report another case of a 68-year-old Japanese man, where AIP developed in IPMN 4 years after the initial radiological detection of branchand gastric-type IPMN. We believe that the 4 previously reported cases also result from the coexistence of AIP and branch-and gastric-type IPMN. Two cases exhibited the occurrence of AIP during IPMN follow up similar to our case. These findings suggest that IPMN, particularly the branch-and gastric-type IPMN, might induce AIP. Further studies are necessary in order to conclusively define the relationship between IPMN and AIP.
C1 [Tajima, Shogo; Koda, Kenji] Fujieda Municipal Gen Hosp, Dept Pathol, 4-1-11 Surugadai, Fujieda, Shizuoka 4268677, Japan.
RP Tajima, S (corresponding author), Fujieda Municipal Gen Hosp, Dept Pathol, 4-1-11 Surugadai, Fujieda, Shizuoka 4268677, Japan.
EM stajima-tky@umin.ac.jp
CR Ban S, 2006, AM J SURG PATHOL, V30, P1561, DOI 10.1097/01.pas.0000213305.98187.d4
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NR 20
TC 0
Z9 0
U1 0
U2 1
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2016
VL 9
IS 2
BP 2402
EP 2408
PG 7
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DG1EU
UT WOS:000371809200237
DA 2025-06-01
ER

PT J
AU Atsumi, S
   Katoh, H
   Komura, D
   Hashimoto, I
   Furuya, G
   Koda, H
   Konishi, H
   Suzuki, R
   Yamamoto, A
   Yuba, S
   Abe, H
   Rino, Y
   Oshima, T
   Ushiku, T
   Fukayama, M
   Seto, Y
   Ishikawa, S
AF Atsumi, Shinichiro
   Katoh, Hiroto
   Komura, Daisuke
   Hashimoto, Itaru
   Furuya, Genta
   Koda, Hirotomo
   Konishi, Hiroki
   Suzuki, Ryohei
   Yamamoto, Asami
   Yuba, Satsuki
   Abe, Hiroyuki
   Rino, Yasushi
   Oshima, Takashi
   Ushiku, Tetsuo
   Fukayama, Masashi
   Seto, Yasuyuki
   Ishikawa, Shumpei
TI Focal adhesion ribonucleoprotein complex proteins are major humoral
   cancer antigens and targets in autoimmune diseases
SO COMMUNICATIONS BIOLOGY
LA English
DT Article
ID PRIMARY BILIARY-CIRRHOSIS; RNA; AUTOANTIBODIES; ANTIBODIES; BLOCKADE;
   CELLS
AB Despite the accumulating evidences of the significance of humoral cancer immunity, its molecular mechanisms have largely remained elusive. Here we show that B-cell repertoire sequencing of 102 clinical gastric cancers and molecular biological analyses unexpectedly reveal that the major humoral cancer antigens are not case-specific neo-antigens but are rather commonly identified as ribonucleoproteins (RNPs) in the focal adhesion complex. These common antigens are shared as autoantigens with multiple autoimmune diseases, suggesting a direct molecular link between cancer- and auto-immunity on the focal adhesion RNP complex. This complex is partially exposed to the outside of cancer cell surfaces, which directly evokes humoral immunity and enables functional bindings of antibodies to cancer cell surfaces in physiological conditions. These findings shed light on humoral cancer immunity in that it commonly targets cellular components fundamental for cytoskeletal integrity and cell movement, pointing to a novel modality of immunotherapy using humoral immunological reactions to cancers. Atsumi et al. identify antigens to B-cell receptors isolated from gastric tumour samples. They find that focal adhesion-related protein complexes, several of which are also targets for autoimmune disease, are major humoral cancer antigens. These findings provide insights into humoral immunity in tumor environments.
C1 [Atsumi, Shinichiro; Katoh, Hiroto; Komura, Daisuke; Hashimoto, Itaru; Furuya, Genta; Koda, Hirotomo; Konishi, Hiroki; Suzuki, Ryohei; Yamamoto, Asami; Yuba, Satsuki; Ishikawa, Shumpei] Univ Tokyo, Grad Sch Med, Dept Prevent Med, Tokyo, Japan.
   [Atsumi, Shinichiro; Seto, Yasuyuki] Univ Tokyo, Grad Sch Med, Dept Gastrointestinal Surg, Tokyo, Japan.
   [Hashimoto, Itaru; Rino, Yasushi; Oshima, Takashi] Yokohama City Univ, Dept Surg, Yokohama, Kanagawa, Japan.
   [Furuya, Genta; Koda, Hirotomo; Abe, Hiroyuki; Ushiku, Tetsuo; Fukayama, Masashi] Univ Tokyo, Grad Sch Med, Dept Pathol, Tokyo, Japan.
   [Yuba, Satsuki] Tokyo Med & Dent Univ, Grad Sch Med & Dent Sci, Dept Mol Pathol, Tokyo, Japan.
   [Oshima, Takashi] Kanagawa Canc Ctr, Dept Gastrointestinal Surg, Yokohama, Kanagawa, Japan.
C3 University of Tokyo; University of Tokyo; Yokohama City University;
   University of Tokyo; Institute of Science Tokyo; Tokyo Medical & Dental
   University (TMDU); Kanagawa Prefectural Cancer Center
RP Katoh, H; Ishikawa, S (corresponding author), Univ Tokyo, Grad Sch Med, Dept Prevent Med, Tokyo, Japan.
EM hkat-prm@m.u-tokyo.ac.jp; ishum-prm@m.u-tokyo.ac.jp
RI Komura, Daisuke/AAF-2481-2019; Ishikawa, Shumpei/NBW-9562-2025; Katoh,
   Hiroto/ADO-8117-2022; Hashimoto, Itaru/HJB-0987-2022; Abe,
   Hiroyuki/JXN-2646-2024
OI Katoh, Hiroto/0000-0001-9440-728X; Komura, Daisuke/0000-0002-0038-728X;
   Furuya, Genta/0000-0001-9730-0947
FU AMED P-CREATE [JP20cm0106551]; KAKENHI [16H02481, 19H01032]; AMED
   Research on Development of New Drugs [JP20ak0101096]; Takeda Science
   Foundation; Mochida Memorial Foundation for Medical and Pharmaceutical
   Research; Relay-for-Life Project Mirai Cancer Research Grants; Princess
   Takamatsu Cancer Research Fund; Joint Usage/Research Program of Medical
   Research Institute, Tokyo Medical and Dental University; Grants-in-Aid
   for Scientific Research [19H01032, 16H02481] Funding Source: KAKEN
FX The authors would like to thank Ms.Miharu Tamukai for her excellent
   office works. This work was supported by AMED P-CREATE (JP20cm0106551),
   and KAKENHI Grant-in-Aid for Scientific Research (A) (16H02481) to S.
   Ishikawa, and AMED Research on Development of New Drugs (JP20ak0101096),
   KAKENHI Grant-in-Aid for Scientific Research (A) (19H01032), Takeda
   Science Foundation, the Mochida Memorial Foundation for Medical and
   Pharmaceutical Research, Relay-for-Life Project Mirai Cancer Research
   Grants, and Princess Takamatsu Cancer Research Fund to H. Katoh. This
   study was also supported by the Joint Usage/Research Program of Medical
   Research Institute, Tokyo Medical and Dental University.
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NR 57
TC 5
Z9 5
U1 0
U2 1
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
EI 2399-3642
J9 COMMUN BIOL
JI Commun. Biol.
PD OCT 16
PY 2020
VL 3
IS 1
AR 588
DI 10.1038/s42003-020-01305-5
PG 15
WC Biology; Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Life Sciences & Biomedicine - Other Topics; Science & Technology - Other
   Topics
GA OI5FY
UT WOS:000583305400013
PM 33067514
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Grozinsky-Glasberg, S
   Alexandraki, KI
   Angelousi, A
   Chatzellis, E
   Sougioultzis, S
   Kaltsas, G
AF Grozinsky-Glasberg, Simona
   Alexandraki, Krystallenia, I
   Angelousi, Anna
   Chatzellis, Eleftherios
   Sougioultzis, Stavros
   Kaltsas, Gregory
TI Gastric Carcinoids
SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
LA English
DT Article
DE Carcinoids; Neuroendocrine; Gastrin; Atrophic gastritis; Endoscopic
   ultrasound
ID ENDOCRINE NEOPLASIA TYPE-1; ZOLLINGER-ELLISON-SYNDROME;
   GASTROENTEROPANCREATIC NEUROENDOCRINE TUMORS; ENETS CONSENSUS
   GUIDELINES; ATROPHIC BODY GASTRITIS; ENTEROCHROMAFFIN-LIKE CELLS;
   AUTOIMMUNE THYROID-DISEASE; TERM-FOLLOW-UP; LONG-TERM; RECEPTOR
   ANTAGONIST
AB Gastric carcinoids, formally named gastric neuroendocrine neoplasms (NENs), are derived from enterochromaffin-like cells of the stomach and are increasingly diagnosed. A majority are designated as type I (related to autoimmune gastritis) and type II (related to gastrinoma) neoplasms that develop secondary to gastrin hypersecretion. Types I and II gastric carcinoids are mostly small (1-2 cm), multiple, low-malignancy potential lesions mainly confined to the gastric mucosa/submucosa. These lesions have an indolent course and low metastatic potential. In contrast, type III gastric carcinoids are single, larger (>2 cm), non-gastrin-related lesions that infiltrate the muscular layers associated with local and distant metastases.
C1 [Grozinsky-Glasberg, Simona] Hadassah Hebrew Univ, Dept Endocrinol, Neuroendocrine Tumor Unit, Med Ctr, POB 12000, IL-91120 Jerusalem, Israel.
   [Alexandraki, Krystallenia, I; Angelousi, Anna; Chatzellis, Eleftherios; Kaltsas, Gregory] Univ Athens, Dept Propaedeut Internal Med 1, Mikras Asias 75, Athens 11527, Greece.
   [Sougioultzis, Stavros] Univ Athens, Dept Pathophysiol, Mikras Asias 75, Athens 11527, Greece.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center;
   National & Kapodistrian University of Athens; National & Kapodistrian
   University of Athens
RP Kaltsas, G (corresponding author), Univ Athens, Dept Propaedeut Internal Med 1, Mikras Asias 75, Athens 11527, Greece.
EM gkaltsas@med.uoa.gr
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OI Alexandraki, Krystallenia/0000-0003-2398-6768; Chatzellis,
   Eleftherios/0000-0002-9173-3271; Kaltsas, Gregory/0000-0002-5876-7883
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NR 79
TC 42
Z9 50
U1 1
U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8529
EI 1558-4410
J9 ENDOCRIN METAB CLIN
JI Endocrinol. Metabol. Clin. North Amer.
PD SEP
PY 2018
VL 47
IS 3
BP 645
EP +
DI 10.1016/j.ecl.2018.04.013
PG 17
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA GT2YV
UT WOS:000444367100014
PM 30098721
DA 2025-06-01
ER

PT J
AU Li, Q
AF Li, Qiao
TI Bacterial infection and microbiota in carcinogenesis and tumor
   development
SO FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
LA English
DT Review
DE microbiota; cancer; tumor microenvironment; sequencing; bacteria
ID HELICOBACTER-PYLORI CAGA; FUSOBACTERIUM-NUCLEATUM; COLORECTAL-CANCER;
   ESCHERICHIA-COLI; GASTRIC-CANCER; INTESTINAL MICROBIOTA; GUT MICROBIOTA;
   TUMORIGENESIS; TRANSLOCATION; ASSOCIATION
AB Microbiota colonize exposed body tissues (e.g., gastrointestinal tract, skin, lungs, female genital tract, and urogenital tracts) and unexposed sites (e.g., breast). Persistent bacterial infection in the host lead to the development of multiple disease. They are implicated in the pathogenesis of various complex diseases, including diabetes, atherosclerosis, autoimmune diseases, Alzheimer's disease, and malignant diseases. Amounting studies have demonstrated the role of bacterial infection in carcinogenesis. The study of microbiota in tumorigenesis is primarily focused on lung cancer, colorectal cancer (CRC), breast cancer, gastric cancer, and gynecologic tumors, and so on. Infection of Helicobacter pylori in gastric cancer carcinogenesis is recognized as class I carcinogen by the World Health Organization (WHO) decades ago. The role of Fusobacterium nucleatum in the development of colorectal cancer is extensively investigated. Variable bacteria have been cultured from the tumor tissues. The identification of microbiota in multiple tumor tissues reveal that bacterial infection and microbiota are associated with tumor development. The microbiota affects multiple aspects of carcinogenesis and tumor development, including favoring epithelial cells proliferation, establishing inflammatory microenvironment, promoting metastasis, and causing resistance to therapy. On the other hand, microbiota can shape a tumor surveillance environment by enhancing cell activity, and sensitize the tumor cells to immune therapy. In the present review, the roles of microbiota in multiple malignancies are summarized, and unraveling the mechanisms of host-microbiota interactions can contribute to a better understanding of the interaction between microbiota and host cells, also the development of potential anti-tumor therapeutic strategies.
C1 [Li, Qiao] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Wuhan, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology
RP Li, Q (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Wuhan, Hubei, Peoples R China.
EM liqiaograce@163.com
FU Tongji Hospital
FX The support from Tongji Hospital is appreciated.
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NR 122
TC 15
Z9 18
U1 3
U2 14
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2235-2988
J9 FRONT CELL INFECT MI
JI Front. Cell. Infect. Microbiol.
PD NOV 15
PY 2023
VL 13
AR 1294082
DI 10.3389/fcimb.2023.1294082
PG 13
WC Immunology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology
GA Z1OQ9
UT WOS:001109850200001
PM 38035341
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Yüksel, C
   Ersen, O
   Cuclu, S
   Bakirarar, B
   Unal, AE
   Demirci, S
AF Yuksel, Cemil
   Ersen, Ogun
   Cuclu, Serdar
   Bakirarar, Batuhan
   Unal, Ali Ekrem
   Demirci, Salim
TI Prognostic Role of Red Distribution Width (RDW) Value in Gastric Cancer
SO JCPSP-JOURNAL OF THE COLLEGE OF PHYSICIANS AND SURGEONS PAKISTAN
LA English
DT Article
DE Gastrectomy; Gastric cancer; Laparoscopy; Surgical oncology; Red
   distribution width; survival
ID CELL DISTRIBUTION WIDTH; PREDICTOR; SURVIVAL
AB Objective: To investigate the prognostic effect of red distribution width (RDW) in patients with gastric cancer.
   Study Design: Observational study.
   Place and Duration of Study: Department of Surgical Oncology, Ankara University School of Medicine, between November 2010 and January 2020.
   Methodology: Patients diagnosed with adenocarcinoma by biopsy, who underwent radical surgery and lymph node dissection, and had preoperative RDW value, were inducted. Patients who had history of active inflammation in the past three months, received treatment for hematology disorder, blood transfusion, malignancy other than gastric cancer, autoimmune disease, venous thrombosis, or under 18 years of age, and those having cardiac and cerebrovascular diseases and distant metastases were excluded from the study. Apart from diagnosis, preoperative blood values, clinicopathologial, demographic features, and follow-up data were included in the study.
   Results: RDW average value was 15.11 +/- 2.87 and median value was 14.3%. For RDW cut off value, 13.4% was accepted as reference from previous studies was divided into two groups as <13.4% and >= 13.4%. While it was <13.4% in 119 patients; in 292 patients, it was >= 13.4W. High RDW value showed poor survival (p<0.001).
   Conclusion: RDW, the current hematological marker, can be used as an important indicator for monitoring the progression and prognosis of gastric cancer.
C1 [Yuksel, Cemil; Cuclu, Serdar] Univ Hlth Sci, Ankara Abdurrahman Yurtaslan Oncol Training & Res, Dept Surg Oncol, Ankara, Turkey.
   [Ersen, Ogun; Unal, Ali Ekrem; Demirci, Salim] Ankara Univ, Dept Surg Oncol, Sch Med, Ankara, Turkey.
   [Bakirarar, Batuhan] Ankara Univ, Dept Biostat, Sch Med, Ankara, Turkey.
C3 University of Health Sciences Turkey; Ankara University; Ankara
   University
RP Yüksel, C (corresponding author), Univ Hlth Sci, Ankara Abdurrahman Yurtaslan Oncol Training & Res, Dept Surg Oncol, Ankara, Turkey.
EM cemil8537@hotmail.com
RI YÜKSEL, CEMiL/AAW-9017-2020; Bakirarar, Batuhan/ACX-5602-2022
OI Unal, Ali Ekrem/0000-0002-2757-4034
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PU COLL PHYSICIANS & SURGEONS PAKISTAN
PI KARACHI
PA SEVENTH CENTRAL ST, DEFENCE HOUSING AUTHORITY, KARACHI, 75500, PAKISTAN
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EI 1681-7168
J9 JCPSP-J COLL PHYSICI
JI JCPSP-J. Coll. Physicians Surg.
PD JAN
PY 2021
VL 31
IS 1
BP 21
EP 26
DI 10.29271/jcpsp.2021.01.21
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA QP7EO
UT WOS:000623996300005
PM 33546528
OA gold
DA 2025-06-01
ER

PT J
AU Wang, KY
   Huang, HY
   Zhan, Q
   Ding, HR
   Li, Y
AF Wang, Kunyu
   Huang, Hanyao
   Zhan, Qi
   Ding, Haoran
   Li, Yi
TI Toll-like receptors in health and disease
SO MEDCOMM
LA English
DT Review
DE cancer; clinical treatment; disease; innate immunity; toll-like
   receptors
ID SQUAMOUS-CELL CARCINOMA; NF-KAPPA-B; PATTERN-RECOGNITION RECEPTORS;
   PLASMACYTOID DENDRITIC CELLS; DOMAIN-CONTAINING ADAPTER; COLON-CANCER
   CELLS; BREAST-CANCER; GASTRIC-CANCER; COLORECTAL-CANCER; INNATE IMMUNITY
AB Toll-like receptors (TLRs) are inflammatory triggers and belong to a family of pattern recognition receptors (PRRs) that are central to the regulation of host protective adaptive immune responses. Activation of TLRs in innate immune myeloid cells directs lymphocytes to produce the most appropriate effector responses to eliminate infection and maintain homeostasis of the body's internal environment. Inappropriate TLR stimulation can lead to the development of general autoimmune diseases as well as chronic and acute inflammation, and even cancer. Therefore, TLRs are expected to be targets for therapeutic treatment of inflammation-related diseases, autoimmune diseases, microbial infections, and human cancers. This review summarizes the recent discoveries in the molecular and structural biology of TLRs. The role of different TLR signaling pathways in inflammatory diseases, autoimmune diseases such as diabetes, cardiovascular diseases, respiratory diseases, digestive diseases, and even cancers (oral, gastric, breast, colorectal) is highlighted and summarizes new drugs and related clinical treatments in clinical trials, providing an overview of the potential and prospects of TLRs for the treatment of TLR-related diseases.
   Interactions of TLRs with inflammation and tumor. TLRs are expressed on a variety of cells, including tumor cells and immune cells. TLRs signaling is involved in the carcinogenesis of the tumor microenvironment. TLRs expressed on immune cells and tumor cells are subjected to activation by pathogen-associated molecular patterns,damage-associated molecular patterns from microorganisms, viruses, parasites, injured and necrotic cancer cells. The release of cytokines and chemokines by these activated cells is an important part of the tumor microenvironment. Moreover, cytokine-activated infiltrating immune cells can subsequently induce additional cytokines that impair the function of antigen-presenting cells, leading to tumor immune tolerance. # image
C1 [Wang, Kunyu; Zhan, Qi; Ding, Haoran; Li, Yi] Sichuan Univ, West China Hosp Stomatol, Dept Head & Neck Oncol Surg, State Key Lab Oral Dis, Chengdu, Peoples R China.
   [Wang, Kunyu; Zhan, Qi; Ding, Haoran; Li, Yi] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Chengdu, Peoples R China.
   [Huang, Hanyao] Sichuan Univ, West China Hosp Stomatol, Dept Oral & Maxillofacial Surg, State Key Lab Oral Dis, Chengdu, Sichuan, Peoples R China.
   [Huang, Hanyao] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Chengdu, Sichuan, Peoples R China.
   [Li, Yi] West China Hosp Stomatol, Dept Head & Neck Oncol Surg, State Key Lab Oral Dis, 14,Unit 3,Renmin Nan Rd, Chengdu 610041, Sichuan, Peoples R China.
   [Li, Yi] West China Hosp Stomatol, Natl ClinicalResearch Ctr Oral Dis, 14,Unit 3,Renmin Nan Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Sichuan University; Sichuan University; Sichuan University; Sichuan
   University; Sichuan University
RP Li, Y (corresponding author), West China Hosp Stomatol, Dept Head & Neck Oncol Surg, State Key Lab Oral Dis, 14,Unit 3,Renmin Nan Rd, Chengdu 610041, Sichuan, Peoples R China.; Li, Y (corresponding author), West China Hosp Stomatol, Natl ClinicalResearch Ctr Oral Dis, 14,Unit 3,Renmin Nan Rd, Chengdu 610041, Sichuan, Peoples R China.
EM Liyi1012@163.com
RI Li, Longjiang/JXL-6904-2024; Huang, Hanyao/AAX-9478-2020
OI Huang, Hanyao/0000-0002-6805-0157
FU Research and Develop Program, West China Hospital of Stomatology Sichuan
   University; Sichuan Postdoctoral Science Foundation [TB2022005]; Sichuan
   Province Science and Technology Support Program [2022NSFSC0371];
   National Natural Science Foundation of China [81972546];  [RD-02-202107]
FX This work was supported by the Research and Develop Program, West China
   Hospital of Stomatology Sichuan University (RD-02-202107), Sichuan
   Postdoctoral Science Foundation (TB2022005), Sichuan Province Science
   and Technology Support Program (2022NSFSC0371), and the National Natural
   Science Foundation of China (82301148). and the National Natural Science
   Foundation of China (No. 81972546). We would also like to thank
   BioRender for the application in drawing Figures 1, 2, 3, and 4.
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VL 5
IS 5
AR e549
DI 10.1002/mco2.549
PG 30
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA OY4Z6
UT WOS:001210838200001
PM 38685971
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU D'Elios, MM
   Andersen, LP
AF D'Elios, Mario M.
   Andersen, Leif P.
TI Inflammation, Immunity, and Vaccines for Helicobacter pylori
SO HELICOBACTER
LA English
DT Review
DE Mucosal immunity; Th1; Th2; Th17; cytokine; regulatory lymphocyte;
   chemokine; VacA; CagA; HP-NAP; vaccine
ID NEUTROPHIL-ACTIVATING PROTEIN; PEPTIC-ULCER DISEASE; GASTRIC
   EPITHELIAL-CELLS; GROWTH-FACTOR RECEPTOR; LYMPHOID-TISSUE TYPE; B-CELL;
   MALT LYMPHOMA; GENE POLYMORPHISMS; UP-REGULATION; EXPRESSION
AB Helicobacter pylori infects almost half of the population worldwide and represents the major cause of gastroduodenal diseases, such as duodenal and gastric ulcer, gastric adenocarcinoma, autoimmune gastritis, and B-cell lymphoma of mucosa-associated lymphoid tissue. Helicobacter pylori induces the activation of a complex and fascinating cytokine and chemokine network in the gastric mucosa. Different bacterial and environmental factors, other concomitant infections, and host genetics may influence the balance between mucosal tolerance and inflammation in the course of H. pylori infection. An inverse association between H. pylori prevalence and the frequencies of asthma and allergies was demonstrated, and the neutrophil activating protein of H. pylori was shown to inhibit the allergic inflammation of bronchial asthma. During the last year, significant progress was made on the road to the first efficient vaccine for H. pylori that will represent a novel and very important bullet against both infection and gastric cancer.
C1 [D'Elios, Mario M.] Univ Florence, Dept Internal Med, I-50134 Florence, Italy.
   [D'Elios, Mario M.] Azienda Osped Univ Careggi, Dept Biomed, Florence, Italy.
   [Andersen, Leif P.] Rigshosp, Copenhagen Univ Hosp, Dept Infect Control 9101, DK-2100 Copenhagen, Denmark.
C3 University of Florence; University of Florence; Azienda Ospedaliero
   Universitaria Careggi; University of Copenhagen; Copenhagen University
   Hospital; Rigshospitalet
RP D'Elios, MM (corresponding author), Univ Florence, Dept Internal Med, Viale Morgagni 85, I-50134 Florence, Italy.
EM delios@unifi.it
RI D'Elios, Mario Milco/Y-9573-2019
OI D'Elios, Mario Milco/0000-0001-9160-0930
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NR 84
TC 25
Z9 25
U1 0
U2 11
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PD SEP
PY 2009
VL 14
SU 1
BP 21
EP 28
DI 10.1111/j.1523-5378.2009.00698.x
PG 8
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Microbiology
GA 487YS
UT WOS:000269316200004
PM 19712164
DA 2025-06-01
ER

PT J
AU Venerito, M
   Link, A
   Rokkas, T
   Malfertheiner, P
AF Venerito, Marino
   Link, Alexander
   Rokkas, Theodoros
   Malfertheiner, Peter
TI Gastric cancer - clinical and epidemiological aspects
SO HELICOBACTER
LA English
DT Article; Proceedings Paper
CT 29th International Workshop on Helicobacter and Microbiota in
   Inflammation and Cancer
CY SEP 15-17, 2016
CL Magdeburg, GERMANY
DE epidemiology; gastric cancer; therapy; prevention
ID CIRCULATING TUMOR-CELLS; CHEMOTHERAPY; COHORT; RISK
AB Gastric cancer (GC) ranks fifth for cancer incidence and second for cancer deaths. Epidemiological data showed that survivors of Hodgkin's lymphoma and patients with pernicious anemia etiologically linked to autoimmune gastritis are at increased risk of GC. Screening of patients with autoimmune thyroid disease by means of pepsinogen (PG) I and PG I/II detected autoimmune gastritis with oxyntic gastric atrophy in one of four patients and may be recommended for GC prevention purposes. The International Agency for Research on Cancer reported a positive association between consumption of processed meet and increased GC risk. A new GC risk prediction model based on biological markers, age, gender, smoking status, family history of GC, and consumption of highly salted food showed good predictive performance, and might prompt individuals to modify their lifestyle habits, attend regular check-up visits or participate in screening programs. A novel GC classification based on gene expression of primary resected cancers correlated with clinicopathological features. Noncoding RNA for GC screening remains the focus of multiple studies. Patients with early GC undergoing endoscopic resection are more likely to develop metachronous lesions than patients undergoing surgery and endoscopic surveillance is warranted in this special cohort. The addition of gastrectomy to chemotherapy did not improve survival of patients with advanced GC and a single noncurable factor. Apatinib, a novel oral vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor, improved the median overall survival of patients with advanced GC and progressive disease after two or more lines of prior chemotherapy of nearly 3months.
C1 [Venerito, Marino; Link, Alexander; Malfertheiner, Peter] Otto von Guericke Univ Hosp, Dept Gastroenterol Hepatol & Infect Dis, Magdeburg, Germany.
   [Rokkas, Theodoros] Henry Dunant Hosp, Gastroenterol Clin, Athens, Greece.
C3 Otto von Guericke University; University Hospital Magdeburg; Henry
   Dunant Hospital
RP Venerito, M (corresponding author), Otto von Guericke Univ Hosp, Dept Gastroenterol Hepatol & Infect Dis, Magdeburg, Germany.
EM m.venerito@med.ovgu.de
RI Link, Alexander/AFK-7535-2022; Malfertheiner, Peter/AEZ-6553-2022;
   Venerito, Marino/AAF-4493-2020
OI Link, Alexander/0000-0002-9514-4562; Malfertheiner,
   Peter/0000-0001-8439-9036; Venerito, Prof. Dr. med.
   Marino/0000-0001-8581-0974
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NR 28
TC 102
Z9 118
U1 0
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PD SEP
PY 2016
VL 21
SU 1
SI SI
BP 39
EP 44
DI 10.1111/hel.12339
PG 6
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology; Microbiology
GA DW3BR
UT WOS:000383517600008
PM 27531538
DA 2025-06-01
ER

PT J
AU Busada, JT
   Khadka, S
   Peterson, KN
   Druffner, SR
   Stumpo, DJ
   Zhou, LC
   Oakley, RH
   Cidlowski, JA
   Blackshear, PJ
AF Busada, Jonathan T.
   Khadka, Stuti
   Peterson, Kylie N.
   Druffner, Sara R.
   Stumpo, Deborah J.
   Zhou, Lecong
   Oakley, Robert H.
   Cidlowski, John A.
   Blackshear, Perry J.
TI Tristetraprolin Prevents Gastric Metaplasia in Mice by Suppressing
   Pathogenic Inflammation
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE gastric inflammation; adrenalectomy; SPEM; gastric cancer
ID NECROSIS-FACTOR-ALPHA; POLYPEPTIDE-EXPRESSING METAPLASIA; RNA-BINDING
   PROTEINS; MESSENGER-RNA; HELICOBACTER-PYLORI; CANCER; CELLS;
   GLUCOCORTICOIDS; DEFICIENCY; STABILITY
AB Aberrant gastric inflammation damages the stomach and induces gastric metaplasia (spasmolytic polypeptideexpressing metaplasia). Increased expression of the RNA binding protein tristetraprolin suppresses adrenalectomy-induced gastric inflammation and spasmolytic polypeptideexpressing metaplasia development.
   BACKGROUND & AIMS: Aberrant immune activation is associated with numerous inflammatory and autoimmune diseases and contributes to cancer development and progression. Within the stomach, inflammation drives a well established sequence from gastritis to metaplasia, eventually resulting in adenocarcinoma. Unfortunately, the processes that regulate gastric inflammation and prevent carcinogenesis remain unknown. Tristetraprolin (TTP) is an RNA binding protein that promotes the turnover of numerous proinflammatory and oncogenic messenger RNAs. Here, we assess the role of TTP in regulating gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM) development.
   METHODS: We used a TTP-overexpressing model, the TTP Delta adenylate-uridylate rich element mouse, to examine whether TTP can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and SPEM.
   RESULTS: We found that TTPDadenylate-uridylate rich element mice were completely protected from ADX-induced gastric inflammation and SPEM. RNA sequencing 5 days after ADX showed that TTP overexpression suppressed the expression of genes associated with the innate immune response. Importantly, TTP overexpression did not protect from highdose-tamoxifen-induced SPEM development, suggesting that protection in the ADX model is achieved primarily by suppressing inflammation. Finally, we show that protection from gastric inflammation was only partially due to the suppression of Tnf, a well-known TTP target.
   CONCLUSIONS: Our results show that TTP exerts broad antiinflammatory effects in the stomach and suggest that therapies that increase TTP expression may be effective treatments of proneoplastic gastric inflammation. Transcript profiling: GSE164349.
C1 [Busada, Jonathan T.; Peterson, Kylie N.; Oakley, Robert H.; Cidlowski, John A.] NIEHS, Mol Endocrinol Grp, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
   [Stumpo, Deborah J.; Blackshear, Perry J.] NIEHS, Posttranscript Gene Express Grp, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
   [Zhou, Lecong] NIEHS, Integrat Bioinformat Support Grp, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
   [Busada, Jonathan T.; Khadka, Stuti; Druffner, Sara R.] West Virginia Univ, Sch Med, Dept Microbiol Immunol & Cell Biol, 64 Med Ctr Dr,POB 9177, Morgantown, WV 26506 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
   Environmental Health Sciences (NIEHS); National Institutes of Health
   (NIH) - USA; NIH National Institute of Environmental Health Sciences
   (NIEHS); National Institutes of Health (NIH) - USA; NIH National
   Institute of Environmental Health Sciences (NIEHS); West Virginia
   University
RP Busada, JT (corresponding author), West Virginia Univ, Sch Med, Dept Microbiol Immunol & Cell Biol, 64 Med Ctr Dr,POB 9177, Morgantown, WV 26506 USA.
EM jonathan.busada@hsc.wvu.edu
RI Blackshear, Perry/C-6206-2019; Cidlowski, John/G-2548-2019
FU National Institute of General Medical Sciences [1Fi2GM123974,
   P20GM121322]; West Virginia University start-up funds; National
   Institutes of Health/National Institute of Environmental Health Sciences
   [1ZIAES090057, 1ZIAES090080]; National Institutes of Health
   [P20RR016440, P30GM103488, U54GM104942, P30GM103503, P20GM103434];
   National Institute of Environmental Health Sciences [ZIAES090080]
   Funding Source: NIH RePORTER
FX This research was supported by the National Institute of General Medical
   Sciences 1Fi2GM123974 (J.T.B.) and P20GM121322 (J.T.B.) , West Virginia
   University start-up funds (J.T.B) , and by the Intramural Research
   Program of the National Institutes of Health/National Institute of
   Environmental Health Sciences 1ZIAES090057 (J.A.C) and 1ZIAES090080
   (P.J.B.) . Confocal microscopy was performed at the West Virginia
   University Microscope Imaging Facility, which is supported by National
   Institutes of Health grants P20RR016440, P30GM103488, U54GM104942,
   P30GM103503, and P20GM103434.
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NR 62
TC 6
Z9 7
U1 2
U2 17
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-345X
J9 CELL MOL GASTROENTER
JI Cell. Mol. Gastroenterol. Hepatol.
PY 2021
VL 12
IS 5
BP 1831
EP 1845
DI 10.1016/j.jcmgh.2021.07.015
EA OCT 2021
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WX0XW
UT WOS:000718329100001
PM 34358715
OA Green Published, Green Submitted
DA 2025-06-01
ER

PT J
AU Nishiura, H
   Iwamoto, S
   Kido, M
   Aoki, N
   Maruoka, R
   Ikeda, A
   Chiba, T
   Watanabe, N
AF Nishiura, Hisayo
   Iwamoto, Satoru
   Kido, Masahiro
   Aoki, Nobuhiro
   Maruoka, Ryutaro
   Ikeda, Aki
   Chiba, Tsutomu
   Watanabe, Norihiko
TI Interleukin-21 and tumor necrosis factor- are critical for the
   development of autoimmune gastritis in mice
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE autoimmune gastritis; autoantibody production; cytokine
ID RECEPTOR-DEFICIENT MICE; NEONATAL THYMECTOMY; PERNICIOUS-ANEMIA;
   T-CELLS; IFN-GAMMA; AUTOANTIBODIES; SUSCEPTIBILITY; PREDNISOLONE;
   DISEASE; ALPHA
AB Background and Aim Autoimmune gastritis (AIG), an organ-specific autoimmune disease, is accompanied by achlorhydria, pernicious anemia, gastric carcinoid tumors, and gastric cancer. Patients with AIG initially respond to corticosteroids but have a great potential to relapse after treatment is withdrawn. This study examines the roles of cytokines in order to identify potential therapeutic options for AIG patients. Methods Using a mouse model of AIG, we monitored disease progression and administered antibodies in vivo to block cytokines. Results We developed a mouse model of AIG with early onset and rapid progression in which neonatal thymectomy (NTx) was performed on programmed cell death 1-deficient (PD-1/) mice on the BALB/c background. Using NTxPD-1/ mice, we found that in AIG lesions, interferon-, and tumor necrosis factor (TNF)- together with interleukin-21 (IL-21) were highly expressed in the inflamed gastric mucosa. In addition, as with the injection of dexamethasone, in vivo administration of either anti-TNF- or anti-IL-21 suppressed the development of AIG in NTxPD-1/ mice. Conclusions These data reveal the essential role of IL-21 in the development of AIG and suggest that in addition to corticosteroids, anti-TNF- as well as anti-IL-21 have the potential to induce the remission of AIG, offering additional therapeutic options for AIG patients.
C1 [Nishiura, Hisayo; Iwamoto, Satoru; Kido, Masahiro; Aoki, Nobuhiro; Maruoka, Ryutaro; Ikeda, Aki; Chiba, Tsutomu; Watanabe, Norihiko] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kyoto 6068501, Japan.
   [Nishiura, Hisayo; Iwamoto, Satoru; Kido, Masahiro; Aoki, Nobuhiro; Maruoka, Ryutaro; Ikeda, Aki; Watanabe, Norihiko] Kyoto Univ, Grad Sch Med, Ctr Innovat Immunoregulat Technol & Therapeut, Sakyo Ku, Kyoto 6068501, Japan.
C3 Kyoto University; Kyoto University
RP Watanabe, N (corresponding author), Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Yoshida Konoe Cho, Kyoto 6068501, Japan.
EM norihiko@kuhp.kyoto-u.ac.jp
FU Japanese Government; Astellas Pharma Inc.; Japan Society for the
   Promotion of Science (JSPS) [20390207, 21229009, 23590973]; Ministry of
   Health, Labour and Welfare, Japan; Japanese Society of Gastroenterology;
   Kato Memorial Trust for Nambyo Research; Waksman Foundation of Japan;
   Grants-in-Aid for Scientific Research [23590973, 20390207] Funding
   Source: KAKEN
FX The Center for Innovation in Immunoregulative Technology and
   Therapeutics is supported in part by the Special Coordination Funds for
   Promoting Science and Technology of the Japanese Government and in part
   by Astellas Pharma Inc. in the Formation of Innovation Center for Fusion
   of Advanced Technologies Program. This work is partially supported by
   Grants-in-aid for Scientific Research 20390207, 21229009, 23590973 from
   Japan Society for the Promotion of Science (JSPS), a Health and Labour
   Sciences Research Grant on Intractable Diseases from the Ministry of
   Health, Labour and Welfare, Japan, Grants-in-Aid for Research by the
   Japanese Society of Gastroenterology, The Kato Memorial Trust for Nambyo
   Research, and The Waksman Foundation of Japan.
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NR 26
TC 16
Z9 16
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD JUN
PY 2013
VL 28
IS 6
BP 982
EP 991
DI 10.1111/jgh.12144
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 149RX
UT WOS:000319339900017
PM 23425147
DA 2025-06-01
ER

PT J
AU De Re, V
   Repetto, O
   Zanussi, S
   Casarotto, M
   Caggiari, L
   Canzonieri, V
   Cannizzaro, R
AF De Re, Valli
   Repetto, Ombretta
   Zanussi, Stefania
   Casarotto, Mariateresa
   Caggiari, Laura
   Canzonieri, Vincenzo
   Cannizzaro, Renato
TI Protein signature characterizing Helicobacter pylori strains of
   patients with autoimmune atrophic gastritis, duodenal ulcer and gastric
   cancer
SO INFECTIOUS AGENTS AND CANCER
LA English
DT Article
DE Adenocarcinoma; Autoimmune atrophic gastritis; Comparative proteomics;
   DIGE; Duodenal ulcer; Gastric cancer; Helicobacter pylori
ID OXIDATIVE STRESS; PATHOGENESIS; INFECTION; VIRULENCE; IDENTIFICATION;
   ACTIVATION; RESISTANCE; PROTEOMICS; IMMUNITY; REVEALS
AB Background: Helicobacter pylori (H. pylori) represents a key factor in the etiology of autoimmune atrophic gastritis (AAG), duodenal ulcer (DU) and gastric cancer (GC). The aim of this study was to characterize the differential protein expression of H. pylori isolated from gastric biopsies of patients affected by either AAG, DU or GC.
   Methods: The H. pylori strains were isolated from endoscopic biopsies from the stomach of patients with gastric disease. Protein profiles of H. pylori were compared by two-dimensional difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS) for the identification of significantly different spots (Student t-test, p < 0.05).
   Results: A total of 47 differentially expressed spots were found between H. pylori isolated from patients with either DU or AAG diseases and those isolated from patients with GC (Anova < 0.05, log fold change > 1.5). These spots corresponded to 35 unique proteins. The identity of 7 protein spots was validated after one-dimensional electrophoresis and MS/MS analyses of excised gel portions. In H. pylori isolated from DU-patients a significant increase in proteins with antioxidant activity emerged (AroQ, AspA, FldA, Icd, OorA and ScoB), together with a higher content of proteins counteracting the high acid environment (KatA and NapA). In H. pylori isolated from AAG-patients proteins neutralizing hydrogen concentrations through organic substance metabolic processes decreased (GroL, TrxB and Tuf). In addition, a reduction of bacterial motility (FlhA) was found to be associated with AAG-H. pylori isolates. In GC-H. pylori strains it was found an increase in nucleic acid-binding proteins (e.g. DnaG, Tuf, RpoA, RplU) which may be involved in a higher demand of DNA-and protein-related processes.
   Conclusion: Our data suggest the presence of specific protein signatures discriminating among H. pylori isolated from either AAG, DU or GC. Changes in protein expression profiles evaluated by DIGE succeeded in deciphering part of the molecular scenarios associated with the different H. pylori-related gastric diseases.
C1 [De Re, Valli; Repetto, Ombretta; Caggiari, Laura; Cannizzaro, Renato] IRCCS CRO Natl Canc Inst, Facil Bioprote Immunopathol & Canc Biomarkers, Via F Gallini 2, I-33081 Aviano, Italy.
   [Zanussi, Stefania; Casarotto, Mariateresa; Cannizzaro, Renato] IRCCS CRO Natl Canc Inst, Microbiol Immunol & Virol, Aviano, Italy.
   [Canzonieri, Vincenzo; Cannizzaro, Renato] IRCCS CRO Natl Canc Inst, Pathol Gastroenterol, Aviano, Italy.
   [Cannizzaro, Renato] IRCCS CRO Natl Canc Inst, Gastroenterol, Aviano, Italy.
C3 IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano
   (CRO)
RP De Re, V (corresponding author), IRCCS CRO Natl Canc Inst, Facil Bioprote Immunopathol & Canc Biomarkers, Via F Gallini 2, I-33081 Aviano, Italy.
EM vdere@cro.it
RI De Re, Valli/K-4121-2016; Canzonieri, Vincenzo/AAA-7951-2019; Repetto,
   Ombretta/V-6342-2019; Cannizzaro, Renato/V-3804-2018; Canzonieri,
   Vincenzo/K-3141-2018; ZANUSSI, STEFANIA/I-2558-2018; DE RE,
   VALLI/AAA-1374-2019; CAGGIARI, LAURA/Q-6125-2019; CASAROTTO,
   MARIATERESA/D-3947-2019
OI Repetto, Ombretta/0000-0002-0785-5066; Cannizzaro,
   Renato/0000-0002-2020-222X; Canzonieri, Vincenzo/0000-0001-6010-0976;
   ZANUSSI, STEFANIA/0000-0003-0608-9766; DE RE, VALLI/0000-0001-6100-9373;
   CAGGIARI, LAURA/0000-0003-1651-6653; CASAROTTO,
   MARIATERESA/0000-0001-5832-2895
FU 5 x 1000 CRO grant; 5 x 1000 Gastric cancer intramural grant
FX This work was supported by O. Repetto (5 x 1000 CRO grant) and L.
   Caggiari fellow (5 x 1000 Gastric cancer intramural grant).
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NR 52
TC 5
Z9 5
U1 0
U2 17
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1750-9378
J9 INFECT AGENTS CANCER
JI Infect. Agents Cancer
PD APR 27
PY 2017
VL 12
AR 22
DI 10.1186/s13027-017-0133-x
PG 12
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA ET4JL
UT WOS:000400246000001
PM 28465717
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Privitera, G
   Williams, JJ
   De Salvo, C
AF Privitera, Giuseppe
   Williams, Joseph J.
   De Salvo, Carlo
TI The Importance of Th2 Immune Responses in Mediating the Progression of
   Gastritis-Associated Metaplasia to Gastric Cancer
SO CANCERS
LA English
DT Review
DE gastric metaplasia; spasmolytic polypeptide-expressing metaplasia
   (SPEM); intestinal metaplasia; IL-33; Th2 immunity; M2 macrophages;
   eosinophils
ID POLYPEPTIDE-EXPRESSING METAPLASIA; HELICOBACTER-PYLORI INFECTION; INNATE
   LYMPHOID-CELLS; INTESTINAL METAPLASIA; INTERFERON-GAMMA; PARIETAL-CELLS;
   MOUSE STOMACH; CHIEF CELLS; ACTIVATED MACROPHAGES; AUTOIMMUNE GASTRITIS
AB Simple Summary Gastric cancer is one of the most prevalent and deadliest neoplasms worldwide. Although significant advances have been made in recent decades to improve its treatment, an incomplete understanding of its etiology and pathogenesis still limits our ability to effectively prevent and treat gastric cancer. It is well established that the most common subtype of gastric cancer (intestinal gastric cancer) develops through a multi-step process, wherein pathologic changes in gastric cells progressively occur, ultimately leading to the development of tumors. Recent evidence suggests that, aside from environmental factors, the immune system plays a key role in the sequela from gastritis to metaplasia, dysplasia and finally, gastric cancer, primarily through type 2 immune responses. In this review, we summarize the current literature and provide an overall interpretation regarding the impact of T helper 2 (Th2) immunity on the development and progression of gastric cancer.Abstract Gastric cancer is one of the leading causes of cancer deaths worldwide, with chronic gastritis representing the main predisposing factor initiating the cascade of events leading to metaplasia and eventually progressing to cancer. A widely accepted classification distinguishes between autoimmune and environmental atrophic gastritis, mediated, respectively, by T cells promoting the destruction of the oxyntic mucosa, and chronic H. pylori infection, which has also been identified as the major risk factor for gastric cancer. The original dogma posits Th1 immunity as a main causal factor for developing gastritis and metaplasia. Recently, however, it has become evident that Th2 immune responses play a major role in the events causing chronic inflammation leading to tumorigenesis, and in this context, many different cell types and cytokines are involved. In particular, the activity of cytokines, such as IL-33 and IL-13, and cell types, such as mast cells, M2 macrophages and eosinophils, are intertwined in the process, promoting chronic gastritis-dependent and more diffuse metaplasia. Herein, we provide an overview of the critical events driving the pathology of this disease, focusing on the most recent findings regarding the importance of Th2 immunity in gastritis and gastric metaplasia.
C1 [Privitera, Giuseppe; Williams, Joseph J.; De Salvo, Carlo] Case Western Reserve Univ, Dept Pathol, Sch Med, Cleveland, OH 44106 USA.
   [Privitera, Giuseppe] Univ Milan, Dipartimento Sci Salute, I-20142 Milan, Italy.
C3 University System of Ohio; Case Western Reserve University; University
   of Milan
RP De Salvo, C (corresponding author), Case Western Reserve Univ, Dept Pathol, Sch Med, Cleveland, OH 44106 USA.
EM gpp.privitera@icloud.com; jxw1519@case.edu; cxd198@case.edu
RI Privitera, Giuseppe/KIA-3145-2024
FU Crohn's & Colitis Foundation Career Development
FX The authors would like to thank Theresa T. Pizarro for critical review
   of the manuscript.
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NR 137
TC 6
Z9 6
U1 2
U2 8
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2024
VL 16
IS 3
AR 522
DI 10.3390/cancers16030522
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HJ3Y0
UT WOS:001159104900001
PM 38339273
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Jannot, AS
   Girardeau, Y
   Chaussade, S
   Cerf-Bensussan, N
   Malamut, G
AF Jannot, Anne-Sophie
   Girardeau, Yannick
   Chaussade, Stanislas
   Cerf-Bensussan, Nadine
   Malamut, Georgia
TI Increased risk of gastric cancer in relation with pernicious anaemia in
   patients with primary antibody deficiency: A nationwide case control
   study
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article; Proceedings Paper
CT Francophone Days of Hepato-gastroenterology and Digestive Oncology
   (JFHOD)
CY JUN 25-28, 2020
CL Paris, FRANCE
DE Common variable immunodeficiency; Gastric cancer; Inflammatory bowel
   diseases; Pernicious anaemia; Primary antibody deficiency
ID COMMON VARIABLE IMMUNODEFICIENCY
AB Background/Aim: We aimed to assess gastrointestinal cancers risks in a large cohort of individuals with primary antibody deficiency (PAD) and their association with risk of autoimmune and inflammatory gastrointestinal diseases. Methods: Investigating a French national database of inpatient admissions between 2010 and 2018, we identified 12,748 patients with PAD and 38,244 control non-exposed individuals. We performed multiple exposed-non-exposed studies using conditional logistic regression. Results: In comparison with non-exposed patients, PAD patients had increased risk of in situ gastric carcinoma (Odds Ratio (OR) = 10.5 [95 % CI 2.2; 50.5]), malignant gastric tumor (OR = 3.2 [95 % CI 2.2; 4.4]) and colorectal cancer (OR = 1.2 [95 % CI 1; 1.5]). PAD patients had also increased risk of pernicious anaemia (OR = 8 |95 % CI 5.6; 11.5]), Crohn's disease (OR = 4.4 [95 % CI 3.5; 5.6]), ulcerative colitis (OR = 2.9 [95 % CI 2.4; 3.6]) and coeliac disease (OR = 13.3 [95 % CI 9.1; 19.5]). Within patients with gastric cancer, those with PAD had increased risk of pernicious anaemia (OR = 8.4 [95 % CI 1.5; 215]; p = 0.01) but not of H. pylori infection. Conclusions: Risk of gastric cancer is particularly high in PAD patients and notably risk of in situ gastric carcinoma in association with pernicious anaemia. It supports indication of early endoscopic screening in these patients. (c) 2024 Published by Elsevier Ltd on behalf of Editrice Gastroenterologica Italiana S.r.l.
C1 [Jannot, Anne-Sophie] Univ Paris Cite, Greater Paris Univ Hosp AP HP, French Natl Rare Dis Registry BNDMR, Paris, France.
   [Jannot, Anne-Sophie] Univ Paris Cite, Ctr Rech Cordeliers, HeKA, INRIA Paris,Inserm, Paris, France.
   [Girardeau, Yannick] Ctr Univ Paris Cite, Hop Europeen Georges Pompidou, AP HP, Dept Clin Invest & Clin Epidemiol, Paris, France.
   [Chaussade, Stanislas; Malamut, Georgia] Univ Paris Cite, Hop Cochin, AP HP Ctr, Dept Gastroenterol, Paris, France.
   [Cerf-Bensussan, Nadine; Malamut, Georgia] Univ Paris, INSERM, UMR 1163, Paris, France.
   [Cerf-Bensussan, Nadine; Malamut, Georgia] Univ Paris Cite, Imagine Inst, Lab Intestinal Immun, Paris, France.
C3 Universite Paris Cite; Universite Paris Cite; Institut National de la
   Sante et de la Recherche Medicale (Inserm); Sorbonne Universite;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Europeen Georges-Pompidou - APHP; Assistance
   Publique Hopitaux Paris (APHP); Universite Paris Cite; Hopital
   Universitaire Cochin - APHP; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Universite Paris Cite; Universite Paris
   Cite; Institut National de la Sante et de la Recherche Medicale (Inserm)
RP Malamut, G (corresponding author), Hop Cochin, Dept Gastroenterol, 27 Rue Faubourg St Jacques, F-75014 Paris, France.
EM georgia.malamut@aphp.fr
RI Jannot, Anne-Sophie/KIL-7043-2024
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NR 17
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD OCT
PY 2024
VL 56
IS 10
BP 1760
EP 1765
DI 10.1016/j.dld.2024.05.032
EA SEP 2024
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Gastroenterology & Hepatology
GA I3G4F
UT WOS:001329172200001
PM 38853087
DA 2025-06-01
ER

PT J
AU Lee, HR
   Lennon, VA
   Camilleri, M
   Prather, CM
AF Lee, HR
   Lennon, VA
   Camilleri, M
   Prather, CM
TI Paraneoplastic gastrointestinal motor dysfunction: Clinical and
   laboratory characteristics
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID PURKINJE-CELL ANTIBODIES; ANTINEURONAL NUCLEAR AUTOANTIBODIES;
   TUMOR-ASSOCIATED GASTROPARESIS; INTESTINAL-PSEUDO-OBSTRUCTION;
   CEREBELLAR DEGENERATION; LUNG-CARCINOMA; ANTI-PURKINJE; AUTONOMIC
   NEUROPATHY; SENSORY NEURONOPATHY; HODGKINS-DISEASE
AB OBJECTIVES: The aim of this study was to describe the clinical, manometric, and serological characteristics of 12 patients with paraneoplastic GI motor dysfunction and to assess the contributory role of diagnostic tests.
   METHODS: Twelve patients diagnosed with malignant tumors and GI motor dysfunction were identified at the Mayo Clinic from 1985 to 1996.
   RESULTS: Cancers identified were: nine small cell lung carcinoma (SCLC), one anaplastic lung adenocarcinoma, one retroperitoneal lymphoma, and one ovarian papillary serous adenocarcinoma. GI symptoms preceded the tumor diagnosis in all cases of SCLC (mean, -8.7 months, range, -1 to -24 months, n = 9). The diagnosis of a malignant tumor preceded the onset of GI symptoms in the three patients with other neoplasms (6, 12, and 24 months). Five of the nine patients found to have SCLC had no evidence of tumor on initial chest x-ray. One or more paraneoplastic autoantibodies were found in 10 of the 11 patients tested by autoimmune serology. Type 1 antineuronal nuclear antibody (ANNA-1 or anti-Hu) was detected in eight of the nine patients with SCLC (one patient was not tested). The patient with ovarian carcinoma had type 1 Purkinje cell cytoplasmic antibody (PCA-1 or anti-Yo). N-type calcium channel antibodies were found in one patient with SCLC, one with a retroperitoneal B cell lymphoma, and one with ovarian carcinoma. Gastric emptying was delayed in 89% (eight of nine tested) and 80% (four of five tested) had esophageal dysmotility. Autonomic reflex tests were abnormal in the seven patients tested.
   CONCLUSIONS: The diagnosis of paraneoplastic GI motor dysfunction requires a high index of clinical suspicion. A panel of serological tests for paraneoplastic autoantibodies, scintigraphic gastric emptying, and esophageal manometry are useful as first-line screening tests. Seropositivity for ANNA-1, PCA-1, or N-type calcium channel-binding antibodies should prompt further evaluation for an underlying malignancy even when routine imaging studies are negative.
C1 Mayo Clin, Gastroenterol Res Unit, Rochester, MN USA.
   Mayo Clin, Dept Immunol, Neuroimmunol Lab, Rochester, MN USA.
   Mayo Clin, Dept Neurol, Rochester, MN USA.
   Mayo Clin, Dept Lab Med, Rochester, MN USA.
   Mayo Clin, Dept Pathol, Rochester, MN USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic
RP Prather, CM (corresponding author), St Louis Univ, Div Gastroenterol & Hepatol, 3635 Vista Ave,FDT-9, St Louis, MO 63110 USA.
FU NCI NIH HHS [CA-37343] Funding Source: Medline
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NR 46
TC 107
Z9 110
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA
SN 0002-9270
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD FEB
PY 2001
VL 96
IS 2
BP 373
EP 379
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 404EH
UT WOS:000167084100017
PM 11232678
DA 2025-06-01
ER

PT J
AU Wang, SM
   Roth, MJ
   Murphy, GA
   Dawsey, SM
   Fan, JH
   Taylor, PR
   Qiao, YL
   Abnet, CC
AF Wang, Shao-Ming
   Roth, Mark J.
   Murphy, Gwen A.
   Dawsey, Sanford M.
   Fan, Jin-Hu
   Taylor, Philip R.
   Qiao, You-Lin
   Abnet, Christian C.
TI Serologic Profile of Antiparietal Cell Antibodies, Pepsinogens, and
   H. pylori and Risk of Upper Gastrointestinal Cancer: A Nested
   Case-Control Study in China
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HELICOBACTER-PYLORI; GASTRIC-CANCER; CARDIA; ESOPHAGEAL; ADENOCARCINOMA;
   INFECTION; SUBSITE; LINXIAN; DISEASE; ATROPHY
AB Background: Autoimmune gastritis is understudied and possibly associated with gastric noncardia adenocarcinoma (GNCA) and esophageal squamous cell carcinoma (ESCC) in Western populations when it presents as pernicious anemia.
   Methods: A nested case-control study within a Chinese cohort included 100 ESCC, 200 gastric cardia adenocarcinoma (GCA), and 200 GNCA cases diagnosed between 1986 and 2001 and 400 controls. Serostatus of anti-parietal cell antibodies (APCA), Helicobacter pylori antibodies, and pepsinogens were measured using commercial kits and serum collected at baseline. We used logistic regression to calculate odds ratios (OR) and 95% confidence interval (CI) for associations between serologic biomarkers and cancer risk adjusted for numerous potential confounders.
   Results: There was an average interval of 8 years between baseline blood draw and cancer diagnosis. The baseline prevalence of APCA seropositivity was 10.0% and 14.5% in subjects who developed GCA and GNCA, respectively. APCA seropositivity was inversely associated with later development of GCA (OR = 0.42; 95% CI, 0.24-0.75), but not significantly associated with later development of GNCA (OR = 0.82; 95% CI, 0.50-1.36) or ESCC (OR = 1.05; 95% CI, 0.58-1.88). APCA seropositivity was significantly associated with low pepsinogen I/II ratios (OR = 3.69; 95% CI, 1.66-8.21), and individuals with low pepsinogen I/II ratios who were seronegative for APCA had the highest risk of both GCA and GNCA.
   Conclusions: APCA seropositivity measured years prior to diagnosis was associated with prevalent atrophic gastritis but inversely associated with incident GCA in this Chinese population.
   Impact: APCA may contribute to a growing list of serologic markers that can improve risk stratification for gastric cancer.
C1 [Wang, Shao-Ming; Fan, Jin-Hu; Qiao, You-Lin] Chinese Acad Med Sci & Peking Union Med Coll, Dept Canc Epidemiol, Natl Canc Ctr, Natl Clin Res Ctr Canc,Canc Hosp, Beijing, Peoples R China.
   [Wang, Shao-Ming; Murphy, Gwen A.; Dawsey, Sanford M.; Taylor, Philip R.; Abnet, Christian C.] NCI, Metab Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
   [Roth, Mark J.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Peking Union Medical College;
   National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); NIH National Cancer Institute- Division of Cancer Epidemiology &
   Genetics; National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI)
RP Abnet, CC (corresponding author), NCI, 9609 Med Ctr Dr,Room 6E430, Rockville, MD 20850 USA.; Qiao, YL (corresponding author), Chinese Acad Med Sci & Peking Union Med Coll, Natl Canc Ctr, Natl Clin Res Ctr Canc, Canc Hosp, 17 South Panjiayuan Lane,POB 2258, Beijing 100021, Peoples R China.
EM qiaoy@cicams.ac.cn; abnetc@mail.nih.gov
RI Qiao, You-Lin/B-4139-2012; Abnet, Christian/JAC-5179-2023; Abnet,
   Christian/C-4111-2015; Murphy, Gwen/AFR-8275-2022
OI Abnet, Christian/0000-0002-3008-7843; fan, jinhu/0000-0003-3159-7893;
   Wang, Shao-Ming/0000-0002-3980-1919; Wang, ShaoMing/0000-0003-0420-2833;
   Murphy, Gwen/0000-0003-0118-5337; Dawsey, Sanford M/0000-0003-2185-0533;
   Qiao, Youlin/0000-0001-6380-0871
FU National Natural Science Fund of China [81502864]; intramural research
   program of the NCI, NIH
FX The authors thank all the people who participated in the study and the
   many individuals not specifically mentioned in the article who have
   supported the study. This work was supported by the Young Scientists
   Fund of the National Natural Science Fund of China (award no. 81502864,
   to S.-M. Wang) and the intramural research program of the NCI, NIH (C.C.
   Abnet).
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NR 31
TC 6
Z9 6
U1 0
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2019
VL 28
IS 12
BP 2022
EP 2029
DI 10.1158/1055-9965.EPI-19-0512
PG 8
WC Oncology; Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Public, Environmental & Occupational Health
GA JV8CX
UT WOS:000502588500011
PM 31501152
OA Green Accepted, Bronze
DA 2025-06-01
ER

PT J
AU Zhang, Y
   Lu, N
   Xue, YW
   Zhang, M
   Li, YJ
   Si, YQ
   Bian, XK
   Jia, YF
   Wang, YS
AF Zhang, Yi
   Lu, Nan
   Xue, Yuwen
   Zhang, Min
   Li, Yingjie
   Si, Yuanquan
   Bian, Xiaokun
   Jia, Yanfei
   Wang, Yunshan
TI Expression of immunoglobulin-like transcript (ILT)2 and ILT3 in human
   gastric cancer and its clinical significance
SO MOLECULAR MEDICINE REPORTS
LA English
DT Article
DE immunoglobulin-like transcript 2; immunoglobulin-like transcript 3;
   gastric cancer; NK cells
ID TOLEROGENIC DENDRITIC CELLS; INHIBITORY RECEPTOR ILT3; REGULATORY
   T-CELLS; HLA-G; MYELOID CELLS; ANTIGEN; GENE; ACTIVATION; INDUCTION;
   MOLECULES
AB Immune inhibitory receptors play an important role in organ transplantation, autoimmune diseases and cancers. Immunoglobulin-like transcript (ILT)2 and ILT3 belong to the inhibitory receptors of the ILT family, which have been reported to regulate a broad range of cellular functions involved in the immune response. They contain immunoreceptor tyrosine-based inhibitory motifs (ITIMs), which are related to immune regulation. Although ILT receptors have been studied in dendritic cells (DCs), T cells, NK cells and other cell types, the expression and clinical significance of ILT2 and ILT3 in gastric cancer have yet to be elucidated. Here, the expression of ILT2 and ILT3 in gastric cancer cell lines and pathologic tissues, as well as their effects on the cytotoxicity of NK92MI against the gastric cancer cell lines MKNI with ILT2(low)ILT3(low) and HGC-27 with ILT2(high)ILT3(high) were detected. The results suggest that ILT2 and ILT3 are expressed with diverse degrees in gastric cancer cells and tissues, and the expression of ILT2 is related with differentiation and size of tumors. Furthermore, the cytotoxic activity of NK92MI against the MKNI cell line was stronger than that against HGC-27. This study indicates that ILT2 and ILT3 play a key role in gastric cancer immune escape, and ILT2 may be a new target in the clinical diagnosis and treatment of gastric cancer.
C1 [Zhang, Yi; Li, Yingjie; Si, Yuanquan; Bian, Xiaokun] Shandong Univ, Qilu Hosp, Dept Clin Lab Med, Jinan 250012, Peoples R China.
   [Lu, Nan] Shandong Univ, Sch Med, Inst Diagnost, Jinan, Peoples R China.
   [Jia, Yanfei; Wang, Yunshan] Shandong Univ, Jinan Cent Hosp, Med Res & Lab Diagnost Ctr, Shandong Prov Key Lab Tumor Target Mol, Jinan 250013, Peoples R China.
   [Xue, Yuwen] Shandong Univ, Qilu Hosp, Dept Med, Jinan, Peoples R China.
   [Zhang, Min] Shandong Chest Hosp, Dept Med, Jinan, Peoples R China.
C3 Shandong University; Shandong University; Shandong University; Shandong
   First Medical University & Shandong Academy of Medical Sciences;
   Shandong University; Shandong University
RP Zhang, Y (corresponding author), Shandong Univ, Qilu Hosp, Dept Clin Lab Med, 107 Wen Hua Rd, Jinan 250012, Peoples R China.
EM yizhang@sdu.edu.cn; sdjnwys@163.com
RI Lu, Nan/AGU-1449-2022; Zhang, Yining/AHB-5771-2022
OI Lu, Nan/0000-0003-0590-7173
FU Shandong Province Science Foundation [2008GG30002017, 2010GSF10274];
   University Innovation Program from Jinan, Shandong Province [201004050]
FX This study was supported in part by grants from the Shandong Province
   Science Foundation for Key Programs (2008GG30002017 and 2010GSF10274)
   and the University Innovation Program from Jinan, Shandong Province
   (201004050).
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NR 42
TC 38
Z9 42
U1 0
U2 8
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1791-2997
J9 MOL MED REP
JI Mol. Med. Rep.
PD APR
PY 2012
VL 5
IS 4
BP 910
EP 916
DI 10.3892/mmr.2012.744
PG 7
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 906DC
UT WOS:000301324100006
PM 22246571
OA Green Accepted, Bronze, Green Published
DA 2025-06-01
ER

PT J
AU Szylberg, L
   Karbownik, D
   Marszalek, A
AF Szylberg, Lukasz
   Karbownik, Dominika
   Marszalek, Andrzej
TI The Role of FOXP3 in Human Cancers
SO ANTICANCER RESEARCH
LA English
DT Review
DE FOXP3; cancer; tumor immunity; review
ID REGULATORY T-CELLS; GASTRIC-CANCER; EXPRESSION; MELANOMA; POPULATION;
   INHIBITION; DEFINES; TUMORS
AB FOXP3 transcription factor can be observed as the main component of the immune system expressed in regulatory T (Treg) cells that regulate hemostasis and self-tolerance. Moreover, the altered expression of FOXP3 was found in autoimmune diseases, benign tumors and carcinomas. Latest reports indicate that the FOXP3 gene mutation can contribute to carcinogenesis, which can be associated with immune response abnormalities. Infiltration of the Treg cells into tumor cells can be associated with prognosis. Understanding the biology of the FOXP3 gene may be crucial in developing new immunotherapeutics.
C1 [Szylberg, Lukasz; Karbownik, Dominika; Marszalek, Andrzej] Nicolaus Copernicus Univ Torun, Coll Med Bydgoszcz, Dept Clin Pathomorphol, Torun, Poland.
   [Marszalek, Andrzej] Poznan Univ Med Sci, Dept Oncol Pathol, Poznan, Poland.
   [Marszalek, Andrzej] Greater Poland Canc Ctr, Poznan, Poland.
C3 Nicolaus Copernicus University; Poznan University of Medical Sciences;
   Wielkopolskie Centrum Onkologii
RP Szylberg, L (corresponding author), A Jurasz Univ Hosp 1, Dept Clin Pathomorphol, Sklodowskiej Curie 9, PL-85094 Bydgoszcz, Poland.
EM l.szylberg@cm.umk.pl
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NR 38
TC 43
Z9 48
U1 0
U2 7
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD AUG
PY 2016
VL 36
IS 8
BP 3789
EP 3794
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DW9QW
UT WOS:000383997800001
PM 27466478
DA 2025-06-01
ER

PT J
AU Ma, XZ
   Zhou, N
   Luo, X
   Guo, SQ
   Mai, P
AF Ma, Xiu-Zhen
   Zhou, Ni
   Luo, Xiu
   Guo, Si-Qi
   Mai, Ping
TI Update understanding on diagnosis and histopathological examination of
   atrophic gastritis: A review
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Atrophic gastritis; Helicobacter pylori infection; Autoimmune gastritis;
   Diagnosis; Operative link for gastritis assessment staging; Gastric
   cancer risk
ID HELICOBACTER-PYLORI INFECTION; NEUROENDOCRINE TUMORS; AUTOIMMUNE
   GASTRITIS; BODY GASTRITIS; CANCER-RISK; SALT INTAKE; DEFICIENCY;
   MANAGEMENT; CELLS; OLGA
AB Chronic atrophic gastritis (CAG) is a complex syndrome in which long-term chronic inflammatory stimulation causes gland atrophy in the gastric mucosa, reducing the stomach's ability to secrete gastric juice and pepsin, and interfering with its normal physiological function. Multiple pathogenic factors contribute to CAG incidence, the most common being Helicobacter pylori infection and the immune reactions resulting from gastric autoimmunity. Furthermore, CAG has a broad spectrum of clinical manifestations, including gastroenterology and extra-intestinal symptoms and signs, such as hematology, neurology, and oncology. Therefore, the initial CAG evaluation should involve the examination of clinical and serological indicators, as well as diagnosis confirmation via gastroscopy and histopathology if necessary. Depending on the severity and scope of atrophy affecting the gastric mucosa, a histologic staging system (Operative Link for Gastritis Assessment or Operative Link on Gastritis intestinal metaplasia) could also be employed. Moreover, chronic gastritis has a higher risk of progressing to gastric cancer (GC). In this regard, early diagnosis, treatment, and regular testing could reduce the risk of GC in CAG patients. However, the optimal interval for endoscopic monitoring in CAG patients remains uncertain, and it should ideally be tailored based on individual risk evaluations and shared decision-making processes. Although there have been many reports on CAG, the precise etiology and histopathological features of the disease, as well as the diagnosis of CAG patients, are yet to be fully elucidated. Consequently, this review offers a detailed account of CAG, including its key clinical aspects, aiming to enhance the overall understanding of the disease.
C1 [Ma, Xiu-Zhen; Luo, Xiu; Mai, Ping] Lanzhou Univ, Sch Clin Med 1, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.
   [Ma, Xiu-Zhen; Guo, Si-Qi; Mai, Ping] Gansu Prov Peoples Hosp, Dept Gastroenterol, Lanzhou 730000, Gansu, Peoples R China.
   [Zhou, Ni] Xian Int Med Ctr, Dept Gastroenterol, Xian 710000, Shaanxi, Peoples R China.
   [Guo, Si-Qi] Gansu Univ Chinese Med, Sch Clin Med 1, Lanzhou 730000, Gansu, Peoples R China.
C3 Lanzhou University; Gansu University of Chinese Medicine
RP Mai, P (corresponding author), Lanzhou Univ, Sch Clin Med 1, 204 Donggang West Rd, Lanzhou 730000, Gansu, Peoples R China.
EM maiping_lz@163.com
RI ma, xiuzhen/LTF-2461-2024
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NR 92
TC 1
Z9 1
U1 6
U2 6
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD OCT 15
PY 2024
VL 16
IS 10
DI 10.4251/wjgo.v16.i10.4080
PG 13
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA K8A5Z
UT WOS:001346055400010
PM 39473965
DA 2025-06-01
ER

PT J
AU Pacheco, A
   Diedisheim, M
   Goulvestre, C
   Alexandre-Heymann, L
   Mallone, R
   Dubois-Laforgue, D
   Larger, E
AF Pacheco, Aude
   Diedisheim, Marc
   Goulvestre, Claire
   Alexandre-Heymann, Laure
   Mallone, Roberto
   Dubois-Laforgue, Daniele
   Larger, Etienne
TI Screening for autoimmune atrophic gastritis by serum gastrin measurement
   in subjects with type 1 diabetes
SO DIABETES & METABOLISM
LA English
DT Article
DE Autoimmune gastritis; Type 1 diabetes; Gastrin; Autoimmune polyglandular
   diseases; Parietal cells
ID PARIETAL-CELL ANTIBODY; DIAGNOSIS; CHILDREN; GHRELIN; MARKER; RISK
AB Introduction: Despite associated risk of anemia and gastric cancer, screening for autoimmune atrophic gastritis (AAG) is underperformed in subjects with type 1 diabetes mellitus (T1DM). We measured the predictive value of serum gastrin as a biomarker of gastric atrophy in subjects with T1DM and parietal cell autoantibodies (PCA). Subjects and Methods: PCA measurements were retrospectively retrieved in 1,425 consecutive subjects with T1DM between 2014 and 2018. Screening for AAG was conducted in PCA+ subjects by measuring blood counts, serum ferritin, vitamin B12 and gastrin; and by performing gastroduodenal fibroscopy, with fundic biopsies for histology and Helicobacter pylori. The performance of blood biomarkers of gastric atrophy was analyzed in comparison with the histopathological gold standard. Results: PCA were found in 185/1,425 subjects (13 %). PCA positivity was associated with female sex, older age, longer T1DM duration, and co-occurrence of anti-GAD and anti-thyroperoxydase autoantibodies. Of the 185 PCA+ subjects, 122 (66 %) participated in screening. AAG was found in 69/122 (57 %) subjects and Helicobacter pylori infection in 20/122 (16 %). Compared to PCA+ subjects without gastric atrophy, those with gastric atrophy had more frequently iron deficiency (65 % vs. 18 %, P < 0.0001), and/or vitamin B12 deficiency (57 % vs. 7 %, P < 0.0001); 44/69 (64 %) presented a pre-tumoral lesion and 6 % a tumor. Using a cut-off of 1.2-fold above the upper normal limit, serum gastrin concentration displayed 91 % sensitivity and 82 % specificity at predicting gastric atrophy. Conclusion: In subjects with T1DM and PCA, serum gastrin is a reliable biomarker of gastric atrophy that can be used to select subjects requiring gastroduodenal fibroscopy.
C1 [Pacheco, Aude; Diedisheim, Marc; Alexandre-Heymann, Laure; Mallone, Roberto; Dubois-Laforgue, Daniele; Larger, Etienne] Univ Paris Cite, Paris, France.
   [Pacheco, Aude; Diedisheim, Marc; Alexandre-Heymann, Laure; Mallone, Roberto; Dubois-Laforgue, Daniele; Larger, Etienne] Ctr Univ Paris Cite, Hop Cochin, AP HP, Serv Diabetol & Immunol Clin, Paris, France.
   [Diedisheim, Marc; Alexandre-Heymann, Laure; Mallone, Roberto; Dubois-Laforgue, Daniele; Larger, Etienne] Univ Paris Cite, Inst Cochin, CNRS, INSERM, Paris, France.
   [Goulvestre, Claire] Ctr Univ Paris Cite, Hop Cochin, AP HP, Lab Immunol, Paris, France.
C3 Universite Paris Cite; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Cochin - APHP; Universite
   Paris Cite; Institut National de la Sante et de la Recherche Medicale
   (Inserm); Centre National de la Recherche Scientifique (CNRS);
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Cochin - APHP
RP Larger, E (corresponding author), Univ Paris Cite, Paris, France.; Larger, E (corresponding author), Ctr Univ Paris Cite, Hop Cochin, AP HP, Serv Diabetol & Immunol Clin, Paris, France.; Larger, E (corresponding author), Univ Paris Cite, Inst Cochin, CNRS, INSERM, Paris, France.
EM etienne.larger@u-paris.fr
FU Borel bequest to the Diabetes Department of the Cochin Hospital
FX This work was supported by the Borel bequest to the Diabetes Department
   of the Cochin Hospital.
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NR 24
TC 0
Z9 0
U1 0
U2 0
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
SN 1262-3636
EI 1878-1780
J9 DIABETES METAB
JI Diabetes Metab.
PD MAY
PY 2025
VL 51
IS 3
AR 101640
DI 10.1016/j.diabet.2025.101640
EA MAR 2025
PG 5
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 0WQ6K
UT WOS:001457787400001
PM 40113012
DA 2025-06-01
ER

PT J
AU Khan, S
   Zhu, LP
   Jiang, K
   Liu, WT
   Chen, X
   Wang, BM
AF Khan, Samiullah
   Zhu, Lan-ping
   Jiang, Kui
   Liu, Wentian
   Chen, Xin
   Wang, Bang-mao
TI Immunoglobulin G4-Related Disease Manifesting as Isolated, Typical, and
   Nontypical Gastroesophageal Lesion: A Research of Literature Review
SO DIGESTION
LA English
DT Review
DE Esophageal immunoglobulin G4-related disease; Gastric immunoglobulin
   G4-related disease; Isolated lesions; Typical lesions; Nontypical
   lesions
ID IGG4-RELATED DISEASE; INFLAMMATORY PSEUDOTUMOR; AUTOIMMUNE PANCREATITIS;
   EOSINOPHILIC ESOPHAGITIS; GASTROINTESTINAL-TRACT; GASTRIC-ULCER; IGG4;
   MALIGNANCIES; CANCER; ADULTS
AB Background:Immunoglobulin G4-related disease (IgG4-RD) is an autoimmune inflammatory and fibrotic condition. The disease is characterized by tissue infiltration with dense lymphoplasmacytes and IgG4-positive plasma cells.Summary:The aim of this study was to provide gastroenterologists with novel insights into evaluating the gastroesophageal involvement with IgG4-RD or mimickers of this condition and to give special attention to clinicopathological features. A literature review was performed using the PubMed database. A total of 39 studies presenting cases in the form of isolated, typical, and nontypical gastroesophageal involvement with IgG4-RD published between 2010 and 2018 were included. These studies were thoroughly reviewed for symptoms, lesion location, lesion type, lesion size, immune-histopathology, associated diseases, treatment, and follow-up. Of the 39 studies reviewed, 9 were esophageal IgG4-RD lesions, isolated esophageal IgG4-RD 66.66% (6/9), a typical form of esophageal IgG4-RD 11.11% (1/9), and nontypical form esophageal IgG4-RD 22.22% (2/9). The 30 gastric IgG4-RD that include isolated gastric IgG4-RD 46.66% (14/30), typical gastric IgG4-RD 40% (12/30), and nontypical gastric IgG4-RD 13.33% (4/30). The majority of lesions were inflammatory tumors, ulceration, nodular lesions, chronic gastritis, and malignant lesions.Key Messages:IgG4-RD may be manifested by isolated, typical and nontypical forms of gastroesophageal lesions and should be taken into consideration in the differential diagnosis. Corticosteroids may be the sole diagnostic treatment for this condition.
C1 [Khan, Samiullah; Zhu, Lan-ping; Jiang, Kui; Liu, Wentian; Chen, Xin; Wang, Bang-mao] Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, 154 Anshan Rd, Tianjin 300052, Peoples R China.
C3 Tianjin Medical University
RP Chen, X; Wang, BM (corresponding author), Tianjin Med Univ, Gen Hosp, Dept Gastroenterol & Hepatol, 154 Anshan Rd, Tianjin 300052, Peoples R China.
EM xchen03@tmu.edu.cn; mwang02@tmu.edu.cn
FU Science and Technology Program of Tianjin [15ZXJZSY00020]; Natural
   Science Foundation of Tianjin [18JCZDJC45200]
FX This study was supported by Science and Technology Program of Tianjin
   (15ZXJZSY00020) and Natural Science Foundation of Tianjin
   (18JCZDJC45200).
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NR 70
TC 15
Z9 16
U1 0
U2 5
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0012-2823
EI 1421-9867
J9 DIGESTION
JI Digestion
PD SEP
PY 2020
VL 101
IS 5
BP 506
EP 521
DI 10.1159/000501513
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA NP5EF
UT WOS:000570198600002
PM 31291621
OA Bronze
DA 2025-06-01
ER

PT J
AU Wang, WW
   Yuan, XL
   Chen, H
   Xie, GH
   Ma, YH
   Zheng, YX
   Zhou, YL
   Shen, LS
AF Wang, Weiwei
   Yuan, Xiangliang
   Chen, Hui
   Xie, Guohua
   Ma, Yanhui
   Zheng, Yingxia
   Zhou, Yunlan
   Shen, Lisong
TI CD19<SUP>+</SUP>CD24<SUP>hi</SUP>CD38<SUP>hi</SUP>Bregs involved in
   downregulate helper T cells and upregulate regulatory T cells in gastric
   cancer
SO ONCOTARGET
LA English
DT Article
DE cgastric cancer; regulatory B cells; IL-10; TGF-beta; regulatory T
   cells; immune escape
ID B-CELLS; SUPPRESSIVE ROLE; AUTOIMMUNITY; FREQUENCIES; METASTASIS;
   INHIBITION; DEFICIENT; RESPONSES; SUBSET; FOXP3
AB Regulatory B cells (Bregs) play a critical role in inflammation and autoimmune disease. We characterized the role of Bregs in the progression of gastric cancer. We detected an increase in Bregs producing IL-10 both in peripheral blood mononuclear cells (PBMCs) and in gastric tumors. Multicolor flow cytometry analysis revealed that a subset of CD19(+)CD24(hi)CD38(hi) B cells produces IL-10. Functional studies indicated that increased Bregs do not inhibit the proliferation of CD3(+)T cells or CD4(+) helper T cells (Th cells). However, Bregs do suppress the secretion of IFN-gamma and TNF-alpha by CD4(+)Th cells. CD19(+)CD24(hi)CD38(hi)Bregs were also found to correlate positively with CD4(+)FoxP3(+) regulatory T cells (Tregs). Neutralization experiments showed that Bregs onvert CD4(+)CD25(-) effector T cells to CD4(+)FoxP3(+)Tregs via TGF-beta 1. Collectively, these findings demonstrate that increased Bregs play a immunosuppressive role in gastric cancer by inhibiting T cells cytokines as well as conversion to Tregs. These results may provide new clues about the underlying mechanisms of immune escape in gastric cancer.
C1 [Wang, Weiwei; Yuan, Xiangliang; Chen, Hui; Xie, Guohua; Ma, Yanhui; Zheng, Yingxia; Zhou, Yunlan; Shen, Lisong] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Clin Lab, Shanghai 200030, Peoples R China.
C3 Shanghai Jiao Tong University
RP Shen, LS (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, Dept Clin Lab, Shanghai 200030, Peoples R China.
EM lisongshen@hotmail.com
FU National Natural Science Foundation of China [81301788]
FX This study was supported by the National Natural Science Foundation of
   China (81301788).
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NR 50
TC 112
Z9 115
U1 0
U2 27
PU IMPACT JOURNALS LLC
PI ORCHARD PARK
PA 6666 E QUAKER ST, STE 1, ORCHARD PARK, NY 14127 USA
EI 1949-2553
J9 ONCOTARGET
JI Oncotarget
PD OCT 20
PY 2015
VL 6
IS 32
BP 33486
EP 33499
DI 10.18632/oncotarget.5588
PG 14
WC Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Cell Biology
GA CU0DQ
UT WOS:000363186600104
PM 26378021
OA Green Submitted, Green Published, gold
DA 2025-06-01
ER

PT J
AU Magris, R
   De Re, V
   Maiero, S
   Fornasarig, M
   Guarnieri, G
   Caggiari, L
   Mazzon, C
   Zanette, G
   Steffan, A
   Canzonieri, V
   Cannizzaro, R
AF Magris, Raffaella
   De Re, Valli
   Maiero, Stefania
   Fornasarig, Mara
   Guarnieri, Giovanni
   Caggiari, Laura
   Mazzon, Cinzia
   Zanette, Giorgio
   Steffan, Agostino
   Canzonieri, Vincenzo
   Cannizzaro, Renato
TI Low Pepsinogen I/II Ratio and High Gastrin-17 Levels Typify Chronic
   Atrophic Autoimmune Gastritis Patients With Gastric Neuroendocrine
   Tumors
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Article
ID ASSOCIATION; CANCER; CLASSIFICATION; THYROIDITIS; DISEASES; RISK
AB INTRODUCTION: Chronic atrophic autoimmune gastritis (CAAG) can lead to the development of gastric neuroendocrine tumors (gNETs) and can be accompanied by other autoimmune diseases. This study aimed to determine, in CAAG patients, the association of gNET development, the prevalence of autoimmune diseases other than CAAG, the association of autoimmunity, and gNET development with pepsinogen I, II, gastrin-17, andHelicobacter pyloriinfection analysis.
   METHODS: We determined the prevalence of gNETs and other autoimmune diseases and analyzed pepsinogen I and II, gastrin-17 serum levels, andH. pyloriinfection in all patients diagnosed with CAAG at our hospital between 2013 and 2017.
   RESULTS: A total of 156 patients were studied and in 15.4% was observed concomitant gNET. Approximately 68.6% had at least 1 other autoimmune disease at diagnosis of CAAG. Approximately 60.9% had autoimmune thyroiditis, followed by diabetes (19.9%) and autoimmune polyendocrine syndrome (12.8%). CAAG patients with and without gNET had similar rates of comorbidity with other autoimmune diseases, but the pepsinogen I/II ratio was lower in patients with gNET (1.6 vs 4.5,P= 0.018). Receiver operating characteristic curve analyses identified a pepsinogen I/II ratio 29.6 pmol/L as cutoffs distinguishing CAAG patients with gNET from those without. The combined use of these cutoff correctly identified 16 of the 18 CAAG patients with gNET (P= 0.007).H. pyloriinfection was observed in 28.7% of cases tested but did not associate with gNET.
   DISCUSSION: This study suggests that a low pepsinogen I/II ratio and high gastrin-17 levels characterize patients with CAAG and gNET and confirms the frequent coexistence of CAAG with other autoimmune diseases.
C1 [Magris, Raffaella; Maiero, Stefania; Fornasarig, Mara; Guarnieri, Giovanni; Cannizzaro, Renato] Ctr Riferimento Oncol Aviano CRO IRCCS, Oncol & Gastroenterol, Aviano, Italy.
   [De Re, Valli; Caggiari, Laura; Steffan, Agostino] Ctr Riferimento Oncol Aviano CRO IRCCS, Immunopathol & Canc Biomarkers, Aviano, Italy.
   [Mazzon, Cinzia] Pordenone Hosp, Div Endocrinol, Pordenone, Italy.
   [Zanette, Giorgio] Pordenone Hosp, Div Diabetol, Pordenone, Italy.
   [Canzonieri, Vincenzo] Ctr Riferimento Oncol Aviano CRO IRCCS, Pathol Unit, Aviano, Italy.
   [Canzonieri, Vincenzo] Univ Trieste, DSM Dept Med Surg & Hlth Sci, Trieste, Italy.
C3 University of Trieste
RP Cannizzaro, R (corresponding author), Ctr Riferimento Oncol Aviano CRO IRCCS, Oncol & Gastroenterol, Aviano, Italy.; De Re, V (corresponding author), Ctr Riferimento Oncol Aviano CRO IRCCS, Immunopathol & Canc Biomarkers, Aviano, Italy.
EM vdere@cro.it; rcannizzaro@cro.it
RI Magris, Raffaella/ABD-7791-2020; De Re, Valli/K-4121-2016; CAGGIARI,
   LAURA/Q-6125-2019; Steffan, Agostino/ABE-5972-2020; Cannizzaro,
   Renato/V-3804-2018; Maiero, Stefania/ABD-6092-2020; Canzonieri,
   Vincenzo/K-3141-2018; Guarnieri, Giovanni/ABE-8112-2020; Fornasarig,
   Mara/ABD-5093-2020
OI Cannizzaro, Renato/0000-0002-2020-222X; Maiero,
   Stefania/0000-0001-5085-1549; Canzonieri, Vincenzo/0000-0001-6010-0976;
   Guarnieri, Giovanni/0000-0002-3245-1047; Fornasarig,
   Mara/0000-0003-3388-0676
FU Italian Ministry of Health (Ricerca Corrente); CRO 5X1000_2010_MdS,
   Italy
FX The project was supported by the Italian Ministry of Health (Ricerca
   Corrente) [no grant number provided]. CRO 5X1000_2010_MdS, Italy.
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NR 32
TC 33
Z9 36
U1 0
U2 19
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD SEP
PY 2020
VL 11
IS 9
AR e00238
DI 10.14309/ctg.0000000000000238
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA NX9AN
UT WOS:000575994700013
PM 33094954
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Fujie, S
   Matsubayashi, H
   Ishiwatari, H
   Hazama, H
   Ito, T
   Sasaki, K
   Ono, H
AF Fujie, Shinya
   Matsubayashi, Hiroyuki
   Ishiwatari, Hirotoshi
   Hazama, Hiromasa
   Ito, Takaaki
   Sasaki, Keiko
   Ono, Hiroyuki
TI Intraductal Tubulopapillary Epithelial Proliferation Associated with
   Type 1 Autoimmune Pancreatitis
SO JOURNAL OF GASTROINTESTINAL AND LIVER DISEASES
LA English
DT Article
DE autoimmune pancreatitis; intraductal tumor; IgG4; K-ras; diagnosis
ID PAPILLARY-MUCINOUS NEOPLASM; FINE-NEEDLE-ASPIRATION; IGG4-RELATED
   DISEASE; DIAGNOSIS; CARCINOMA; LESIONS; CANCER; TUMOR; DUCT;
   CLASSIFICATION
AB A 70-year-old man was referred to our hospital with exacerbation of diabetes. His blood tests showed elevated levels of serum IgG4 and HbAlc. Computed tomography of the pancreatic body demonstrated a weakly enhanced mass, 2 cm in size, with indistinct borders. Magnetic resonance cholangiopancreatography revealed a narrowing of the main pancreatic duct (MPD) at the pancreatic body, a markedly dilated upstream duct, and a slightly dilated downstream duct. Endoscopic ultrasonography demonstrated an iso-hypoechoic heterogeneous mass, protruding and spreading in the pancreatic duct. The histology of a fine needle aspiration sample demonstrated fibrous tissue containing abundant IgG4-positive plasma cells and atypical epithelial cells. The imaging findings and histology were not typical for either pancreatic ductal adenocarcinoma or type 1 autoimmune pancreatitis (AIP), but these were not completely excluded, and a distal pancreatectomy was performed. Histological examination showed an intraductal tubulopapillary epithelial proliferation, which contained cytoplasmic mucin (MUC5AC and MUC6), and severe IgG4-positive lymphoplasmacytic infiltration in the interstitium around the MPD. Next-generation sequencing using DNA extracted from the tumor revealed no mutation of K-ras, GNAS, or TP53. The entire lesion was ultimately diagnosed as AIP with an intraductal tubular and papillary epithelial hyperplasia producing gastric-type mucin. Some recent reports have described AIP development in the background of intraductal papillary mucinous neoplasms, and some have hypothesized a paraneoplastic occurrence of IgG4-related disease. The current case indicates issues in the clinical diagnosis of rare variants of AIP, and raises questions about the relationship between AIP and pancreatic epithelial lesions.
C1 [Fujie, Shinya; Matsubayashi, Hiroyuki; Ishiwatari, Hirotoshi; Hazama, Hiromasa; Ono, Hiroyuki] Shizuoka Canc Ctr, Div Endoscopy, 1007 Shimonagakubo, Suntogun, Shizuoka 4118777, Japan.
   [Ito, Takaaki] Shizuoka Canc Ctr, Div Hepatopancreaticobiliary Surg, Suntogun, Shizuoka 4118777, Japan.
   [Sasaki, Keiko] Shizuoka Canc Ctr, Div Pathol, Suntogun, Shizuoka 4118777, Japan.
C3 Shizuoka Cancer Center; Shizuoka Cancer Center; Shizuoka Cancer Center
RP Matsubayashi, H (corresponding author), Shizuoka Canc Ctr, Div Endoscopy, 1007 Shimonagakubo, Suntogun, Shizuoka 4118777, Japan.
EM h.matsubayashi@scchr.jp
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NR 32
TC 5
Z9 5
U1 1
U2 2
PU MEDICAL UNIV PRESS
PI CLUJ-NAPOCA
PA 3RD MEDICAL CLINIC, STR CROITORILOR NO 19-21, CLUJ-NAPOCA, 400162,
   ROMANIA
SN 1841-8724
EI 1842-1121
J9 J GASTROINTEST LIVER
JI J. Gastrointest. Liver Dis.
PD MAR
PY 2018
VL 27
IS 1
BP 83
EP 87
DI 10.15403/jgld.2014.1121.271.fuj
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GD6YZ
UT WOS:000430656700014
PM 29557419
DA 2025-06-01
ER

PT J
AU Piscione, M
   Mazzone, M
   Di Marcantonio, MC
   Muraro, R
   Mincione, G
AF Piscione, Mariagrazia
   Mazzone, Mariangela
   Di Marcantonio, Maria Carmela
   Muraro, Raffaella
   Mincione, Gabriella
TI Eradication of Helicobacter pylori and Gastric Cancer: A
   Controversial Relationship
SO FRONTIERS IN MICROBIOLOGY
LA English
DT Review
DE gastric cancer; Helicobacter pylori; inflammation; gut microbiota;
   eradication
ID VACUOLATING CYTOTOXIN; GUT MICROBIOTA; THYROID-DISEASE; IRON-DEFICIENCY;
   INFECTION; EXPRESSION; MUCOSA; CAGA; ASSOCIATION; HYGIENE
AB Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a "type I carcinogen." Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa's cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett's esophagus, but also asthma and allergies, through discussion of the "hygiene hypothesis. " This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa's cascade, to improve prevention and therapy of gastric carcinoma.
C1 [Piscione, Mariagrazia; Mazzone, Mariangela; Di Marcantonio, Maria Carmela; Muraro, Raffaella; Mincione, Gabriella] Univ G dAnnunzio, Dept Innovat Technol Med & Dent, Chieti, Italy.
C3 G d'Annunzio University of Chieti-Pescara
RP Mincione, G (corresponding author), Univ G dAnnunzio, Dept Innovat Technol Med & Dent, Chieti, Italy.
EM gabriella.mincione@unich.it
RI Mazzone, M/AAQ-9306-2021; Di Marcantonio, Maria Carmela/AAB-9564-2022
OI Mazzone, Mariangela/0000-0002-7002-1291
FU Ministero dell'Universita e della Ricerca (MUR) [FAR2020]
FX This work was financed by intramural grants by the Ministero
   dell'Universita e della Ricerca (MUR) FAR2020 (ex 60%), held by GM.
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NR 109
TC 74
Z9 78
U1 1
U2 31
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-302X
J9 FRONT MICROBIOL
JI Front. Microbiol.
PD FEB 4
PY 2021
VL 12
AR 630852
DI 10.3389/fmicb.2021.630852
PG 18
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA QI5MX
UT WOS:000619022900001
PM 33613500
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Soykan, I
   Yakut, M
   Keskin, O
   Bektas, M
AF Soykan, Irfan
   Yakut, Mustafa
   Keskin, Onur
   Bektas, Mehmet
TI Clinical Profiles, Endoscopic and Laboratory Features and Associated
   Factors in Patients with Autoimmune Gastritis
SO DIGESTION
LA English
DT Article
DE Autoimmune gastritis; Iron/vitamin B-12 deficiency; Antiparietal cell
   antibody; Bloating; Helicobacter pylori
ID ATROPHIC BODY GASTRITIS; HELICOBACTER-PYLORI; PERNICIOUS-ANEMIA;
   INTRINSIC-FACTOR; THYROID-DISEASE; HYPERGASTRINEMIA; VITAMIN-B-12;
   PREVALENCE; DIAGNOSIS; CELLS
AB Background/Aims: Autoimmune gastritis (AIG) may predispose to gastric carcinoid tumors or adenocarcinomas and may also cause unexplained iron and/or vitamin B-12 deficiency. The aims of this study were to explore clinical manifestations, endoscopic findings and laboratory features of patients with AIG. Methods: 109 patients with AIG were enrolled into the study. In addition to demographic and clinical data, gastric lesions, serum gastrin, vitamin B-12, antiparietal cell antibody (APA), current Helicobacter pylori status, and anti-H. pylori IgG were also investigated. Results: The mean age of the patients was 53.06 +/- 12.7 years (range 24-81; 72 (66.1%) women). The most common main presenting symptom was abdominal symptoms in 51 patients, consultation for iron and/or vitamin B-12 deficiency in 36, and non-specific symptoms including intermittent diarrhea in 15 patients. Endoscopic lesions were detected in 17 patients, hyperplastic polyps in 8, gastric carcinoid tumor in 4, fundic gland polyps in 3, and adenomatous polyps in 2 patients. H. pylori was negative in all patients in biopsy specimens; however, anti-H. pylori IgG was positive in 30 (27.5%) patients. 91 patients (83.4%) were positive for APA. Conclusion: In patients with AIG, the main symptoms prompted for clinical investigation were: abdominal symptoms, iron/B-12 deficiency and non-specific symptoms. 20% of patients with AIG had various gastric lesions including type I gastric carcinoids. None of the patients were positive for H. pylori by means of invasive tests; however, anti-H. pylori IgG was found in 27.5% of patients. Patients referring with non-specific abdominal symptoms such as bloating, diarrhea and iron/B-12 deficiency should be investigated for the presence of AIG. Copyright (C) 2012 S. Karger AG, Basel
C1 [Soykan, Irfan; Yakut, Mustafa; Keskin, Onur; Bektas, Mehmet] Ankara Univ, Fac Med, Ibni Sina Hosp, Div Gastroenterol, TR-06100 Ankara, Turkey.
C3 Ankara University
RP Soykan, I (corresponding author), Ankara Univ, Fac Med, Ibni Sina Hosp, Div Gastroenterol, TR-06100 Ankara, Turkey.
EM isoykan@medicine.ankara.edu.tr
RI BEKTAŞ, Mehmet/AAA-3663-2020; Keskin, Onur/P-2213-2015
CR Annibale B, 2001, HELICOBACTER, V6, P225, DOI 10.1046/j.1083-4389.2001.00032.x
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NR 29
TC 36
Z9 36
U1 0
U2 8
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0012-2823
EI 1421-9867
J9 DIGESTION
JI Digestion
PY 2012
VL 86
IS 1
BP 20
EP 26
DI 10.1159/000338295
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 987QA
UT WOS:000307431000004
PM 22710370
DA 2025-06-01
ER

PT J
AU Tu, SP
   Quante, M
   Bhagat, G
   Takaishi, S
   Cui, GL
   Yang, XD
   Muthuplani, S
   Shibata, W
   Fox, JG
   Pritchard, DM
   Wang, TC
AF Tu, Shui Ping
   Quante, Michael
   Bhagat, Govind
   Takaishi, Shigeo
   Cui, Guanglin
   Yang, Xiang Dong
   Muthuplani, Sureshkumar
   Shibata, Wataru
   Fox, James G.
   Pritchard, D. Mark
   Wang, Timothy C.
TI IFN-γ Inhibits Gastric Carcinogenesis by Inducing Epithelial Cell
   Autophagy and T-Cell Apoptosis
SO CANCER RESEARCH
LA English
DT Article
ID HELICOBACTER-PYLORI; INTERFERON-GAMMA; CANCER; INFLAMMATION; INDUCTION;
   INFECTION; SURVIVAL; INTERLEUKIN-10; EXPRESSION; RESPONSES
AB IFN-gamma mediates responses to bacterial infection and autoimmune disease, but it is also an important tumor suppressor. It is upregulated in the gastric mucosa by chronic Helicobacter infection; however, whether it plays a positive or negative role in inflammation-associated gastric carcinogenesis is unexplored. To study this question, we generated an H+/K+-ATPase-IFN-gamma transgenic mouse that overexpresses murine IFN-gamma in the stomach mucosa. In contrast to the expected proinflammatory role during infection, we found that IFN-gamma overexpression failed to induce gastritis and instead inhibited gastric carcinogenesis induced by interleukin-1beta (IL-1 beta) and/or Helicobacter infection. Helper T cell (Th) 1 and Th17 immune responses were inhibited by IFN-gamma through Fas induction and apoptosis in CD4 T cells. IFN-gamma also induced autophagy in gastric epithelial cells through increased expression of Beclin-1. Finally, in the gastric epithelium, IFN-gamma also inhibited IL-1 beta-and Helicobacterinduced epithelial apoptosis, proliferation, and Dckl1(+) cell expansion. Taken together, our results suggest that IFN-gamma coordinately inhibits bacterial infection and carcinogenesis in the gastric mucosa by suppressing putative gastric progenitor cell expansion and reducing epithelial cell apoptosis via induction of an autophagic program. Cancer Res; 71(12); 4247-59. (C)2011 AACR.
C1 [Wang, Timothy C.] Columbia Univ, Coll Phys & Surg, Med Ctr, Dept Med, New York, NY 10032 USA.
   [Bhagat, Govind] Columbia Univ, Coll Phys & Surg, Dept Pathol & Cell Biol, New York, NY 10032 USA.
   [Tu, Shui Ping] Rutgers State Univ, Ctr Canc Prevent, Dept Biol Chem, Susam L Cullman Lab Canc Res, Piscataway, NJ USA.
   [Muthuplani, Sureshkumar; Fox, James G.] MIT, Div Comparat Med, Cambridge, MA 02139 USA.
   [Pritchard, D. Mark] Univ Liverpool, Sch Clin Sci, Div Gastroenterol, Liverpool L69 3BX, Merseyside, England.
C3 Columbia University; Columbia University; Rutgers University System;
   Rutgers University New Brunswick; Massachusetts Institute of Technology
   (MIT); University of Liverpool
RP Wang, TC (corresponding author), Columbia Univ, Coll Phys & Surg, Med Ctr, Dept Med, New York, NY 10032 USA.
EM tcw21@columbia.edu
RI wang, tim/JXM-8048-2024; Takaishi, Shigeo/AAS-3319-2021; Bhagat,
   Govind/AAE-9493-2021
OI Bhagat, Govind/0000-0001-6250-048X; Wang, Timothy/0000-0001-5730-3019;
   Pritchard, David Mark/0000-0001-7971-3561
FU NIH [1U54CA126513, RO1CA093405, R01CA120979, R21CA149865];
   Mildred-Scheel-Stiftung, Deutsche Krebshilfe; Grants-in-Aid for
   Scientific Research [23590919] Funding Source: KAKEN
FX This project was supported by NIH grants 1U54CA126513, RO1CA093405, and
   R01CA120979 (T.C. Wang), NIH grant R21CA149865 (S-P. Tu). M. Quante was
   supported by a grant from the Mildred-Scheel-Stiftung, Deutsche
   Krebshilfe.
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NR 50
TC 94
Z9 106
U1 0
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD JUN 15
PY 2011
VL 71
IS 12
BP 4247
EP 4259
DI 10.1158/0008-5472.CAN-10-4009
PG 13
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 777PZ
UT WOS:000291637100020
PM 21512143
OA Green Submitted, Green Accepted
DA 2025-06-01
ER

PT J
AU Kunovsky, L
   Dite, P
   Jabandziev, P
   Dolina, J
   Vaculova, J
   Blaho, M
   Bojkova, M
   Dvorackova, J
   Uvirova, M
   Kala, Z
   Trna, J
AF Kunovsky, Lumir
   Dite, Petr
   Jabandziev, Petr
   Dolina, Jiri
   Vaculova, Jitka
   Blaho, Martin
   Bojkova, Martina
   Dvorackova, Jana
   Uvirova, Magdalena
   Kala, Zdenek
   Trna, Jan
TI Helicobacter pylori infection and other bacteria in pancreatic
   cancer and autoimmune pancreatitis
SO WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY
LA English
DT Review
DE Helicobacter pylori; Pancreatic cancer; Autoimmune pancreatitis;
   Carcinogenesis; Microbiome; Molecular mimicry
ID ATROPHIC GASTRITIS; RISK; TERM; METAANALYSIS; ASSOCIATION; MULTICENTER;
   ERADICATION; PROGRESSION; MICROBIOTA; OUTCOMES
AB Helicobacter pylori (H. pylori) is an infectious agent influencing as much as 50% of the world's population. It is the causative agent for several diseases, most especially gastric and duodenal peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma of the stomach. A number of other, extragastric manifestations also are associated with H. pylori infection. These include neurological disorders, such as Alzheimer's disease, demyelinating multiple sclerosis and Parkinson's disease. There is also evidence for a relationship between H. pylori infection and such dermatological diseases as psoriasis and rosacea as well as a connection with infection and open-angle glaucoma. Generally little is known about the relationship between H. pylori infection and diseases of the pancreas. Most evidence about H. pylori and its potential role in the development of pancreatic diseases concerns pancreatic adenocarcinoma and autoimmune forms of chronic pancreatitis. There is data (albeit not fully consistent) indicating modestly increased pancreatic cancer risk in H. pylori-positive patients. The pathogenetic mechanism of this increase is not yet fully elucidated, but several theories have been proposed. Reduction of antral D-cells in H. pylori-positive patients causes a suppression of somatostatin secretion that, in turn, stimulates increased secretin secretion. That stimulates pancreatic growth and thus increases the risk of carcinogenesis. Alternatively, H. pylori, as a part of microbiome dysbiosis and the so-called oncobiome, is proven to be associated with pancreatic adenocarcinoma development via the promotion of cellular proliferation. The role of H. pylori in the inflammation characteristic of autoimmune pancreatitis seems to be explained by a mechanism of molecular mimicry among several proteins (mostly enzymes) of H. pylori and pancreatic tissue. Patients with autoimmune pancreatitis often show positivity for antibodies against H. pylori proteins. H. pylori, as a part of microbiome dysbiosis, also is viewed as a potential trigger of autoimmune inflammation of the pancreas. It is precisely these relationships (and associated equivocal conclusions) that constitute a center of attention among pancreatologists, immunologists and pathologists. In order to obtain clear and valid results, more studies on sufficiently large cohorts of patients are needed. The topic is itself sufficiently significant to draw the interest of clinicians and inspire further systematic research. Next-generation sequencing could play an important role in investigating the microbiome as a potential diagnostic and prognostic biomarker for pancreatic cancer.
C1 [Kunovsky, Lumir; Kala, Zdenek] Masaryk Univ, Univ Hosp Brno, Dept Surg, Brno 62500, Czech Republic.
   [Kunovsky, Lumir; Dite, Petr; Jabandziev, Petr; Dolina, Jiri; Vaculova, Jitka; Kala, Zdenek; Trna, Jan] Masaryk Univ, Fac Med, Brno 62500, Czech Republic.
   [Kunovsky, Lumir; Dite, Petr; Dolina, Jiri; Vaculova, Jitka; Trna, Jan] Masaryk Univ, Dept Gastroenterol & Internal Med, Univ Hosp Brno, Brno 62500, Czech Republic.
   [Jabandziev, Petr; Blaho, Martin; Bojkova, Martina] Univ Hosp Ostrava, Dept Gastroenterol & Internal Med, Ostrava 70800, Czech Republic.
   [Dite, Petr; Blaho, Martin; Bojkova, Martina; Dvorackova, Jana] Univ Ostrava, Fac Med, Ostrava 70300, Czech Republic.
   [Jabandziev, Petr] Masaryk Univ, Univ Hosp Brno, Dept Pediat, Brno 61300, Czech Republic.
   [Jabandziev, Petr] Masaryk Univ, Cent European Inst Technol, Brno 62500, Czech Republic.
   [Dvorackova, Jana] Univ Hosp Ostrava, Dept Intens Med Emergency Med & Forens Studies, Ostrava 70800, Czech Republic.
   [Uvirova, Magdalena] CGB Lab Ostrava As Ostrava, Ostrava 70300, Czech Republic.
   [Trna, Jan] Masaryk Mem Canc Inst, Dept Gastroenterol & Digest Endoscopy, Zluty Kopec 7, Brno 65653, Czech Republic.
   [Trna, Jan] Hosp Boskovice, Dept Internal Med, Boskovice 68001, Czech Republic.
C3 University Hospital Brno; Masaryk University Brno; Masaryk University
   Brno; University Hospital Brno; Masaryk University Brno; University
   Hospital Ostrava; University of Ostrava; Masaryk University Brno;
   University Hospital Brno; Masaryk University Brno; University Hospital
   Ostrava; Masaryk Memorial Cancer Institute
RP Trna, J (corresponding author), Masaryk Mem Canc Inst, Dept Gastroenterol & Digest Endoscopy, Zluty Kopec 7, Brno 65653, Czech Republic.
EM jan.trna@mou.cz
RI Kunovsky, Lumir/HCI-3910-2022; Blaho, Martin/T-7383-2019
OI Blaho, Martin/0000-0002-5291-9102
FU Ministry of Health of the Czech Republic [NU20-0300126]; Ministry of
   Health of the Czech Republic-conceptual development of research
   organization [65269705, SUp 3/21]
FX Supported by Ministry of Health of the Czech Republic, No. NU20-0300126;
   and Ministry of Health of the Czech Republic-conceptual development of
   research organization, No. FNBr, 65269705, SUp 3/21.
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NR 62
TC 26
Z9 28
U1 1
U2 25
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1948-5204
J9 WORLD J GASTRO ONCOL
JI World J. Gastrointest. Oncol.
PD AUG 15
PY 2021
VL 13
IS 8
BP 835
EP 844
DI 10.4251/wjgo.v13.i8.835
PG 10
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA UJ2BP
UT WOS:000691097800005
PM 34457189
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Dore, MP
   Manca, A
   Pensamiento, MCA
   Delitala, AP
   Fanciulli, G
   Piana, AF
   Pes, GM
AF Dore, Maria Pina
   Manca, Alessandra
   Pensamiento, Maria Carolina Alfonso
   Delitala, Alessandro Palmerio
   Fanciulli, Giuseppe
   Piana, Andrea Fausto
   Pes, Giovanni Mario
TI Male Predominance of Gastric Cancer among Patients with Hypothyroidism
   from a Defined Geographic Area
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Article
DE gastric cancer; hypothyroidism; Helicobacter pylori infection
ID AUTOIMMUNE THYROID-DISEASE; STOMACH-CANCER; GOITER; RISK; MORTALITY;
   IODINE; ADENOCARCINOMA; PREVALENCE
AB In the past, hypothyroidism has been associated with an increased susceptibility to gastric cancer (GC). Although several epidemiological studies have corroborated this association, a precise mechanistic explanation remains elusive. In this study, this hypothesis was tested by using a large database of subjects who underwent upper endoscopy for various reasons. This was a retrospective, case-control, single-center study. Subjects with GC (cases) were compared with subjects without (controls), according to hypothyroidism status. Overall, the prevalence of GC was 0.73% in the total cohort and was significantly higher in males compared to females (1.4% versus 0.4%, p < 0.0001). Multivariate logistic regression analysis confirmed an increased risk in males with hypothyroidism (OR 5.10; p < 0.0001) after adjusting for potential confounders, especially H. pylori infection. Interestingly, only hypothyroidism and not treatment with levothyroxine was a significant predictor of GC, ruling out a possible direct carcinogenic effect of the replacement therapy. The present study suggests a male-restricted association of gastric carcinogenesis with a hypothyroid state. If the results of this study are confirmed by longitudinal studies, an attractive perspective could open up for the better management of males with concomitant hypothyroidism and a higher risk of GC.
C1 [Dore, Maria Pina; Manca, Alessandra; Delitala, Alessandro Palmerio; Fanciulli, Giuseppe; Piana, Andrea Fausto; Pes, Giovanni Mario] Univ Sassari, Dipartimento Sci Med Chirurg & Sperimentali, I-07100 Sassari, Italy.
   [Dore, Maria Pina] Baylor Coll Med, One Baylor Plaza, Houston, TX 77030 USA.
   [Pensamiento, Maria Carolina Alfonso] Univ San Carlos, Fac Ciencias Med, Guatemala City 01012, Guatemala.
   [Fanciulli, Giuseppe] Azienda Osped Univ, Endocrine Unit, I-07100 Sassari, Italy.
   [Pes, Giovanni Mario] Sardinia Longev Blue Zone Observ, I-08040 Ogliastra, Italy.
C3 University of Sassari; Baylor College of Medicine; Universidad de San
   Carlos de Guatemala
RP Dore, MP (corresponding author), Univ Sassari, Dipartimento Sci Med Chirurg & Sperimentali, I-07100 Sassari, Italy.; Dore, MP (corresponding author), Baylor Coll Med, One Baylor Plaza, Houston, TX 77030 USA.
EM mpdore@uniss.it; alessandra.manca@aousassari.it;
   carolinealpen28@gmail.com; aledelitala@tiscali.it; gfanciu@uniss.it;
   piana@uniss.it; gmpes@uniss.it
RI DORE, Maria/AAV-7918-2021; Delitala, Alessandro/L-3194-2016; Pes,
   Giovanni Mario/AAH-3340-2019; Fanciulli, Giuseppe/IAP-0357-2023
OI PIANA, Andrea Fausto/0000-0002-6609-8886; DORE, Maria
   Pina/0000-0001-7305-3531; Pes, Giovanni Mario/0000-0003-3265-2823;
   Fanciulli, Giuseppe/0000-0002-8367-5649
FU Regione Autonoma della Sardegna, Fondo di Sviluppo e Coesione
   [RASSR38231]
FX This research and the APC was funded by Regione Autonoma della Sardegna,
   Fondo di Sviluppo e Coesione 2014/2020, grant number RASSR38231.
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NR 39
TC 3
Z9 3
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD JAN
PY 2020
VL 9
IS 1
AR 135
DI 10.3390/jcm9010135
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA KO2OF
UT WOS:000515388400135
PM 31947827
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Dworzanska, A
   Polz-Dacewicz, M
AF Dworzanska, Anna
   Polz-Dacewicz, Malgorzata
TI The role of Toll-like receptors (TLRs) in virus-related cancers: a mini
   review
SO CURRENT ISSUES IN PHARMACY AND MEDICAL SCIENCES
LA English
DT Review
DE TLR9; EBV; HPV; nasopharyngeal cancer; gastric cancer
ID EPSTEIN-BARR-VIRUS; ONCOGENESIS; CARCINOMA
AB The modulation of the host innate immune system is a well-established carcinogenesis feature of several tumors, including human Epstein-Barr (EBV) and Papillomavirus-(HPV) related cancers. These viruses are able to interrupt the initial events of the immune response, including the expression of Toll-like receptors (TLRs), cytokines, and inflammation. The aim of the study is to review current data and summarize knowledge on the TLRs and their role in the development of cancer, especially viral-related cancers (EBV and HPV). Research work shows a correlation between the TLRs polymorphism and the development of oropharyngeal and gastric cancer (GC), especially related to viral infections. Many studies suggest the important role for TLRs in inflammatory, autoimmune disease and human cancers. However, further efforts are necessary to draw a precise conclusion.
C1 [Dworzanska, Anna] Masovian Specialist Hosp, PL-26617 Radom, Poland.
   [Polz-Dacewicz, Malgorzata] Med Univ Lublin, Dept Virol, PL-20059 Lublin, Poland.
C3 Medical University of Lublin
RP Polz-Dacewicz, M (corresponding author), Med Univ Lublin, Dept Virol, PL-20059 Lublin, Poland.
EM m.polz@umlub.pl
RI Dworzanska, Anna/AAT-6977-2020; Polz-Dacewicz, Malgorzata/ABI-3021-2020
OI Polz-Dacewicz, Malgorzata/0000-0002-3222-184X
FU Medical University of Lublin, Poland [DS 233]
FX This study was supported by a Research Grant from the Medical University
   of Lublin, Poland (DS 233).
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NR 20
TC 1
Z9 1
U1 0
U2 0
PU SCIENDO
PI WARSAW
PA BOGUMILA ZUGA 32A, WARSAW, MAZOVIA, POLAND
SN 2084-980X
EI 2300-6676
J9 CURR ISS PHARM MED S
JI Curr. Iss. Pharm. Med. Sci.
PD DEC
PY 2020
VL 33
IS 4
BP 225
EP 227
DI 10.2478/cipms-2020-0038
PG 3
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA QR5TM
UT WOS:000625279600008
OA gold
DA 2025-06-01
ER

PT J
AU Kim, B
   Kim, KM
AF Kim, Binnari
   Kim, Kyoung-Mee
TI Role of Exosomes and Their Potential as Biomarkers in Epstein-Barr
   Virus-Associated Gastric Cancer
SO CANCERS
LA English
DT Review
DE exosome; EBV; gastric cancer; biomarker; immunotherapy
ID NUCLEAR ANTIGEN 1; EPITHELIAL-CELLS; CARCINOMA-CELLS; NASOPHARYNGEAL
   CARCINOMA; NONCODING RNAS; LATENT INFECTION; TUMOR-SUPPRESSOR;
   DOWN-REGULATION; PROTEIN; MICRORNAS
AB Simple Summary Exosomes are considered to be involved in the pathogenesis of various diseases, including cancer, viral infections, and autoimmune diseases. Research on exosomes is critical, since understanding the pathogenesis of diseases is crucial for their diagnosis and treatment. Epstein-Barr virus (EBV)-infected cells have been found to secrete exosomes for intercellular communication. Exosomal pathways play vital roles in the pathogenesis of EBV-related malignancies. This review aims to summarize the role of exosomes in EBV-associated gastric cancer and to serve as a basis for future diagnostic and therapeutic development. Exosomes are a subtype of extracellular vesicles ranging from 30 to 150 nm and comprising many cellular components, including DNA, RNA, proteins, and metabolites, encapsulated in a lipid bilayer. Exosomes are secreted by many cell types and play important roles in intercellular communication in cancer. Viruses can hijack the exosomal pathway to regulate viral propagation, cellular immunity, and the microenvironment. Cells infected with Epstein-Barr virus (EBV), one of the most common oncogenic viruses, have also been found to actively secrete exosomes, and studies on their roles in EBV-related malignancies are ongoing. In this review, we focus on the role of exosomes in EBV-associated gastric cancer and their clinical applicability in diagnosis and treatment.
C1 [Kim, Binnari] Ulsan Univ Hosp, Univ Ulsan Coll Med, Dept Pathol, Ulsan 44610, South Korea.
   [Kim, Kyoung-Mee] Sungkyunkwan Univ Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul 06351, South Korea.
   [Kim, Kyoung-Mee] Ctr Compan Diagnost, Samsung Med Ctr, Seoul 06351, South Korea.
C3 University of Ulsan; Ulsan University Hospital; Sungkyunkwan University
   (SKKU); Samsung Medical Center; Sungkyunkwan University (SKKU); Samsung
   Medical Center
RP Kim, KM (corresponding author), Sungkyunkwan Univ Sch Med, Samsung Med Ctr, Dept Pathol & Translat Genom, Seoul 06351, South Korea.; Kim, KM (corresponding author), Ctr Compan Diagnost, Samsung Med Ctr, Seoul 06351, South Korea.
EM kkmkys@skku.edu
OI Kim, Binnari/0000-0002-0934-3056; Kim, Kyoung Mee/0000-0002-1162-9205
FU Korea Health Technology R&D Project via the Korea Health Industry
   Development Institute - Ministry of Health and Welfare, Republic of
   Korea [HR20C0025, HI21C1137]
FX This work was supported by a grant from the Korea Health Technology R&D
   Project via the Korea Health Industry Development Institute, funded by
   the Ministry of Health and Welfare, Republic of Korea (grant numbers:
   HR20C0025 and HI21C1137).
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NR 138
TC 6
Z9 9
U1 2
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2023
VL 15
IS 2
AR 469
DI 10.3390/cancers15020469
PG 15
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 7Y0ZL
UT WOS:000914618400001
PM 36672418
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Xue, LJ
   Su, QS
   Yang, JH
   Lin, Y
AF Xue, Li-Jun
   Su, Quan-Sheng
   Yang, Ji-Hong
   Lin, Yong
TI Autoimmune responses induced by Helicobacter pylori improve the
   prognosis of gastric carcinoma
SO MEDICAL HYPOTHESES
LA English
DT Article
ID MICROSATELLITE INSTABILITY; ANTI-CAGA; PATHOGENESIS; INFECTION;
   ACTIVATION; METAPLASIA; ANTIBODIES; DISEASES; MIMICRY; PROTEIN
AB Gastric carcinoma (GC) remains one of most serious malignant tumors worldwide, with Helicobacter pylori being the definite carcinogen. The H. pylori components, cytotoxin-associated gene A (CagA), vacuolating toxin A (VacA) and blood-group antigen-binding adhesin gene (BabA), can mimic and bind to specific receptors or surface molecules both on gastric epithelial cells and platelets, in which CagA and VacA may also be directly involved in loosening of tight junctions in monolayers; of polarized gastric epithelial cells. It has been shown that a history of H. pylori infection is found in the majority of patients with GC, and that anti-CagA, anti-VacA and anti-BabA antibodies targeting both H. pylori components and host mimic molecules can be detected in them with increased levels.
   Patients with GC who are positive for H. pylori prospectively have a better outlook than those negative. The stimulation of mentioned autoantibodies in antigen processing and presentation and subsequent T-cell activation and proliferation improves host immune status. On the other hand, in an autoimmune response, autoantibodies can induce the cross-reaction against those localized or circulating GC cells, which are characterized by mimic or absorbed H. pylori antigens, and. lead to the killing and even suppressing of metastasis of cancer cells. Therefore, we here hypothesize that autoimmune responses induced by H. pylori components may play a key role in improving the prognosis of patients with gastric carcinoma. (C) 2007 Published by Elsevier Ltd.
C1 [Xue, Li-Jun; Su, Quan-Sheng; Yang, Ji-Hong; Lin, Yong] Jinling Hosp, Dept Oncol, Nanjing 210002, Peoples R China.
RP Xue, LJ (corresponding author), Jinling Hosp, Dept Oncol, Nanjing 210002, Peoples R China.
EM xljhy2001@hotmail.com
RI Xue, Li-Jun/AFE-7346-2022
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NR 38
TC 27
Z9 30
U1 0
U2 1
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PY 2008
VL 70
IS 2
BP 273
EP 276
DI 10.1016/j.mehy.2007.05.045
PG 4
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 258WT
UT WOS:000252901500013
PM 17681432
DA 2025-06-01
ER

PT J
AU Noh, SJ
   Park, SY
   Kim, KR
   Kim, CY
   Kwon, KS
   Park, HS
   Lee, H
   Chung, MJ
   Moon, WS
   Jang, KY
AF Noh, Sang Jae
   Park, Shin Young
   Kim, Kyung Ryoul
   Kim, Chan Young
   Kwon, Keun Sang
   Park, Ho Sung
   Lee, Ho
   Chung, Myoung Ja
   Moon, Woo Sung
   Jang, Kyu Yun
TI The Prognostic Significance of the Tumor-Infiltrating FoxP3-Positive
   Regulatory T Cells in Gastric Carcinoma
SO KOREAN JOURNAL OF PATHOLOGY
LA English
DT Article
DE T-lymphocytes, regulatory; FoxP3 protein, human; Stomach neoplasms
ID TRANSCRIPTION FACTOR FOXP3; CANCER-PATIENTS; ESOPHAGEAL CANCERS;
   PERIPHERAL-BLOOD; DENDRITIC CELLS; LYMPH-NODES; IN-VITRO; EXPRESSION;
   ANGIOGENESIS; LYMPHOCYTES
AB Background : Regulatory T cells (Tregs) are known to be key regulators of immune responses in patients with autoimmune disease and infection and also for attenuating antitumor immunity by the host. It has been reported that high numbers of tumor-infiltrating Tregs might be associated with poor clinical outcomes for several malignant tumors. Therefore, this study aimed to examine the impact of tumor-infiltrating Tregs on the prognosis of gastric carcinoma patients. Methods : The immunohistochemical staining for anti-fork head Box P3 (FoxP3) antibody was performed by using a 3 mm core from the tumor specimens of each of the 173 gastric cancer patients for constructing a tissue microarray. FoxP3-positive Tregs were quantified by calculating the numbers of positive cells per 5 high-power fields on light microscopy. Thereafter, the 173 patients were subdivided into the low Tregs group (<= 3/5 high power fields [HPF], n = 41) and the high Tregs group (>3/5 HPF, n = 132). Results : The high Tregs group was significantly associated with a higher stage, more invasion depth and lymph node metastasis (p = 0.009, p = 0.036, p = 0.006, respectively). The high Tregs group showed significantly poorer overall survival and event-free survival (p = 0.004, p = 0.017, respectively) on the univariate analysis. The Tregs group and the tumor, node and metastasis stage were also independent prognostic factors that were significantly associated with overall survival (p = 0.025, p < 0.001, respectively) by multivariate analysis. Conclusions : Our results indicated that a high number of tumor-infiltrating FoxP3-positive Tregs could be an indicator of poor long term survival for gastric carcinoma patients.
C1 [Noh, Sang Jae; Park, Shin Young; Park, Ho Sung; Chung, Myoung Ja; Moon, Woo Sung; Jang, Kyu Yun] Chonbuk Natl Univ, Dept Pathol, Sch Med, Res Inst Clin Med, Jeonju 561180, South Korea.
   [Noh, Sang Jae; Park, Shin Young; Park, Ho Sung; Lee, Ho; Chung, Myoung Ja; Moon, Woo Sung; Jang, Kyu Yun] Chonbuk Natl Univ, Inst Med Sci, Sch Med, Jeonju 561180, South Korea.
   [Kim, Kyung Ryoul] Natl Inst Sci Invest, Dept Forens Med, Seoul, South Korea.
   [Kim, Chan Young] Chonbuk Natl Univ, Dept Surg, Sch Med, Jeonju 561180, South Korea.
   [Kwon, Keun Sang] Chonbuk Natl Univ, Dept Prevent Med, Sch Med, Jeonju 561180, South Korea.
   [Lee, Ho] Chonbuk Natl Univ, Dept Forens Med, Res Inst Clin Med, Sch Med, Jeonju 561180, South Korea.
C3 Jeonbuk National University; Jeonbuk National University; Jeonbuk
   National University; Jeonbuk National University; Jeonbuk National
   University
RP Jang, KY (corresponding author), Chonbuk Natl Univ, Dept Pathol, Sch Med, Res Inst Clin Med, San 2-20 Geumam Dong, Jeonju 561180, South Korea.
EM kyjang@chonbuk.ac.kr
RI NOH, SANG/R-4395-2019
OI Noh, Sang Jae/0000-0002-7005-056X
FU Ministry of Science & Technology/Korea Science & engineering Foundation
   through the Diabetes Research Center of Chonbuk National University
   [R13-2008-005-0000-0]
FX This study was supported by a grant of the Ministry of Science &
   Technology/Korea Science & engineering Foundation through the Diabetes
   Research Center of Chonbuk National University (R13-2008-005-0000-0).
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TC 3
Z9 3
U1 0
U2 5
PU KOREAN SOCIETY PATHOLOGISTS
PI SEOUL
PA ROOM 702 KOREAN MED ASSOC BLDG, 302-75 ICHON, 1 DONG, YOUNGSAN-GU,
   SEOUL, 140-721, SOUTH KOREA
SN 1738-1843
J9 KOREAN J PATHOL
JI Korean J. Pathol.
PY 2010
VL 44
IS 1
BP 9
EP 15
DI 10.4132/KoreanJPathol.2010.44.1.9
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 570EK
UT WOS:000275654500002
OA Bronze
DA 2025-06-01
ER

PT J
AU De Block, CEM
   De Leeuw, IH
   Van Gaal, LF
AF De Block, Christophe E. M.
   De Leeuw, Ivo H.
   Van Gaal, Luc F.
TI Autoimmune gastritis in type 1 diabetes: A clinically oriented review
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Review
ID PARIETAL-CELL ANTIBODIES; HELICOBACTER-PYLORI INFECTION; ATROPHIC BODY
   GASTRITIS; INTRINSIC-FACTOR ANTIBODY; IRON-DEFICIENCY ANEMIA; SERUM
   PEPSINOGEN-I; PERNICIOUS-ANEMIA; FOLLOW-UP; H+,K+-ADENOSINE
   TRIPHOSPHATASE; CARCINOID-TUMORS
AB Context: Autoimmune gastritis and pernicious anemia are common autoimmune disorders, being present in up to 2% of the general population. In patients with type 1 diabetes or autoimmune thyroid disease, the prevalence is 3- to 5-fold increased. This review addresses the epidemiology, pathogenesis, diagnosis, clinical consequences, and management of autoimmune gastritis in type 1 diabetic patients.
   Synthesis: Autoimmune gastritis is characterized by: 1) atrophy of the corpus and fundus; 2) autoantibodies to the parietal cell and to intrinsic factor; 3) achlorhydria; 4) iron deficiency anemia; 5) hypergastrinemia; 6) pernicious anemia may result from vitamin B12 deficiency; and 7) in up to 10% of patients, autoimmune gastritis may predispose to gastric carcinoid tumors or adenocarcinomas. This provides a strong rationale for screening, early diagnosis, and treatment. The management of patients with autoimmune gastritis implies yearly determination of gastrin, iron, vitamin B12 levels, and a complete blood count. iron or vitamin B12 should be supplemented in patients with iron deficiency or pernicious anemia. Whether regular gastroscopic surveillance, including biopsies, is needed in patients with autoimmune gastritis/pernicious anemia is controversial. The gastric carcinoids that occur in these patients generally do not pose a great threat to life, whereas the danger of developing carcinoma is controversial. Nevertheless, awaiting a consensus statement, we suggest performing gastroscopy and biopsy at least once in patients with autoantibodies to the parietal cell, iron, or vitamin B12-deficiency anemia, or high gastrin levels.
   Conclusion: The high prevalence of autoimmune gastritis in type 1 diabetic patients and its possible adverse impact on the health of the patient provide a strong rationale for screening, early diagnosis, periodic surveillance by gastroscopy, and treatment.
C1 [De Block, Christophe E. M.; De Leeuw, Ivo H.; Van Gaal, Luc F.] Univ Antwerp Hosp, Dept Diabet Endocrinol, B-2650 Edegem, Belgium.
   [De Block, Christophe E. M.; De Leeuw, Ivo H.; Van Gaal, Luc F.] Univ Antwerp, B-2650 Edegem, Belgium.
C3 University of Antwerp; University of Antwerp
RP De Block, CEM (corresponding author), Univ Antwerp Hosp, Dept Diabet Endocrinol, Wilrijkstr 10, B-2650 Edegem, Belgium.
EM christophe.deblock@ua.ac.be
RI De+Block, Christophe/ABE-1600-2020
OI De Block, Christophe/0000-0002-0679-3203
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NR 106
TC 137
Z9 141
U1 0
U2 6
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD FEB
PY 2008
VL 93
IS 2
BP 363
EP 371
DI 10.1210/jc.2007-2134
PG 9
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 262RN
UT WOS:000253165800006
PM 18029461
DA 2025-06-01
ER

PT J
AU Dilaghi, E
   Esposito, G
   Ligato, I
   Del Forno, A
   Rossi, RE
   Hassan, C
   Annibale, B
   Zullo, A
AF Dilaghi, Emanuele
   Esposito, Gianluca
   Ligato, Irene
   Del Forno, Alessandro
   Rossi, Roberta Elisa
   Hassan, Cesare
   Annibale, Bruno
   Zullo, Angelo
TI Real-Time Gastric Juice Analysis to Rule Out the Presence of Autoimmune
   Gastritis: A Case-Control Study
SO GE PORTUGUESE JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune gastritis; Gastric juice analysis; pH value; Precancerous
   lesions
ID ATROPHIC GASTRITIS; CLASSIFICATION
AB Background: Autoimmune gastritis (AIG) is an infrequent disease predisposing to both neuroendocrine tumours and cancer. This study aimed to evaluate whether pH measurement of gastric juice allows accurate exclusion of the presence of AIG in real time so that gastric mucosa sampling on normal-appearing mucosa may be avoided. Methods: This study enrolled patients diagnosed with AIG and matched controls (ratio 1:5) who underwent upper endoscopy with standard gastric mucosa sampling and real-time, gastric juice pH assessment. A threshold of pH less than 4.5 was adopted as cut-off to rule out the presence of a feature of AIG. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), overall accuracy, positive likelihood ratio (LR+), and negative likelihood ratio (LR-) were calculated. Results: Data of 40 patients (M/F: 19/21; mean age: 58 years, range: 18-89) with AIG and 212 matched controls were evaluated. Among AIG patients, the feature of atrophy/metaplasia of the oxyntic mucosa was staged as mild in 9 cases, moderate in 9, and severe in the remaining 22 patients. Gastric juice analysis showed a pH value >4.5 in 29 (72.5%) patients and 12 (5.7%) controls. Sensitivity, specificity, accuracy, PPV, NPV, LR+, and LR- were 73% (95% CI = 0.57-0.84), 94% (95% CI = 0.90-0.97), 71% (95% CI = 0.64-0.74), 95% (95% CI = 0.93-0.97), 91% (95% CI = 0.87-0.95), 12.9 (95% CI = 7.19-23.03), and 0.29 (95% CI = 0.18-0.48), respectively. The histological assessment of false-negative cases showed the presence of only mild-moderate atrophy of oxyntic mucosa in 6 (54.5%) cases, and severe in the others. Conclusions: Our data found that real-time pH evaluation of gastric juice allows ruling out AIG with a very high NPV, but further studies are needed.
C1 [Dilaghi, Emanuele; Esposito, Gianluca; Ligato, Irene; Annibale, Bruno] Sapienza Univ Rome, St Andrea Hosp, Dept Med & Surg Sci & Translat Med, Rome, Italy.
   [Del Forno, Alessandro; Zullo, Angelo] Nuovo Regina Margher Hosp, Gastroenterol & Digest Endoscopy, Rome, Italy.
   [Rossi, Roberta Elisa] IRCCS Humanities Res Hosp, Gastroenterol & Endoscopy Unit, Milan, Italy.
   [Hassan, Cesare] Humanitas Univ, Dept Biomed Sci, Pieve Emanuele, Italy.
   [Hassan, Cesare] Humanitas Clin & Res Ctr IRCCS, Endoscopy Unit, Rozzano, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea;
   Poliambulatorio Nuovo Regina Margherita; Humanitas University
RP Zullo, A (corresponding author), Nuovo Regina Margher Hosp, Gastroenterol & Digest Endoscopy, Rome, Italy.
EM angelozullo66@yahoo.it
RI Esposito, Gianluca/J-7200-2019; Annibale, Bruno/A-5372-2008; Zullo,
   Angelo/AAV-7092-2020; Rossi, Roberta Elisa/LFS-1897-2024; hassan,
   cesare/H-2844-2012
OI hassan, cesare/0000-0001-7167-1459
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NR 28
TC 2
Z9 2
U1 3
U2 3
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 2341-4545
EI 2387-1954
J9 GE PORT J GASTROENT
JI GE Port. J. Gastroenterol.
PD FEB
PY 2025
VL 32
IS 1
BP 37
EP 42
DI 10.1159/000540117
EA AUG 2024
PG 6
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA 0HR6N
UT WOS:001296132600001
PM 39906511
OA gold
DA 2025-06-01
ER

PT J
AU Noto, CN
   Hoft, SG
   DiPaolo, RJ
AF Noto, Christine N.
   Hoft, Stella G.
   DiPaolo, Richard J.
TI Mast Cells as Important Regulators in Autoimmunity and Cancer
   Development
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE mast cell; autoimmunity; cancer; rheumatoid arthritis; multiple
   sclerosis; type 1 diabetes
ID NECROSIS-FACTOR-ALPHA; INFLAMMATORY-BOWEL-DISEASE; EXPERIMENTAL ALLERGIC
   ENCEPHALOMYELITIS; TO-MESENCHYMAL TRANSITION; TYPE-1 DIABETES-MELLITUS;
   MULTIPLE-SCLEROSIS; RHEUMATOID-ARTHRITIS; PROTUMORIGENIC ROLE;
   COLORECTAL-CANCER; HISTAMINE-RELEASE
AB Mast cells are an essential part of the immune system and are best known as important modulators of allergic and anaphylactic immune responses. Upon activation, mast cells release a multitude of inflammatory mediators with various effector functions that can be both protective and damage-inducing. Mast cells can have an anti-inflammatory or pro-inflammatory immunological effect and play important roles in regulating autoimmune diseases including rheumatoid arthritis, type 1 diabetes, and multiple sclerosis. Importantly, chronic inflammation and autoimmunity are linked to the development of specific cancers including pancreatic cancer, prostate cancer, colorectal cancer, and gastric cancer. Inflammatory mediators released from activated mast cells regulate immune responses and promote vascular permeability and the recruitment of immune cells to the site of inflammation. Mast cells are present in increased numbers in tissues affected by autoimmune diseases as well as in tumor microenvironments where they co-localize with T regulatory cells and T effector cells. Mast cells can regulate immune responses by expressing immune checkpoint molecules on their surface, releasing anti-inflammatory cytokines, and promoting vascularization of solid tumor sites. As a result of these immune modulating activities, mast cells have disease-modifying roles in specific autoimmune diseases and cancers. Therefore, determining how to regulate the activities of mast cells in different inflammatory and tumor microenvironments may be critical to discovering potential therapeutic targets to treat autoimmune diseases and cancer.</p>
C1 [Noto, Christine N.; Hoft, Stella G.; DiPaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63103 USA.
C3 Saint Louis University
RP Noto, CN; DiPaolo, RJ (corresponding author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, St Louis, MO 63103 USA.
EM christine.noto@slu.edu; Richard.Dipaolo@health.slu.edu
OI Noto, Christine/0000-0002-4445-6793; DiPaolo,
   Richard/0000-0002-2191-6689
FU American Cancer Society [RSG-12-171-01-LIB]; National Institutes of
   Health/National Institute of Diabetes and Digestive and Kidney Diseases
   [R01 DK110406]; Digestive Diseases Research Core Center of the
   Washington University School of Medicine National Institute of Diabetes
   and Digestive and Kidney Diseases [P30DK52574]; American
   Gastroenterological Association Funderburg Research Award
FX Funding This work was supported by the American Cancer Society (Grant
   RSG-12-171-01-LIB), the National Institutes of Health/National Institute
   of Diabetes and Digestive and Kidney Diseases (Grant R01 DK110406), the
   Digestive Diseases Research Core Center of the Washington University
   School of Medicine National Institute of Diabetes and Digestive and
   Kidney Diseases (Grant P30DK52574), and the American Gastroenterological
   Association Funderburg Research Award (RD).
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NR 166
TC 27
Z9 27
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD OCT 12
PY 2021
VL 9
AR 752350
DI 10.3389/fcell.2021.752350
PG 13
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA WP9IA
UT WOS:000713437300001
PM 34712668
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Dawson, RE
   Deswaerte, V
   West, AC
   Tang, K
   West, AJ
   Balic, JJ
   Gearing, LJ
   Saad, M
   Yu, L
   Wu, YH
   Bhathal, PS
   Kumar, B
   Chakrabarti, JT
   Zavros, Y
   Oshima, H
   Klinman, DM
   Oshima, M
   Tan, P
   Jenkins, BJ
AF Dawson, Ruby E.
   Deswaerte, Virginie
   West, Alison C.
   Tang, Ke
   West, Alice J.
   Balic, Jesse J.
   Gearing, Linden J.
   Saad, Mohamed, I
   Yu, Liang
   Wu, Yonghui
   Bhathal, Prithi S.
   Kumar, Beena
   Chakrabarti, Jayati T.
   Zavros, Yana
   Oshima, Hiroko
   Klinman, Dennis M.
   Oshima, Masanobu
   Tan, Patrick
   Jenkins, Brendan J.
TI STAT3-mediated upregulation of the AIM2 DNA sensor links innate immunity
   with cell migration to promote epithelial tumourigenesis
SO GUT
LA English
DT Article
DE cytokines; gastric cancer; cell migration; immunology; molecular biology
ID TOLL-LIKE RECEPTORS; PATTERN-RECOGNITION RECEPTORS; INTESTINAL
   HOMEOSTASIS; GASTRIC TUMORIGENESIS; INFLAMMASOME; CANCER; TUMOR; EB1;
   ACTIVATION; IDENTIFICATION
AB Objective The absent in melanoma 2 (AIM2) cytosolic pattern recognition receptor and DNA sensor promotes the pathogenesis of autoimmune and chronic inflammatory diseases via caspase-1-containing inflammasome complexes. However, the role of AIM2 in cancer is ill-defined. Design The expression of AIM2 and its clinical significance was assessed in human gastric cancer (GC) patient cohorts. Genetic or therapeutic manipulation of AIM2 expression and activity was performed in the genetically engineered gp130 (F/F) spontaneous GC mouse model, as well as human GC cell line xenografts. The biological role and mechanism of action of AIM2 in gastric tumourigenesis, including its involvement in inflammasome activity and functional interaction with microtubule-associated end-binding protein 1 (EB1), was determined in vitro and in vivo. Results AIM2 expression is upregulated by interleukin-11 cytokine-mediated activation of the oncogenic latent transcription factor STAT3 in the tumour epithelium of GC mouse models and patients with GC. Genetic and therapeutic targeting of AIM2 in gp130 (F/F) mice suppressed tumourigenesis. Conversely, AIM2 overexpression augmented the tumour load of human GC cell line xenografts. The protumourigenic function of AIM2 was independent of inflammasome activity and inflammation. Rather, in vivo and in vitro AIM2 physically interacted with EB1 to promote epithelial cell migration and tumourigenesis. Furthermore, upregulated expression of AIM2 and EB1 in the tumour epithelium of patients with GC was independently associated with poor patient survival. Conclusion AIM2 can play a driver role in epithelial carcinogenesis by linking cytokine-STAT3 signalling, innate immunity and epithelial cell migration, independent of inflammasome activation.
C1 [Dawson, Ruby E.; Deswaerte, Virginie; West, Alison C.; Tang, Ke; West, Alice J.; Balic, Jesse J.; Gearing, Linden J.; Saad, Mohamed, I; Yu, Liang; Jenkins, Brendan J.] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic 3168, Australia.
   [Dawson, Ruby E.; Deswaerte, Virginie; West, Alison C.; Tang, Ke; West, Alice J.; Balic, Jesse J.; Gearing, Linden J.; Saad, Mohamed, I; Yu, Liang; Bhathal, Prithi S.; Jenkins, Brendan J.] Monash Univ, Dept Mol & Translat Sci, Fac Med Nursing & Hlth Sci, Clayton, Vic, Australia.
   [Wu, Yonghui] Natl Canc Ctr Singapore, Cellular & Mol Res, Singapore, Singapore.
   [Kumar, Beena] Monash Hlth, Dept Anat Pathol, Clayton, Vic, Australia.
   [Chakrabarti, Jayati T.; Zavros, Yana] Univ Arizona, Coll Med, Dept Cellular & Mol Med, Tucson, AZ USA.
   [Oshima, Hiroko; Oshima, Masanobu] Kanazawa Univ, Canc Res Inst, Div Genet, Kanazawa, Ishikawa, Japan.
   [Klinman, Dennis M.] NCI, Ctr Canc Res, Bethesda, MD USA.
   [Tan, Patrick] Duke NUS Grad Med Sch, Canc & Stem Cell Biol, Singapore, Singapore.
   [Tan, Patrick] Genome Inst Singapore, Singapore, Singapore.
   [Tan, Patrick] Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore.
C3 Hudson Institute of Medical Research; Monash University; National Cancer
   Centre Singapore (NCCS); Monash Health; University of Arizona; Kanazawa
   University; National Institutes of Health (NIH) - USA; NIH National
   Cancer Institute (NCI); National University of Singapore; Agency for
   Science Technology & Research (A*STAR); A*STAR - Genome Institute of
   Singapore (GIS); National University of Singapore
RP Jenkins, BJ (corresponding author), Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic 3168, Australia.; Jenkins, BJ (corresponding author), Monash Univ, Dept Mol & Translat Sci, Fac Med Nursing & Hlth Sci, Clayton, Vic, Australia.
EM brendan.jenkins@hudson.org.au
RI Oshima, Masanobu/F-9958-2014; jenkins, brendan/J-7854-2012; Saad,
   Mohamed/AAE-8887-2019
OI West, Alice/0000-0001-5701-4874; Gearing, Linden/0000-0003-3508-3056;
   Saad, Mohamed I./0000-0002-4855-2360; Dawson, Ruby/0000-0001-9797-7800
FU National Health and Medical Research Council (NHMRC) of Australia;
   Operational Infrastructure Support Program by the Victorian Government
   of Australia; Australian Postgraduate Awards from the Australian
   Government; NHMRC Early Career Fellowship; NHMRC Senior Medical Research
   Fellowship
FX This work was funded by the National Health and Medical Research Council
   (NHMRC) of Australia (BJ), and the Operational Infrastructure Support
   Program by the Victorian Government of Australia. JB and AJW were
   supported by Australian Postgraduate Awards from the Australian
   Government, and ACW was supported by an NHMRC Early Career Fellowship.
   BJ was supported by an NHMRC Senior Medical Research Fellowship.
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NR 54
TC 30
Z9 32
U1 4
U2 22
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD AUG
PY 2022
VL 71
IS 8
DI 10.1136/gutjnl-2020-323916
EA SEP 2021
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 3G2NO
UT WOS:000724322400001
PM 34489308
DA 2025-06-01
ER

PT J
AU Clouston, AD
AF Clouston, AD
TI Timely topic: Premalignant lesions associated with adenocarcinoma of the
   upper gastrointestinal tract
SO PATHOLOGY
LA English
DT Article
DE Barrett's oesophagus; Barrett's esophagus; intestinal metaplasia;
   dysplasia; adenocarcinoma
ID GASTROESOPHAGEAL REFLUX DISEASE; SEGMENT BARRETTS-ESOPHAGUS; INTESTINAL
   METAPLASIA; HELICOBACTER-PYLORI; GASTRIC-CANCER; ESOPHAGOGASTRIC
   JUNCTION; COLUMNAR CELLS; FOLLOW-UP; DYSPLASIA; PREVALENCE
AB The changing incidence of adenocarcinomas, particularly in the oesophagus and gastric cardia, has led to the rapid expansion of screening programmes aimed at detecting the precursor lesion of dysplasia before adenocarcinoma develops. The pathologist now has an important role in first diagnosing patients at risk for developing dysplasia, and then correctly classifying dysplasia when it occurs. Barrett's oesophagus has had different diagnostic criteria in previous years but is currently diagnosed by the presence of intestinal metaplasia of any length in the true oesophagus. Intestinal metaplasia confined only to the gastro-oesophageal junction or cardia is of uncertain significance but is probably common, with less risk of progressing to dysplasia or malignancy. In the stomach, patients with autoimmune atrophic gastritis and Helicobacter-associated multifocal atrophic gastritis have an increased risk of adenocarcinoma, but screening protocols are not well-developed compared with those used for Barrett's oesophagus. Dysplasia of glandular epithelium can be classified using well-described criteria. Low grade dysplasia is the most common type and regresses or remains stable in the majority of patients. High grade dysplasia is more ominous clinically, with a propensity to coexist with or progress to adenocarcinoma.
C1 Univ Queensland, Mayne Med Sch, Dept Pathol, Herston, Qld 4006, Australia.
C3 University of Queensland
RP Clouston, AD (corresponding author), Univ Queensland, Mayne Med Sch, Dept Pathol, Herston Rd, Herston, Qld 4006, Australia.
RI Clouston, Andrew/E-7199-2011
OI Clouston, Andrew/0000-0002-9601-7952
CR [Anonymous], WHO CLASSIFICATION T
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NR 48
TC 17
Z9 21
U1 0
U2 2
PU CARFAX PUBLISHING
PI BASINGSTOKE
PA RANKINE RD, BASINGSTOKE RG24 8PR, HANTS, ENGLAND
SN 0031-3025
J9 PATHOLOGY
JI Pathology
PD AUG
PY 2001
VL 33
IS 3
BP 271
EP 277
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 465BX
UT WOS:000170569500002
PM 11523923
DA 2025-06-01
ER

PT J
AU Anderson, WF
   Rabkin, CS
   Turner, N
   Fraumeni, JF 
   Rosenberg, PS
   Camargo, MC
AF Anderson, William F.
   Rabkin, Charles S.
   Turner, Natalie
   Fraumeni, Joseph F., Jr.
   Rosenberg, Philip S.
   Camargo, M. Constanza
TI The Changing Face of Noncardia Gastric Cancer Incidence Among US
   Non-Hispanic Whites
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID HELICOBACTER-PYLORI; ATROPHIC GASTRITIS; AUTOIMMUNE; TRENDS; SEX;
   PREVALENCE; SUBSITE; STOMACH; SMOKING; DISEASE
AB Background: The initial step for noncardia gastric carcinogenesis is atrophic gastritis, driven by either Helicobacter pylori infection or autoimmunity. In recent decades, the prevalence rates of these two major causes declined and increased, respectively, with changes in Western lifestyles. We therefore assessed gastric cancer incidence trends for US race/ethnic groups, 1995-2013.
   Methods: Age-standardized rates (ASRs) from 45 North American Association of Central Cancer Tumor Registries were summarized by estimated annual percentage change (EAPC) and 95% confidence intervals (CIs). Age period cohort models supplemented standard descriptive techniques and projected future trends.
   Results: There were 137947 noncardia cancers in 4.4 billion person-years of observation. Among non-Hispanic whites, the ASR was 2.2 per 100 000 person-years, with an EAPC of -2.3% (95% CI = -2.0% to -2.6%). Notwithstanding this overall decline, EAPCs rose 1.3% (95% CI = 0.6% to 2.1%) for persons younger than age 50 years and fell -2.6% (95% CI = -2.4% to -2.9%) for older individuals. These converging trends manifested a birth cohort effect more pronounced among women than men, with incidence among women born in 1983 twofold (95% CI = 1.1-fold to 3.6-fold) greater than those born in 1951. Age interaction was also statistically significant among Hispanic whites, with slightly increasing vs decreasing EAPCs for younger and older individuals, respectively. Incidence declined regardless of age for other races. Current trends foreshadow expected reversals in both falling incidence and male predominance among non-Hispanic whites.
   Conclusions: Dysbiosis of the gastric microbiome associated with modem living conditions may be increasing risk of autoimmune gastritis and consequent noncardia cancer. The changing face by age and sex of gastric cancer warrants analytical studies to identify potential causal mechanisms.
C1 [Anderson, William F.; Rabkin, Charles S.; Turner, Natalie; Fraumeni, Joseph F., Jr.; Rosenberg, Philip S.; Camargo, M. Constanza] NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E-338, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); NIH National Cancer Institute- Division of Cancer Epidemiology &
   Genetics
RP Camargo, MC (corresponding author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 6E-338, Bethesda, MD 20892 USA.
EM camargomc@mail.nih.gov
RI Camargo, M. Constanza/R-9891-2016
OI Turner, Natalie/0000-0002-0351-458X; Rosenberg,
   Philip/0000-0001-6349-9126
FU Intramural Research Program of the National Institutes of Health (NIH),
   National Cancer Institute (NCI); National Cancer Institute [ZIACP010181]
   Funding Source: NIH RePORTER
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health (NIH), National Cancer Institute (NCI).
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NR 44
TC 175
Z9 181
U1 2
U2 20
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD JUN
PY 2018
VL 110
IS 6
BP 608
EP 615
AR djx262
DI 10.1093/jnci/djx262
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GU6AD
UT WOS:000445379100012
PM 29361173
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Song, ZC
   Guo, CJ
   Li, Y
   Tan, BB
   Fan, LQ
   Xiao, JW
AF Song, Zhenchuan
   Guo, Chenjun
   Li, Yong
   Tan, Bibo
   Fan, Liqiao
   Xiao, Jianwei
TI Enhanced antitumor effects of a dendritic cell vaccine transfected with
   gastric cancer cell total RNA carrying the 4-1BBL gene in vitro
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE dendritic cell vaccine; 4-1BB ligand; gene transfection; murine
   forestomach carcinoma cell
ID T-CELLS; IMMUNE-RESPONSES; PROLIFERATION; ANTIGEN
AB T cell-mediated antitumor immunity is a cellular immune response that requires two signals. The dendritic cell (DC) has been considered as the most efficient antigen-presenting cell (APC). It plays essential roles in the induction, regulation and maintenance of antitumor immunity in humans. The 4-1BB/4-1BB ligand (4-1BBL) pathway plays crucial roles in immune response, tumor immunity and autoimmune diseases through transduction of T cell co-stimulatory signals. The aim of this study was to generate the preparation protocol for a DC vaccine transfected with gastric cancer cell total ribonucleic acid (RNA) carrying the 4-1 BBL gene in vitro and to investigate its antitumor effects in murine forestomach carcinoma (MFC). The vaccine was prepared by transfecting MFC total RNAs carrying the 4-1BBL gene into the DCs that were isolated from 615 mouse bones. The T cell proliferation rate in the MFC/4-1BBL/DC group was higher than that in the DC group. The tumor cell kill rate in the MFC/4-1BBL/DC group was higher than that in the DC group. ELISA analysis showed that IL-12 and IFN-gamma in the MFC/4-1BBL/DC group were more highly expressed compared to the other group. Collectively, our data demonstrate that the DC vaccine transfected with gastric cancer cell total RNA carrying the 4-1BBL gene has a stronger ability to kill gastric cancer cells through promoting T cell proliferation and enhancing the ability of cytotoxic T lymphocytes (CTLs) to kill gastric carcinoma cells and to secrete IL-12 and IFN-gamma. Our results provide an effective therapeutic strategy for treating gastric cancer using a DC vaccine.
C1 [Song, Zhenchuan; Guo, Chenjun; Li, Yong; Tan, Bibo; Fan, Liqiao; Xiao, Jianwei] Hebei Med Univ, Hosp 4, Dept Surg, Shijiazhuang 050011, Hebei, Peoples R China.
C3 Hebei Medical University
RP Li, Y (corresponding author), Hebei Med Univ, Hosp 4, Dept Surg, 12 Jiankang Rd, Shijiazhuang 050011, Hebei, Peoples R China.
EM songzhch@yahoo.com.cn
RI 郭, 辰峻/KCL-1080-2024; Song, Zhenchuan/HLG-5036-2023
FU Hebei Natural Sciences Foundation [C2008000966]
FX This study was supported by the Hebei Natural Sciences Foundation (No.
   C2008000966).
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NR 22
TC 8
Z9 9
U1 0
U2 5
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD FEB
PY 2012
VL 3
IS 2
BP 319
EP 323
DI 10.3892/etm.2011.394
PG 5
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 879WP
UT WOS:000299363900028
PM 22969889
OA Bronze, Green Published
DA 2025-06-01
ER

PT J
AU Varricchi, G
   Pecoraro, A
   Crescenzi, L
   Marone, G
   Travaglino, A
   D'Armiento, FP
   Genovese, A
   Spadaro, G
AF Varricchi, Gilda
   Pecoraro, Antonio
   Crescenzi, Ludovica
   Marone, Giancarlo
   Travaglino, Antonio
   D'Armiento, Francesco Paolo
   Genovese, Arturo
   Spadaro, Giuseppe
TI Gastroduodenal Disorders in Patients with CVID Undergoing Immunoglobulin
   Therapy
SO CURRENT PHARMACEUTICAL BIOTECHNOLOGY
LA English
DT Article
DE CVID; duodenitis; gastritis; IELs; Giardia lamblia; Helicobacter pylori;
   immunodeficiency; immunoglobulin therapy
ID COMMON VARIABLE IMMUNODEFICIENCY; ANTIBODY DEFICIENCY; REPLACEMENT
   THERAPY; IMMUNE-DEFICIENCY; DIAGNOSIS; PATHOLOGY; DISEASE; CANCER;
   COHORT; HELICOBACTER
AB Background: Common variable immunodeficiency (CVID) encompasses a heterogeneous group of primary antibody deficiency disorders characterized by recurrent infections, autoimmunity and malignancies. Gastrointestinal manifestations are frequently associated with CVID.
   Objective: In this cross-sectional study, we evaluated gastric and duodenal involvement in a cohort of adult patients with CVID.
   Methods: Upper gastrointestinal endoscopy was performed in 58 patients (26 males, mean age 47.8 +/- 15.6 years), diagnosed with CVID according to 2014 ESID criteria. Random biopsies were collected from gastric antrum and descending duodenum for the all enrolled subjects. Intraepithelial lymphocytosis in descending duodenum was defined as the presence of 25 lymphocytes per 100 enterocytes.
   Results: The major histopathological findings that we found were: a) chronic active gastritis (44.8%), Helicobacter pylori-associated (8.6%), b) chronic duodenitis (39.6%) with intraepithelial lymphocytosis (31%) and absence of plasma cells (18.9%) and c) autoimmune atrophic gastritis (5.2%). Three patients (5.2%) presented Intestinal Metaplasia (IM) of the gastric antrum. This finding was associated with H. pylori infection and persisted after the eradication in one patient. IM was associated with autoimmune atrophic gastritis in two cases. Giardia lamblia infection was observed in the duodenum samples from three patients (5.2%). A diagnosis of Gastric adenocarcinoma was made in a 58-year- old woman diagnosed with gastric dysplasia one year earlier.
   Conclusion: In our cohort of CVID patients, gastro-duodenal histopathological findings, including malignancies, are frequent and can affect long-term prognosis. A rigorous endoscopic follow-up is needed in CVID patients irrespective of the gastrointestinal symptoms.
C1 [Varricchi, Gilda; Pecoraro, Antonio; Crescenzi, Ludovica; Genovese, Arturo; Spadaro, Giuseppe] Dept Translat Med Sci DISMET, Naples, Italy.
   [Varricchi, Gilda; Pecoraro, Antonio; Crescenzi, Ludovica; Genovese, Arturo; Spadaro, Giuseppe] Univ Naples Federico II, Ctr Basic & Clin Immunol Res CISI, Via S Pansini 5, I-80131 Naples, Italy.
   [Varricchi, Gilda; Pecoraro, Antonio; Crescenzi, Ludovica; Genovese, Arturo; Spadaro, Giuseppe] WAO Ctr Excellence, Naples, Italy.
   [Marone, Giancarlo] Univ Naples Federico II, Dept Publ Hlth, Naples, Italy.
   [Marone, Giancarlo] Monaldi Hosp Pharm, Naples, Italy.
   [Travaglino, Antonio; D'Armiento, Francesco Paolo] Univ Naples Federico II, Dept Adv Biomed Sci, Naples, Italy.
C3 University of Naples Federico II; University of Naples Federico II;
   University of Naples Federico II
RP Varricchi, G; Pecoraro, A (corresponding author), Univ Naples Federico II, Ctr Basic & Clin Immunol Res CISI, Via S Pansini 5, I-80131 Naples, Italy.; Varricchi, G; Pecoraro, A (corresponding author), Univ Naples Federico II, Dept Translat Med Sci, Via S Pansini 5, I-80131 Naples, Italy.
EM gilda.varricchi@unina.it; spadaro@unina.it
RI Travaglino, Antonio/M-7877-2019; VARRICCHI, GILDA/A-4620-2014
OI VARRICCHI, GILDA/0000-0002-9285-4657; Travaglino,
   Antonio/0000-0003-4002-1618
FU Regione Campania CISI-Lab; TIMING Project
FX The authors apologize to the authors who have contributed importantly to
   this field and whose work has not been cited due to space and citation
   restrictions. The authors thank Dr. Gjada Criscuolo for critical reading
   of the manuscript. This work was supported in part by Regione Campania
   CISI-Lab and TIMING Project.
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NR 49
TC 9
Z9 10
U1 0
U2 1
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-2010
EI 1873-4316
J9 CURR PHARM BIOTECHNO
JI Curr. Pharm. Biotechnol.
PY 2018
VL 19
IS 9
BP 734
EP 741
DI 10.2174/1389201019666181010170630
PG 8
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA HD4XU
UT WOS:000452532500007
PM 30336770
DA 2025-06-01
ER

PT J
AU Huang, Z
   Xu, YS
   Wan, MP
   Zeng, XX
   Wu, JM
AF Huang, Zheng
   Xu, Yesha
   Wan, Maoping
   Zeng, Xixi
   Wu, Jianmin
TI miR-340: A multifunctional role in human malignant diseases
SO INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
LA English
DT Review
DE microRNAs; miR-340; malignant diseases; cancers; drug resistance
ID MICRORNA-340 INDUCES APOPTOSIS; CANCER CELL-PROLIFERATION; HUMAN
   GASTRIC-CANCER; COLORECTAL-CANCER; HEPATOCELLULAR-CARCINOMA;
   DOWN-REGULATION; TUMOR-GROWTH; CISPLATIN RESISTANCE; OSTEOSARCOMA CELLS;
   BONE-MARROW
AB MicroRNAs (miRNAs) are a class of short non-coding RNAs of approximately 22 nucleotides in length, which function by binding to the 3' UTR sequences of their target mRNAs. It has been reported that dysregulated miRNAs play pivotal roles in numerous diseases, including cancers, such as gastric, breast, colorectal, ovarian, and other cancers. Recent research efforts have been devoted to translating these basic discoveries into clinical applications that could improve the therapeutic outcome in patients with cancer. Early studies have shown that miR-340 may act either as an oncogene or a tumor suppressor by targeting genes related to proliferation, apoptosis, and metastasis, as well as those associated with diagnosis, treatment, chemoresistance, and prognosis. miR-340 has been shown to have a role in other diseases, such as autoimmune diseases, acute stroke, and alcoholic steatohepatitis. Nevertheless, the roles of miR-340 in human malignancies are still unclear, and the associated mechanisms are complex, involving a variety of signaling pathways, such as Wnt/beta-catenin and the JAK-STAT pathways. Herein, we review the crucial roles of miR-340 in human cancers through the analysis of the latest research studies, with the aim of clarifying miR-340 function in malignant disease diagnosis, treatment, and prognosis, and to propose further investigations.
C1 [Huang, Zheng; Xu, Yesha; Wan, Maoping; Zeng, Xixi; Wu, Jianmin] Wenzhou Med Univ, Inst Genom Med, 1 Cent North Rd, Wenzhou 325035, Zhejiang, Peoples R China.
   [Huang, Zheng] Chinese Univ Hong Kong, Dept Anesthesia & Intens Care, Hong Kong, Peoples R China.
C3 Wenzhou Medical University; Chinese University of Hong Kong
RP Wu, JM (corresponding author), Wenzhou Med Univ, Inst Genom Med, 1 Cent North Rd, Wenzhou 325035, Zhejiang, Peoples R China.
EM jianminwu81@hotmail.com
RI Zeng, Xixi/LZE-4162-2025
FU National Natural Sciences Foundation of China [NSFC-81472651]; Zhejiang
   Provincial Natural Sciences Foundation [LY20H160016]
FX This work was supported by the National Natural Sciences Foundation of
   China (grant NSFC-81472651) and Zhejiang Provincial Natural Sciences
   Foundation (LY20H160016). We would like to thank Editage
   (www.editage.cn) for English language editing.
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NR 118
TC 29
Z9 30
U1 1
U2 12
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1449-2288
J9 INT J BIOL SCI
JI Int. J. Biol. Sci.
PY 2021
VL 17
IS 1
BP 236
EP 246
DI 10.7150/ijbs.51123
PG 11
WC Biochemistry & Molecular Biology; Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics
GA QL5MG
UT WOS:000621120800010
PM 33390846
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Shi, LH
   Li, XG
   Qian, H
AF Shi, Luhuai
   Li, Xiaoguang
   Qian, Hua
TI Anti-Laminin 332-Type Mucous Membrane Pemphigoid
SO BIOMOLECULES
LA English
DT Review
DE mucous membrane pemphigoid; cicatricial pemphigoid; laminin 332;
   diagnosis; treatment; tumor
ID INDUCE SUBEPIDERMAL BLISTERS; ANTIEPILIGRIN LAMININ-5;
   GASTRIC-CARCINOMA; MEDICAL-TREATMENT; BULLOUS DISEASES; LUNG-CARCINOMA;
   EPILIGRIN; AUTOANTIBODIES; AUTOIMMUNE; ADENOCARCINOMA
AB Anti-laminin (LM) 332-type mucous membrane pemphigoid (MMP) is a rare autoimmune bullous disease and was originally discovered as anti-epiligrin cicatricial pemphigoid. Anti-LM332-type MMP has clinical manifestations similar to those of other types of MMP and can only be distinguished through the detection of circulating autoantibodies against LM332. Our group and others have established a number of immunological methods with varying sensitivity and specificity for detection of anti-LM332 autoantibodies; however, none of the established methods has been widely used for clinical diagnosis. There is currently no unified standard treatment, and it is very difficult to completely cure anti-LM332-type MMP. In addition, an increasing body of evidence suggests that there may be a strong correlation between anti-LM332-type MMP and tumors. In this article, we review the current progression of diagnosis and treatment of anti-LM332-type MMP, as well as the possible correlation between anti-LM332-type MMP and tumors.
C1 [Shi, Luhuai] Nanchang Univ, Dermatol Hosp Jiangxi Prov, Jiangxi Prov Clin Res Ctr Skin Dis, Affiliated Dermatol Hosp,Candidate Branch,Natl Cl, Nanchang 330001, Jiangxi, Peoples R China.
   [Li, Xiaoguang; Qian, Hua] Dalian Univ, Med Coll, Chron Dis Res Ctr, Dept Lab Med, Dalian 116622, Peoples R China.
C3 Nanchang University; Dalian University
RP Qian, H (corresponding author), Dalian Univ, Med Coll, Chron Dis Res Ctr, Dept Lab Med, Dalian 116622, Peoples R China.
EM qianhua@s.dlu.edu.cn
OI Shi, Luhuai/0000-0002-8652-4029
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NR 98
TC 13
Z9 13
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD OCT
PY 2022
VL 12
IS 10
AR 1461
DI 10.3390/biom12101461
PG 12
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 5O1MB
UT WOS:000872244800001
PM 36291670
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Liang, F
   Qin, WX
   Zeng, YL
   Wang, D
AF Liang, Fang
   Qin, Weixiao
   Zeng, Yilan
   Wang, Dan
TI Modulation of Autoimmune and Autoinflammatory Diseases by Gasdermins
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE gasdermins; autoimmune diseases; autoinflammatory disease; pyroptosis;
   inflammasome
ID NONSYNDROMIC HEARING IMPAIRMENT; ONCOSTATIN-M; DFNA5 GENE; CELL-DEATH;
   GASTROINTESTINAL-TRACT; MOLECULAR-MECHANISMS; GASTRIC-CANCER; PROTEIN
   FAMILY; MUTATION; EXPRESSION
AB Autoimmune diseases and autoinflammatory diseases are two types of the immune system disorders. Pyroptosis, a highly inflammatory cell death, plays an important role in diseases of immune system. The gasdermins belong to a pore-forming protein gene family which are mainly expressed in immune cells, gastrointestinal tract, and skin. Gasdermins are regarded as an executor of pyroptosis and have been shown to possess various cellular functions and pathological effects such as pro-inflammatory, immune activation, mediation of tumor, etc. Except for infectious diseases, the vital role of gasdermins in autoimmune diseases, autoinflammatory diseases, and immune-related neoplastic diseases has been proved recently. Therefore, gasdermins have been served as a potential therapeutic target for immune disordered diseases. The review summarizes the basic molecular structure and biological function of gasdermins, mainly discusses their role in autoimmune and autoinflammatory diseases, and highlights the recent research on gasdermin family inhibitors so as to provide potential therapeutic prospects.
C1 [Liang, Fang; Qin, Weixiao] Cent South Univ, Xiangya Hosp 3, Dept Hematol, Changsha, Peoples R China.
   [Zeng, Yilan; Wang, Dan] Cent South Univ, Xiangya Hosp 3, Dept Dermatol, Changsha, Peoples R China.
C3 Central South University; Central South University
RP Wang, D (corresponding author), Cent South Univ, Xiangya Hosp 3, Dept Dermatol, Changsha, Peoples R China.
EM Drdanwang@163.com
FU Longitudinal subject of Municipal Science and Technology Bureau
   [XY050033]
FX Funding This study was supported by Longitudinal subject of Municipal
   Science and Technology Bureau (grant number XY050033).
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NR 98
TC 4
Z9 4
U1 2
U2 14
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUN 1
PY 2022
VL 13
AR 841729
DI 10.3389/fimmu.2022.841729
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 2D2KA
UT WOS:000811381400001
PM 35720396
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bizzaro, N
   Antico, A
   Villalta, D
AF Bizzaro, Nicola
   Antico, Antonio
   Villalta, Danilo
TI Autoimmunity and Gastric Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE autoimmune diseases; autoimmune gastritis; gastric cancer; Helicobacter
   pylori infection; intrinsic factor antibodies; parietal cell antibodies
ID HELICOBACTER-PYLORI INFECTION; CHRONIC ATROPHIC GASTRITIS; SERUM
   ANTI-P53 ANTIBODIES; NON-HODGKINS-LYMPHOMA; CLINICAL-SIGNIFICANCE;
   PERNICIOUS-ANEMIA; BODY GASTRITIS; PARIETAL-CELL; CIRCULATING
   ANTIBODIES; ANTINUCLEAR ANTIBODIES
AB Alterations in the immune response of patients with autoimmune diseases may predispose to malignancies, and a link between chronic autoimmune gastritis and gastric cancer has been reported in many studies. Intestinal metaplasia with dysplasia of the gastric corpus-fundus mucosa and hyperplasia of chromaffin cells, which are typical features of late-stage autoimmune gastritis, are considered precursor lesions. Autoimmune gastritis has been associated with the development of two types of gastric neoplasms: intestinal type and type I gastric carcinoid. Here, we review the association of autoimmune gastritis with gastric cancer and other autoimmune features present in gastric neoplasms.
C1 [Bizzaro, Nicola] Azienda Sanit Univ Integrata, Lab Patol Clin, I-33100 Udine, Italy.
   [Antico, Antonio] Lab Anal ULSS 4, I-36014 Santorso, Italy.
   [Villalta, Danilo] Presidio Osped S Maria Angeli, Immunol & Allergol, I-33170 Pordenone, Italy.
RP Villalta, D (corresponding author), Presidio Osped S Maria Angeli, Immunol & Allergol, I-33170 Pordenone, Italy.
EM nic.bizzaro@gmail.com; antonio.antico@aulss7.veneto.it;
   danilo.villalta@aas5.sanita.fvg.it
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NR 119
TC 65
Z9 69
U1 1
U2 25
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2018
VL 19
IS 2
AR 377
DI 10.3390/ijms19020377
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA FZ3YN
UT WOS:000427527400061
PM 29373557
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Freeman, HJ
AF Freeman, HJ
TI Neoplastic disorders in 100 patients with adult celiac disease
SO CANADIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE celiac disease; colon cancer; dermatitis herpetiformis; hypothyroidism;
   lymphoma; small bowel carcinoma
ID T-CELL LYMPHOMA; SPRUE; MALIGNANCY
AB Previous reports have suggested that the incidence of some neoplastic disorders, particularly malignant lymphoma, is increased in patients with celiac disease. In this study, the type and number of neoplastic disorders detected in 100 consecutive celiac disease patients were explored, Sixty-five patients were initially diagnosed with celiac disease before, and 35 after, age 60 years. Ten elderly celiac patients had lymphoma or small intestinal adenocarcinoma. Although the overall incidence of malignant lymphoma was 8%, similar to that in other centres, the incidence in elderly celiac patients was 23% in this study. Celiac disease was detected before or after the diagnosis of lymphoma or small intestinal adenocarcinoma. In some patients, epithelial lymphocytosis was evident in the gastric, colonic or biliary tract epithelium. In addition, other immune mediated disorders, dermatitis herpetiformis and autoimmune thyroiditis, were common. Finally, other malignant disorders of the esophagus, stomach and colon were not detected.
C1 UNIV BRITISH COLUMBIA,DEPT MED GASTROENTEROL,VANCOUVER,BC V5Z 1M9,CANADA.
C3 University of British Columbia
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NR 26
TC 14
Z9 14
U1 0
U2 0
PU MEDICARE PUBL INC, PULSUS GROUP INC
PI OAKVILLE
PA 2902 S SHERIDAN WAY, OAKVILLE ON L6J 7L6, CANADA
SN 0835-7900
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol.
PD MAY-JUN
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VL 10
IS 3
BP 163
EP 166
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PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UU206
UT WOS:A1996UU20600005
OA gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Correa, P
   Piazuelo, MB
AF Correa, Pelayo
   Piazuelo, M. Blanca
TI Evolutionary History of the Helicobacter pylori Genome:
   Implications for Gastric Carcinogenesis
SO GUT AND LIVER
LA English
DT Review
DE Helicobacter pylori; Genome; Gastric carcinogenesis
ID VACUOLATING CYTOTOXIN; BIOLOGICAL-ACTIVITY; GENETIC DIVERSITY; CANCER
   INCIDENCE; ETHNIC-GROUPS; CAGA; STRAINS; INFECTION; VIRULENCE; VACA
AB The genome of the bacterium Helicobacter pylori has evolved over the millennia since its migration out of Africa along with its human host approximately 60,000 years ago. Human migrations, after thousands of years of permanent settlement in those lands, resulted in seven prototypes of genetic populations of H. pylori with distinct geographical distributions. In all continents, present day isolates of H. pylori have molecular markers that reflect population migrations. The colonization of the Americas as well as the slave trade introduced European and African strains to the New World. The relationship between H. pylori genome and gastric cancer rates is linked to the presence of the cagA gene, but the knowledge on this subject is incomplete because other genes may be involved in certain populations. A new situation for Homo sapiens is the absence of H. pylori colonization in certain, mostly affluent, populations, apparently brought about by improved home sanitation and widespread use of antibiotics during the last decades. The disappearance of H. pylori from the human microbiota may be linked to emerging epidemics of esophageal adenocarcinoma, some allergic diseases such as asthma and some autoimmune disorders. (Gut Liver 2012;6:21-28)
C1 [Correa, Pelayo; Piazuelo, M. Blanca] Vanderbilt Univ, Med Ctr, Dept Med, Div Gastroenterol, Nashville, TN 37232 USA.
C3 Vanderbilt University
RP Correa, P (corresponding author), Vanderbilt Univ, Med Ctr, Dept Med, Div Gastroenterol, 2215 Garland Ave,1030 MRB 4, Nashville, TN 37232 USA.
EM pelayo.correa@vanderbilt.edu
FU U.S. National Cancer Institute [P01-CA28842]
FX This work was supported by the grant P01-CA28842 from the U.S. National
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NR 71
TC 33
Z9 44
U1 0
U2 5
PU EDITORIAL OFFICE GUT & LIVER
PI SEOUL
PA 305 LOTTE GOLD ROSE II, 890-59, DAECHI 4-DONG, GANGNAM-GU, SEOUL,
   135-839, SOUTH KOREA
SN 1976-2283
EI 2005-1212
J9 GUT LIVER
JI Gut Liver
PD JAN
PY 2012
VL 6
IS 1
BP 21
EP 28
DI 10.5009/gnl.2012.6.1.21
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 879XY
UT WOS:000299367400003
PM 22375167
OA gold, Green Published, Green Submitted
DA 2025-06-01
ER

PT J
AU Singh, S
   Jha, HC
AF Singh, Shyam
   Jha, Hem Chandra
TI Status of Epstein-Barr Virus Coinfection with Helicobacter pylori
   in Gastric Cancer
SO JOURNAL OF ONCOLOGY
LA English
DT Review
ID B-CELL LYMPHOMA; NECROSIS-FACTOR-ALPHA; IMMUNOGLOBULIN-G IGG; IV
   SECRETION SYSTEM; EPITHELIAL-CELLS; OXIDATIVE STRESS; TUMOR-SUPPRESSOR;
   CARCINOMA CELLS; INCREASED RISK; E-CADHERIN
AB Epstein-Barr virus is a ubiquitous human herpesvirus whose primary infection causes mononucleosis, Burkett's lymphoma, nasopharyngeal carcinoma, autoimmune diseases, and gastric cancer (GC). The persistent infection causes malignancies in lymph and epithelial cells. Helicobacter pylori causes gastritis in human with chronic inflammation. This chronic inflammation is thought to be the cause of genomic instability. About 45%-word population have a probability of having both pathogens, namely, H. pylori and EBV. Approximately 180 per hundred thousand population is developing GC along with many gastric abnormalities. This makes GC the third leading cause of cancer-related death worldwide. Although lots of research are carried out individually for EBV and H. pylori, still there are very few reports available on coinfection of both pathogens. Recent studies suggested that EBV and H. pylori coinfection increases the occurrence of GC as well as the early age of GC detection comparing to individual infection. The aim of this review is to present status on coinfection of both pathogens and their association with GC.
C1 [Singh, Shyam; Jha, Hem Chandra] Indian Inst Technol, Ctr Biosci & Biomed Engn, Indore, Madhya Pradesh, India.
C3 Indian Institute of Technology System (IIT System); Indian Institute of
   Technology (IIT) - Indore
RP Jha, HC (corresponding author), Indian Inst Technol, Ctr Biosci & Biomed Engn, Indore, Madhya Pradesh, India.
EM hemcjha@iiti.ac.in
RI Jha, Hem Chandra/T-2293-2019
OI Jha, Hem Chandra/0000-0002-9698-4547
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NR 286
TC 54
Z9 57
U1 0
U2 18
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-8450
EI 1687-8469
J9 J ONCOL
JI J. Oncol.
PY 2017
VL 2017
AR 3456264
DI 10.1155/2017/3456264
PG 17
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EQ2OM
UT WOS:000397909400001
PM 28421114
OA Green Published, hybrid, Green Submitted
DA 2025-06-01
ER

PT J
AU Garcia-Marquez, MA
   Thelen, M
   Bauer, E
   Maas, L
   Wennhold, K
   Lehmann, J
   Keller, D
   Nikolic, M
   George, J
   Zander, T
   Schröder, W
   Müller, P
   Yazbeck, AM
   Bruns, C
   Thomas, R
   Gathof, B
   Quaas, A
   Peifer, M
   Hillmer, AM
   von Bergwelt-Baildon, M
   Schlösser, HA
AF Garcia-Marquez, Maria Alejandra
   Thelen, Martin
   Bauer, Eugen
   Maas, Lukas
   Wennhold, Kerstin
   Lehmann, Jonas
   Keller, Diandra
   Nikolic, Milos
   George, Julie
   Zander, Thomas
   Schroeder, Wolfgang
   Mueller, Philipp
   Yazbeck, Ali M.
   Bruns, Christiane
   Thomas, Roman
   Gathof, Birgit
   Quaas, Alexander
   Peifer, Martin
   Hillmer, Axel M.
   von Bergwelt-Baildon, Michael
   Schloesser, Hans Anton
TI Germline homozygosity and allelic imbalance of HLA-I are common in
   esophagogastric adenocarcinoma and impair the repertoire of immunogenic
   peptides
SO JOURNAL FOR IMMUNOTHERAPY OF CANCER
LA English
DT Article
DE Antigen Presentation; Antigens; Computational Biology; Gastrointestinal
   Neoplasms; Tumor Escape
ID MHC CLASS-I; LUNG-CANCER; OPEN-LABEL; EXPRESSION; ESOPHAGEAL; MELANOMA;
   ANTIGENS; SURVIVAL; PHASE-3
AB Background The individual HLA-I genotype is associated with cancer, autoimmune diseases and infections. This study elucidates the role of germline homozygosity or allelic imbalance of HLA-I loci in esophago-gastric adenocarcinoma (EGA) and determines the resulting repertoires of potentially immunogenic peptides.Methods HLA genotypes and sequences of either (1) 10 relevant tumor-associated antigens (TAAs) or (2) patient-specific mutation-associated neoantigens (MANAs) were used to predict good-affinity binders using an in silico approach for MHC-binding (www.iedb.org). Imbalanced or lost expression of HLA-I-A/B/C alleles was analyzed by transcriptome sequencing. FluoroSpot assays and TCR sequencing were used to determine peptide-specific T-cell responses.Results We show that germline homozygosity of HLA-I genes is significantly enriched in EGA patients (n=80) compared with an HLA-matched reference cohort (n=7605). Whereas the overall mutational burden is similar, the repertoire of potentially immunogenic peptides derived from TAAs and MANAs was lower in homozygous patients. Promiscuity of peptides binding to different HLA-I molecules was low for most TAAs and MANAs and in silico modeling of the homozygous to a heterozygous HLA genotype revealed normalized peptide repertoires. Transcriptome sequencing showed imbalanced expression of HLA-I alleles in 75% of heterozygous patients. Out of these, 33% showed complete loss of heterozygosity, whereas 66% had altered expression of only one or two HLA-I molecules. In a FluoroSpot assay, we determined that peptide-specific T-cell responses against NY-ESO-1 are derived from multiple peptides, which often exclusively bind only one HLA-I allele.Conclusion The high frequency of germline homozygosity in EGA patients suggests reduced cancer immunosurveillance leading to an increased cancer risk. Therapeutic targeting of allelic imbalance of HLA-I molecules should be considered in EGA.
C1 [Garcia-Marquez, Maria Alejandra; Thelen, Martin; Wennhold, Kerstin; Lehmann, Jonas; Keller, Diandra; Mueller, Philipp; Yazbeck, Ali M.; Peifer, Martin; Hillmer, Axel M.; Schloesser, Hans Anton] Univ Cologne, Ctr Mol Med Cologne, Cologne, Germany.
   [Garcia-Marquez, Maria Alejandra; Thelen, Martin; Wennhold, Kerstin; Lehmann, Jonas; Keller, Diandra; Schroeder, Wolfgang; Bruns, Christiane; Schloesser, Hans Anton] Univ Cologne, Dept Gen Visceral Canc & Transplantat Surg, Cologne, Germany.
   [Bauer, Eugen; Gathof, Birgit] Univ Cologne, Inst Transfus Med, Cologne, Germany.
   [Maas, Lukas; Nikolic, Milos; George, Julie; Thomas, Roman; Peifer, Martin] Univ Cologne, Dept Translat Genom, Cologne, Germany.
   [George, Julie] Univ Hosp Cologne, Dept Otorhinolaryngol Head & Neck Surg, Cologne, Germany.
   [Zander, Thomas] Univ Hosp Cologne, Dept Internal Med 1, Departmentof Internal Med 1, Cologne, Germany.
   [Zander, Thomas] Univ Hosp Cologne, Ctr Integrated Oncol CIO Aachen Bonn Cologne Duess, Cologne, Germany.
   [Mueller, Philipp; Yazbeck, Ali M.; Thomas, Roman; Quaas, Alexander; Hillmer, Axel M.] Univ Cologne, Inst Pathol, Cologne, Germany.
   [Thomas, Roman; von Bergwelt-Baildon, Michael] German Canc Consortium DKTK, Heidelberg, Germany.
   [von Bergwelt-Baildon, Michael] Ludwig Maximilians Univ Munchen, Gene Ctr, Munich, Germany.
   [von Bergwelt-Baildon, Michael] Ludwig Maximilians Univ Munchen, Dept Med 3, Munich, Germany.
C3 University of Cologne; University of Cologne; University of Cologne;
   University of Cologne; University of Cologne; University of Cologne;
   University of Cologne; University of Cologne; Helmholtz Association;
   German Cancer Research Center (DKFZ); University of Munich; University
   of Munich
RP Garcia-Marquez, MA (corresponding author), Univ Cologne, Ctr Mol Med Cologne, Cologne, Germany.; Garcia-Marquez, MA (corresponding author), Univ Cologne, Dept Gen Visceral Canc & Transplantat Surg, Cologne, Germany.
EM maria.garcia-marquez@uk-koeln.de
RI Schroeder, Wolfgang/K-8728-2013; Hillmer, Axel/B-7485-2015; Quaas,
   Alexander/LXB-4339-2024; Schlößer, Hans Anton/JMB-8546-2023; Thelen,
   Martin/D-6869-2016
OI Thelen, Martin/0000-0002-2785-9726; Garcia-Marquez, Maria
   Alejandra/0000-0002-5923-5942; Keller, Diandra/0009-0000-2266-3698;
   Schlosser, Hans Anton/0000-0002-1304-7719
FU Deutsche Forschungsgemeinschaft; Institute of Transfusion Medicine of
   the University Hospital Cologne [INST 216/512/1FUGG]; Stefan Morsch
   Foundation
FX We thank the Institute of Transfusion Medicine of the University
   Hospital Cologne and the Stefan Morsch Foundation for their support. We
   thank the technicians Monika Keiten-Schmitz and Alina Manu for their
   support. We furthermore thank the Regional Computing Center of the
   University of Cologne (RRZK) for providing computing time on the
   DFG-funded (Funding number: INST 216/512/1FUGG) High Performance
   Computing (HPC) system CHEOPS as well for their support.
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NR 46
TC 0
Z9 0
U1 1
U2 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 2051-1426
J9 J IMMUNOTHER CANCER
JI J. Immunother. Cancer
PD APR
PY 2024
VL 12
IS 4
AR e007268
DI 10.1136/jitc-2023-007268
PG 14
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA SM4L6
UT WOS:001234856000012
PM 38631707
OA gold
DA 2025-06-01
ER

PT J
AU Wu, MY
   Hou, YT
   Ke, JY
   Yiang, GT
AF Wu, Meng-Yu
   Hou, Yueh-Tseng
   Ke, Jian-Yu
   Yiang, Giou-Teng
TI Case of internal jugular vein thrombosis and fever: Lemierre's syndrome
   or Trousseau's syndrome?
SO TZU CHI MEDICAL JOURNAL
LA English
DT Article
DE Internal jugular vein thrombosis; Lemierre's syndrome; Signet-ring cell
   adenocarcinoma; Trousseau's syndrome
ID GASTRIC-CANCER; VENOUS THROMBOEMBOLISM; D-DIMER; PATIENT; CHEMOTHERAPY;
   MALIGNANCY; MECHANISMS; HEPARIN; RISK
AB Internal jugular vein thrombosis is a rare critical cardiovascular emergency, which has potential catastrophic clinical outcomes by resulting in stroke and pulmonary embolism. Several etiologies have been reported; however, there are limited data on Lemierre's and Trousseau's syndromes, which are both rare conditions with advanced disease progression and poor clinical outcomes. Lemierre's syndrome may present with typical progressively infectious symptoms and signs, including sore throat, neck mass, and fever, whereas Trousseau's syndrome may present with thrombophlebitis and painful edema. Without antibiotic agents controlling the infection, the condition of patients with Lemierre's syndrome may progress to sepsis or septic shock. The infection pattern plays an important role for differential diagnosis. Herein, we describe the case of a 46-year-old woman presenting with atypical symptoms of Trousseau's syndrome mimicking Lemierre's syndrome. Laboratory analysis including protein C, protein S, rheumatoid factor, and antinuclear antibody ruled out hypercoagulopathy and autoimmune vasculitis. Abdominal computed tomography and panendoscopy revealed ulcerative tumor at the antrum. Pathological examination confirmed the presence of signet-ring cell adenocarcinoma. We highlight the clinical features and etiologies of internal jugular vein thrombosis, especially in Lemierre's syndrome and Trousseau's syndrome, to aid physicians in making an early diagnosis and providing timely management.
C1 [Wu, Meng-Yu; Hou, Yueh-Tseng; Ke, Jian-Yu; Yiang, Giou-Teng] Buddhist Tzu Chi Med Fdn, Taipei Tzu Chi Hosp, Dept Emergency Med, 289 Jianguo Rd, New Taipei, Taiwan.
   [Wu, Meng-Yu; Hou, Yueh-Tseng; Ke, Jian-Yu; Yiang, Giou-Teng] Tzu Chi Univ, Sch Med, Dept Emergency Med, Hualien, Taiwan.
C3 Buddhist Tzu Chi General Hospital; Taipei Tzu Chi Hospital; Tzu Chi
   University
RP Yiang, GT (corresponding author), Buddhist Tzu Chi Med Fdn, Taipei Tzu Chi Hosp, Dept Emergency Med, 289 Jianguo Rd, New Taipei, Taiwan.
EM gtyiang@gmail.com
RI Yiang, Giou-Teng/IVU-7155-2023; Wu, Meng/J-8772-2019; KE,
   JIANYU/A-8479-2015
OI HOU, YUEH-TSENG/0009-0003-5125-0771; Wu, Meng-Yu/0000-0002-8773-1847
FU Taipei Tzu Chi Hospital [TCRD-TPE-108-5]
FX This study was supported by a grant from the Taipei Tzu Chi Hospital
   (TCRD-TPE-108-5).
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NR 36
TC 3
Z9 3
U1 0
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, 400059, INDIA
SN 1016-3190
EI 2223-8956
J9 TZU CHI MED J
JI Tzu Chi Med. J.
PD JAN-MAR
PY 2020
VL 32
IS 1
BP 91
EP 95
DI 10.4103/tcmj.tcmj_34_19
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA KB3OI
UT WOS:000506408800017
PM 32110528
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Fei, YC
   Cao, YF
   Gu, Y
   Fang, HJ
   Chen, YF
   Wang, JT
   Liu, X
   Lv, KP
   He, XD
   Lin, C
   Liu, H
   Li, H
   He, HY
   Li, RC
   Zhang, H
   Zhang, WJ
AF Fei, Yuchao
   Cao, Yifan
   Gu, Yun
   Fang, Hanji
   Chen, Yifan
   Wang, Jieti
   Liu, Xin
   Lv, Kunpeng
   He, Xudong
   Lin, Chao
   Liu, Hao
   Li, He
   He, Hongyong
   Li, Ruochen
   Zhang, Heng
   Zhang, Weijuan
TI Intratumoral Foxp3<SUP>+</SUP>RORγt<SUP>+</SUP> T cell infiltration
   determines poor prognosis and immunoevasive contexture in gastric cancer
   patients
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Gastric cancer; Foxp3(+)ROR&#947; t(+) T cells; Prognosis; Adjuvant
   chemotherapy; Chemotherapeutic responsiveness
AB Background Foxp3(+)ROR gamma t(+) T cells possess both characteristics of regulatory T cells and T helper 17 cells and show significant immunoregulatory functions in autoimmune diseases. However, the role and clinical significance of Foxp3(+)ROR gamma t(+) T cells in gastric cancer remains unclear. Methods We enrolled 452 gastric cancer tissue microarray samples and 60 fresh tumor tissue samples from Zhongshan Hospital. The infiltration of Foxp3(+)ROR gamma t(+) T cells and immune contexture were examined by immunohistochemistry and flow cytometry. Survival analyses of patient subgroups were conducted by Kaplan-Meier curves, log-rank test and Cox proportional model. Results High infiltration of Foxp3(+)ROR gamma t(+) T cells predicted poor overall survival (P = 0.0222 and 0.0110) and inferior therapeutic response (P = 0.003 for interaction) in gastric cancer. Foxp3(+)ROR gamma t(+) T cells were associated with impaired effective function of CD8(+) T cells featured by decreased interferon-gamma, granzyme B and CD107a expression. Co-evaluation of Foxp3(+)ROR gamma t(+) T cells and CD8(+) T cells could predict survival outcomes and chemotherapeutic responsiveness more precisely. Conclusions We found that Foxp3(+)ROR gamma t(+) T cells could potentially attenuate effective functions of CD8(+) T cells and led to adverse survival outcomes and inferior chemotherapeutic responsiveness. Moreover, the novel co-evaluation system might be useful for prognosis prediction for appropriate treatment in gastric cancer. Novelty and impact statements Clinical significance of Foxp3(+)ROR gamma ts(+) T cells has not been studied in gastric cancer. Herein, we investigated the prognostic value of Foxp3+ROR gamma t+ T cells in 452 patients. We demonstrated that intratumoral Foxp3(+)ROR gamma t(+) T cell infiltration was a prognostic biomarker for overall survival and the identification of patients might benefit from post-gastrectomy 5-fluorouracil. These findings allow a more precise stratification upon the co-evaluation with CD8(+) T cells to better clinical management for patients who would benefit from 5-fluorouracil.
C1 [Fei, Yuchao; Gu, Yun; Fang, Hanji; Liu, Xin; Lv, Kunpeng; He, Xudong] Fudan Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Shanghai, Peoples R China.
   [Cao, Yifan; Lin, Chao; Liu, Hao; Li, He; He, Hongyong; Li, Ruochen; Zhang, Heng] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.
   [Chen, Yifan; Zhang, Weijuan] Fudan Univ, Sch Basic Med Sci, Dept Immunol, Shanghai 200032, Peoples R China.
   [Wang, Jieti] Fudan Univ, Shanghai Canc Ctr, Dept Gastr Surg, Shanghai, Peoples R China.
C3 Fudan University; Fudan University; Fudan University; Fudan University
RP Li, RC; Zhang, H (corresponding author), Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China.; Zhang, WJ (corresponding author), Fudan Univ, Sch Basic Med Sci, Dept Immunol, Shanghai 200032, Peoples R China.
EM rcli12@fudan.edu.cn; zhang.heng@zs-hospital.sh.cn;
   weijuanzhang@fudan.edu.cn
RI Chen, Yifan/AAA-1970-2020; He, Hang/ABF-4074-2020; Liu,
   Hao/GZG-4191-2022; Liu, Tianshu/H-6879-2019; Li, Ruochen/HHC-6630-2022;
   Gu, Yun/NHP-1484-2025; Zhang, Weijuan/Q-1645-2019; Fang,
   Hanji/MAI-3734-2025
OI HE, HONGYONG/0000-0001-7371-4133
FU National Natural Science Foundation of China [81671628, 81871306,
   81871930, 81902402, 81902901, 81972219, 82003019]; Shanghai Sailing
   Program [17YF1402200, 18YF1404600, 19YF1407500, 21YF1407600]
FX This study was funded by grants from National Natural Science Foundation
   of China (81671628, 81871306, 81871930, 81902402, 81902901, 81972219,
   82003019) and Shanghai Sailing Program (17YF1402200, 18YF1404600,
   19YF1407500, 21YF1407600). All these study sponsors have no roles in the
   study design, in the collection, analysis and interpretation of data.
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NR 29
TC 8
Z9 10
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD JAN
PY 2022
VL 71
IS 1
BP 1
EP 11
DI 10.1007/s00262-021-02950-3
EA MAY 2021
PG 11
WC Oncology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Immunology
GA YC9AF
UT WOS:000650086500001
PM 33978826
OA Green Published
DA 2025-06-01
ER

PT J
AU Palacio, A
   Tamariz, L
   Berger, J
   Patarca, R
AF Palacio, A
   Tamariz, L
   Berger, J
   Patarca, R
TI Enteropathy-associated T-cell lymphoma and its immunocarcinogenic
   correlates: Case report and review of the literature
SO CRITICAL REVIEWS IN ONCOGENESIS
LA English
DT Review
DE celiac disease; cytokines; gluten; tumor necrosis factor; eotaxin;
   gliadin; endomysium
ID DEPENDENT DIABETES-MELLITUS; ADULT CELIAC-DISEASE; GLUTEN-SENSITIVE
   ENTEROPATHY; HUMAN UMBILICAL-CORD; EPSTEIN-BARR-VIRUS; PRIMARY
   SCLEROSING CHOLANGITIS; SYSTEMIC LUPUS-ERYTHEMATOSUS; AUTOIMMUNE
   THYROID-DISEASE; IGA ANTIGLIADIN ANTIBODIES; SMALL-BOWEL ADENOCARCINOMA
AB We report a case of enteropathy-associated T-cell lymphoma (EATL), diagnosed by small intestine and gastric biopsies, who presented with manifestations of hypocalcemia and malabsorption. Immunonological assessment revealed increased expression levels of tumor necrosis factor system components and eotaxin, an observation that is consistent with the cytotoxic T-cell phenotype characteristic of EATL, and decreased numbers of circulating activated (CD8+CD38+ and CD4+CD25+) and suppressor (CD11b+) T cells, a feature which can contribute to lymphomagenesis in patients with celiac disease. The acute clinical presentation of the patient resolved with mineral and vitamin supplementation and a gluten-free diet. The novel immunological findings described are discussed in the context of a review of our current knowledge of the immunopathogenesis of celiac disease and associated intestinal neoplasia.
C1 Jackson Mem Hosp, Dept Internal Med, Miami, FL 33136 USA.
RP Jackson Mem Hosp, Dept Internal Med, 1611 NW 12th Ave, Miami, FL 33136 USA.
OI Tamariz, Leonardo/0000-0003-1583-3534
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NR 346
TC 2
Z9 2
U1 0
U2 5
PU BEGELL HOUSE INC
PI DANBURY
PA 50 NORTH ST, DANBURY, CT 06810 USA
SN 0893-9675
EI 2162-6448
J9 CRIT REV ONCOGENESIS
JI Crit. Rev. Oncog.
PY 1998
VL 9
IS 1
BP 63
EP 81
DI 10.1615/CritRevOncog.v9.i1.50
PG 19
WC Biochemistry & Molecular Biology; Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology
GA 119LW
UT WOS:000075898800005
PM 9754448
DA 2025-06-01
ER

PT J
AU Thieblemont, C
   Bertoni, F
   Copie-Bergman, C
   Ferreri, AJM
   Ponzoni, M
AF Thieblemont, Catherine
   Bertoni, Francesco
   Copie-Bergman, Christiane
   Ferreri, Andres J. M.
   Ponzoni, Maurilio
TI Chronic inflammation and extra-nodal marginal-zone lymphomas of
   MALT-type
SO SEMINARS IN CANCER BIOLOGY
LA English
DT Review
DE MALT lymphoma; Chronic inflammation; Marginal zone; Microbial pathogen
   autoimmune disease
ID NF-KAPPA-B; HELICOBACTER-PYLORI ERADICATION; VH GENE ANALYSIS; CELL
   LYMPHOMA; TISSUE LYMPHOMA; GASTRIC-LYMPHOMA; SOMATIC HYPERMUTATION;
   CHROMOSOMAL-ABERRATION; GERMAN MULTICENTER; MUTATION ANALYSIS
AB Extranodal marginal zone lymphoma of mucosa associated lymphoid tissue (MALT) is an indolent B-cell non-Hodgkin lymphoma (NHL) arising in lymphoid populations that are induced by chronic inflammation in extra nodal sites. The stomach is the most commonly affected organ, and MALT lymphoma is clearly associated with a gastroduodenitis induced by a microbial pathogen, Helicobacter pylori, thus gastric MALT lymphoma represents a paradigm for evaluating inflammatory-associated lymphomagenesis. Variable levels of evidence have indicated a possible association between other microorganisms and non-gastric MALT lymphomas. In addition to infectious etiology, chronic inflammation arising as a result of autoimmune diseases such as Sjogren's syndrome or Hashimoto thyroiditis, poses a significant risk factor for developing NHL Recently, genetic alterations affecting the NF-kappa B pathway, a major signaling pathway involved in many cancers, have been identified in MALT lymphoma. This review will present MALT lymphoma as an example of the close pathogenetic link between chronic microenvironmental inflammation and tumor development, showing how these observations can be integrated into daily clinical practice, also in terms of therapeutic implications, with particular focus on the NF-kappa B pathway. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Thieblemont, Catherine] Univ Paris 07, INSERM, Hop St Louis, APHP,Dept Hematooncol,U728, Paris, France.
   [Bertoni, Francesco] IOR Inst Oncol Res, Lymphoma & Genom Res Program, Bellinzona, Switzerland.
   [Bertoni, Francesco] Oncol Inst Southern Switzerland, Lymphoma Unit, Bellinzona, Switzerland.
   [Copie-Bergman, Christiane] Hop Henri Mondor, APHP, Dept Pathol, F-94010 Creteil, France.
   [Ferreri, Andres J. M.] Ist Sci San Raffaele, Dept Oncohematol, I-20132 Milan, Italy.
   [Ferreri, Andres J. M.; Ponzoni, Maurilio] Ist Sci San Raffaele, Unit Lymphoid Malignancies, I-20132 Milan, Italy.
   [Ponzoni, Maurilio] Ist Sci San Raffaele, Pathol Unit, I-20132 Milan, Italy.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Saint-Louis - APHP; Institut National de la Sante
   et de la Recherche Medicale (Inserm); Hopital Universitaire Hotel-Dieu -
   APHP; Hopital Universitaire Ambroise-Pare - APHP; Universita della
   Svizzera Italiana; Institute of Oncology Research (IOR); Institute of
   Oncology Research (IOR); Universite Paris-Est-Creteil-Val-de-Marne
   (UPEC); Assistance Publique Hopitaux Paris (APHP); Hopital Universitaire
   Henri-Mondor - APHP; Hopital Universitaire Ambroise-Pare - APHP;
   Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
   Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
   Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele
RP Ponzoni, M (corresponding author), Ist Sci San Raffaele, Pathol Unit, Via Olgettina 60, I-20132 Milan, Italy.
EM ponzoni.maurilio@hsr.it
RI Ferreri, Andrés/A-6662-2013; Thieblemont, Catherine/AAZ-8423-2020;
   Bertoni, Francesco/G-6922-2014
OI copie bergman, christiane/0000-0001-5408-894X; Bertoni,
   Francesco/0000-0001-5637-8983
FU Special Program in Molecular Clinical Oncology AIRC 5xmille grant
   [9965]; Nelia and Amadeo Barletta Foundation
FX The authors would like to thank our colleague Afua Adjeiwaa Mensah
   (Bellinzona, Switzerland) for manuscript editing. MP and AJMF are
   recipients of Special Program in Molecular Clinical Oncology AIRC
   5xmille grant number 9965, FB of a grant from Nelia and Amadeo Barletta
   Foundation.
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NR 154
TC 73
Z9 77
U1 0
U2 10
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-579X
EI 1096-3650
J9 SEMIN CANCER BIOL
JI Semin. Cancer Biol.
PD FEB
PY 2014
VL 24
BP 33
EP 42
DI 10.1016/j.semcancer.2013.11.005
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AB0LF
UT WOS:000331482800005
PM 24333758
DA 2025-06-01
ER

PT J
AU Liu, YW
   Shao, ZW
   Shangguan, GQ
   Bie, QL
   Zhang, B
AF Liu, Yuwan
   Shao, Zewei
   Shangguan, Guoqiang
   Bie, Qingli
   Zhang, Bin
TI Biological Properties and the Role of IL-25 in Disease Pathogenesis
SO JOURNAL OF IMMUNOLOGY RESEARCH
LA English
DT Review
ID INTERLEUKIN-17 FAMILY; AIRWAY INFLAMMATION; ALLERGIC RHINITIS;
   PERIPHERAL-BLOOD; CELLS; EXPRESSION; IL-17; EOSINOPHILS; RECEPTOR;
   CYTOKINES
AB The interleukin-(IL-) 17 superfamily, a T cell-derived cytokine, consists of 6 ligands (IL-17A-IL-17F) and 5 receptors (IL-17RA-IL-17RE). IL-17A, a prototype member of this family, is involved in the pathogenesis of allergies, autoimmune diseases, allograft transplantations, and malignancies. By contrast, IL-17B is reported to be closely related to certain diseases, particularly tumors such as breast cancer, gastric cancer, and pancreatic cancer. Recently, the biological function of IL-17E (also called IL-25) in disease, particularly airway diseases, has attracted the attention of researchers. However, studies on IL-25 are scant. In this review, we detail the structural characteristics, expression patterns, responder cells, biological properties, and role of IL-25 in disease pathogenesis.
C1 [Liu, Yuwan; Bie, Qingli; Zhang, Bin] Jining Med Univ, Dept Lab Med, Affiliated Hosp, Jining, Shandong, Peoples R China.
   [Shao, Zewei; Shangguan, Guoqiang; Zhang, Bin] Jining Med Univ, Inst Forens Med & Lab Med, Jining, Shandong, Peoples R China.
C3 Jining Medical University; Jining Medical University
RP Bie, QL; Zhang, B (corresponding author), Jining Med Univ, Dept Lab Med, Affiliated Hosp, Jining, Shandong, Peoples R China.; Zhang, B (corresponding author), Jining Med Univ, Inst Forens Med & Lab Med, Jining, Shandong, Peoples R China.
EM xiaobie890101@163.com; zhb861109@163.com
RI B, Zhang/R-4316-2019
FU National Natural Science Foundation of China [81702439, 81802446];
   Postdoctoral Science Foundation of China [2016M600383]; Special Funded
   Projects of China Postdoctoral Science Fund [2017T100337]
FX The authors acknowledge the National Natural Science Foundation of China
   (81702439, 81802446), the Postdoctoral Science Foundation of China
   (2016M600383), and the Special Funded Projects of China Postdoctoral
   Science Fund (2017T100337).
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NR 70
TC 35
Z9 38
U1 0
U2 11
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2314-8861
EI 2314-7156
J9 J IMMUNOL RES
JI J Immunol. Res.
PY 2018
VL 2018
AR 6519465
DI 10.1155/2018/6519465
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GW3AL
UT WOS:000446761600001
PM 30345318
OA gold, Green Published, Green Submitted
DA 2025-06-01
ER

PT J
AU Sutton, S
   Haran, K
   Mullins, A
   Lamerson, C
AF Sutton, Sarah
   Haran, Kathryn
   Mullins, Amanda
   Lamerson, Cindy
TI A Rare Coexistence: Cutaneous Lobular Carcinoma with Pyoderma
   Gangrenosum
SO AMERICAN JOURNAL OF CASE REPORTS
LA English
DT Article
DE Breast Carcinoma In Situ; Dermatology; Pyoderma Gangrenosum
ID PATIENT; COMPLICATION; MANAGEMENT
AB Objective: Unusual clinical course Background: Pyoderma gangrenosum (PG) is a neutrophilic inflammatory disease associated with inflammatory and autoimmune conditions and malignancies. Previously identified links between PG and cancer have included hematological malignancies, solid-organ tumors such as gastric adenocarcinoma, and breast cancer. While specific histologic subtypes of breast cancer such as ductal carcinoma have been associated with PG of the extremities, the literature is limited on the association between PG and cutaneous metastatic lobular carcinoma. Case Report: We describe the case of an 84-year-old woman with recurrent cutaneous metastatic lobular carcinoma of the left anterior chest with concurrent pyoderma gangrenosum on her bilateral lower extremities. The patient was initially diagnosed with lobular carcinoma of the breast and underwent a left breast mastectomy and was in remission. One year later, she developed 2 lower-extremity ulcerations, which at the time were attributed to an injury and underlying venous stasis. She was referred to a wound care clinic, where the lesions worsened with surgical debridement. Six years later, she presented to the dermatology clinic with a rash on her chest wall and worsening of the ulcerations on her ankles bilaterally. Biopsies revealed lobular carcinoma metastatic to the skin of her anterior chest wall and histopathology consistent with pyoderma gangrenosum on her ankles. Conclusions: This case demonstrates a unique presentation of worsening pyoderma gangrenosum due to metastatic malignancy in conjunction with a cutaneous manifestation of lobular carcinoma.
C1 [Sutton, Sarah; Haran, Kathryn] Univ Nevada, Sch Med, Reno, NV USA.
   [Mullins, Amanda] Diagnost Pathol Medial Grp, Dept Dermatopathol, Sacramento, CA USA.
   [Lamerson, Cindy] Nevada Ctr Dermatol, Dept Dermatol, Reno, NV 89511 USA.
C3 Nevada System of Higher Education (NSHE); University of Nevada Reno
RP Lamerson, C (corresponding author), Nevada Ctr Dermatol, Dept Dermatol, Reno, NV 89511 USA.
EM saxkw@sbcglobal.net
OI Haran, Kathryn/0000-0001-8166-4826
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NR 18
TC 1
Z9 1
U1 0
U2 0
PU INT SCIENTIFIC INFORMATION, INC
PI MELVILLE
PA 150 BROADHOLLOW RD, STE 114, MELVILLE, NY 11747 USA
EI 1941-5923
J9 AM J CASE REP
JI Am. J. Case Rep.
PD MAR 12
PY 2024
VL 25
AR e942488
DI 10.12659/A1CR.942488
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA LJ3K0
UT WOS:001186387400001
PM 38531543
DA 2025-06-01
ER

PT J
AU Kamada, T
   Watanabe, H
   Furuta, T
   Terao, S
   Maruyama, Y
   Kawachi, H
   Kushima, R
   Chiba, T
   Haruma, K
AF Kamada, Tomoari
   Watanabe, Hidenobu
   Furuta, Takahisa
   Terao, Shuichi
   Maruyama, Yasuhiko
   Kawachi, Hiroshi
   Kushima, Ryoji
   Chiba, Tsutomu
   Haruma, Ken
TI Diagnostic criteria and endoscopic and histological findings of
   autoimmune gastritis in Japan
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Autoimmune gastritis; Type A gastritis; Diagnostic criteria; Early-stage
   AIG; Corpus-predominant atrophy
ID ATROPHIC BODY GASTRITIS; PERNICIOUS-ANEMIA; THYROID-DISEASE; CANCER;
   CELLS; RISK; AUTOANTIBODIES; MANAGEMENT
AB The Japanese diagnostic criteria for autoimmune gastritis (AIG) were established by the "Study Group on the establishment of diagnostic criteria for type A gastritis," which is related to a workshop associated with the Japan Gastroenterological Endoscopy Society (JGES) and the Committee of AIG Research Group (CARP). The criteria were set as follows: the cases of confirmed diagnosis are patients in whom either the endoscopic or histological findings, or both, meet the requirements for AIG and who are confirmed to be positive for gastric autoantibodies (either anti-parietal cell or anti-intrinsic factor antibodies, or both). The presentation of endoscopic findings of early-stage AIG in the diagnostic criteria was withheld owing to the need for further accumulation and characterization of endoscopic clinical data. Therefore, diagnosis of early-stage AIG only requires histological confirmation and gastric autoantibody positivity. Suspected cases are patients in whom either the endoscopic or histological findings, or both, meet only the requirements for AIG. Histological findings only meet the requirements for early stage. AIG has been underdiagnosed in the past, but our study group's newly proposed diagnostic criteria will enable a more accurate and early diagnosis of AIG. The criteria can be used to stratify patients into various high-risk groups for gastric tumors and pernicious anemia. They would allow the establishment of an appropriate surveillance system in the coming years. Nevertheless, issues such as establishing the endoscopic findings of early-stage AIG and obtaining Japanese insurance coverage for gastric autoantibody tests require attention.
C1 [Kamada, Tomoari] Kawasaki Med Sch, Dept Hlth Care Med, Gen Med Ctr, 2-6-1,Nakasange,Kita Ku, Okayama 7008505, Japan.
   [Watanabe, Hidenobu] Pathol & Cytol Labs Japan, Tokyo, Japan.
   [Furuta, Takahisa] Hamamatsu Univ Sch Med, Ctr Clin Res, Hamamatsu, Japan.
   [Terao, Shuichi] Kakogawa Cent City Hosp, Dept Gastroenterol, Kakogawa, Japan.
   [Maruyama, Yasuhiko] Fujieda Municipal Gen Hosp, Dept Gastroenterol, Fujieda, Japan.
   [Kawachi, Hiroshi] Japanese Fdn Canc Res, Canc Inst Hosp, Dept Pathol, Tokyo, Japan.
   [Kushima, Ryoji] Shiga Univ Med Sci, Dept Pathol, Otsu, Japan.
   [Chiba, Tsutomu] Kansai Elect Power Hosp, Osaka, Japan.
   [Haruma, Ken] Kawasaki Med Sch, Dept Gen Internal Med 2, Kurashiki, Japan.
C3 Hamamatsu University School of Medicine; Japanese Foundation for Cancer
   Research; Shiga University of Medical Science; Kawasaki Medical School
RP Kamada, T (corresponding author), Kawasaki Med Sch, Dept Hlth Care Med, Gen Med Ctr, 2-6-1,Nakasange,Kita Ku, Okayama 7008505, Japan.
EM tkamada@med.kawasaki-m.ac.jp
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NR 70
TC 25
Z9 28
U1 3
U2 18
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD MAR
PY 2023
VL 58
IS 3
BP 185
EP 195
DI 10.1007/s00535-022-01954-9
EA MAR 2023
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9T0TH
UT WOS:000940900900001
PM 36855000
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Koukourakis, MI
   Kambouromiti, G
   Pitsiava, D
   Tsousou, P
   Tsiarkatsi, M
   Kartalis, G
AF Koukourakis, Michael I.
   Kambouromiti, Georgia
   Pitsiava, Dimitra
   Tsousou, Pelagia
   Tsiarkatsi, Maria
   Kartalis, George
TI Serum C-reactive Protein (CRP) Levels in Cancer Patients are Linked with
   Tumor Burden and are Reduced by Anti-hypertensive Medication
SO INFLAMMATION
LA English
DT Article
DE CRP; cancer; hypertension; coronary disease; obesity
ID COLORECTAL-CANCER; GASTRIC-CANCER; BLOOD-PRESSURE; INTERLEUKIN-6; CELLS;
   RISK; HYPERTENSION; APOPTOSIS; SURVIVAL; BINDS
AB High levels of CRP relate with advanced disease and poor prognosis of cancer patients. CRP serum levels were measured in 684 cancer patients who had undergone complete surgery or inoperable patients. Patients with inoperable tumors had significantly higher CRP levels (1.21 +/- 2.2 vs. 0.40 +/- 0.4 mg/dL; p < 0.0001). No association with gender, diabetes, autoimmune disease, thyroid disease or allergy was noted. Significantly higher CRP levels were noted in operated patients with hypertension (0.55 +/- 0.5 vs. 0.35 +/- 0.4; p = 0.001), coronary disease (0.73 +/- 0.8 vs. 0.39 +/- 0.4; p = 0.01) and obesity (0.51 +/- 0.5 vs. 0.37 +/- 0.4; p = 0.04). On the contrary, analysis in the group of inoperable patients showed that hypertensive patients had significantly lower CRP levels (0.64 +/- 1.0 vs. 1.36 +/- 2.4; p = 0.008). Although the tumor itself is the main factor defining increased CRP levels in cancer patients, hypertension, coronary disease and obesity are also linked with high CRP levels. Anti-hypertensive drugs appear as potent suppressors of the tumor-induced CRP production.
C1 [Koukourakis, Michael I.; Tsousou, Pelagia; Tsiarkatsi, Maria] Democritus Univ Thrace, Univ Hosp Alexandroupolis, Dept Radiotherapy Oncol, Alexandroupolis 68100, Greece.
   [Kambouromiti, Georgia] Democritus Univ Thrace, Univ Hosp Alexandroupolis, Dept Biochem, Alexandroupolis 68100, Greece.
   [Pitsiava, Dimitra; Kartalis, George] Democritus Univ Thrace, Univ Hosp Alexandroupolis, Dept Internal Med, Alexandroupolis 68100, Greece.
C3 Democritus University of Thrace; Democritus University of Thrace;
   Democritus University of Thrace
RP Koukourakis, MI (corresponding author), Democritus Univ Thrace, Univ Hosp Alexandroupolis, Dept Radiotherapy Oncol, Alexandroupolis 68100, Greece.
EM targ@her.forthnet.gr
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NR 41
TC 25
Z9 26
U1 0
U2 6
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0360-3997
EI 1573-2576
J9 INFLAMMATION
JI Inflammation
PD JUN
PY 2009
VL 32
IS 3
BP 169
EP 175
DI 10.1007/s10753-009-9116-4
PG 7
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA 445YZ
UT WOS:000266088700005
PM 19373547
DA 2025-06-01
ER

PT J
AU Hassan, MM
   Phan, A
   Li, D
   Dagohoy, CG
   Leary, C
   Yao, JC
AF Hassan, Manal M.
   Phan, Alexandria
   Li, Donghui
   Dagohoy, Cecile G.
   Leary, Colleen
   Yao, James C.
TI Risk factors associated with neuroendocrine tumors: A US-based
   case-control study
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE carcinoids; risk factors; epidemiology; case-control; NET
ID BOWEL CARCINOID-TUMOR; SMALL-INTESTINE; AUTOIMMUNE GASTRITIS; CANCER;
   DIAGNOSIS; HEPATITIS; PATIENT
AB Carcinoids are rare neuroendocrine tumors (NETs); however, their incidence has significantly increased in the United States over the past 30 years. Little is known about the epidemiology of these cancers and their associated risk factors. We evaluated the independent effects of multiple risk factors associated with NETs arising at 5 disease sites (small intestine, stomach, lung, pancreas and rectum). We conducted a retrospective, hospital-based, case-control study involving 740 patients with histologically confirmed NETs and 924 healthy controls. Information on different risk factors was collected, and unconditional logistic regression analysis was used to determine adjusted odds ratios (AORs) and 95% confidence interval (CI) by the maximum-likelihood method. Smoking and alcohol consumption were not associated with NETs development in either men or women. However, a family history of cancer was a significant risk factor for all NETs. A long-term history of diabetes mellitus was a significant risk factor for gastric NETs (AOR = 5.6; 95% CI, 2.1-14.5), particularly in women (AOR = 8.4; 95% CI, 1.9-38.1). Diabetes modified the risk among women with a positive family history of cancer for the development of gastric NETs (AOR = 52.2; 95% CI, 5.5-491.5). Our results suggest that the risk of NETs may mostly explained by genetic factors. The increased risk of gastric NETs in women with both diabetes and a positive family history of cancer suggest that women may have a greater genetic susceptibility to NETs than men. (c) 2008 Wiley-Liss, Inc.
C1 [Hassan, Manal M.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Unit 426, Houston, TX 77030 USA.
C3 University of Texas System; UTMD Anderson Cancer Center
RP Hassan, MM (corresponding author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Unit 426, 1515 Holcombe Bldg, Houston, TX 77030 USA.
EM mhassan@mdanderson.org
OI Yao, James/0000-0002-1875-3962
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NR 34
TC 165
Z9 174
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD AUG 15
PY 2008
VL 123
IS 4
BP 867
EP 873
DI 10.1002/ijc.23529
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 328SL
UT WOS:000257818000017
PM 18491401
OA Bronze
DA 2025-06-01
ER

PT J
AU Díaz-Alberola, I
   Espuch-Oliver, A
   Fernández-Segovia, F
   López-Nevot, MA
AF Diaz-Alberola, Irene
   Espuch-Oliver, Andrea
   Fernandez-Segovia, Francisco
   Lopez-Nevot, Miguel angel
TI Possible Role of Cytomegalovirus in Gastric Cancer Development and
   Recurrent Macrolide-Resistant Campylobacter jejuni Infection in
   Common Variable Immunodeficiency: A Case Report and Literature
   Discussion
SO MICROORGANISMS
LA English
DT Review
DE common variable immunodeficiency; CVID; infections; cytomegalovirus;
   Campylobacter jejuni; gastric cancer; case report
ID PATIENT
AB Common variable immunodeficiency (CVID) is the most common symptomatic immunodeficiency in adults. It comprises a group of syndromes whose etiology involves genetic, epigenetic, microbiota, and environmental factors. We present the case of a 46-year-old Caucasian male patient with CVID and an immune dysregulation phenotype. The particular elements of the case consisted of an atypical clinical course, which undoubtedly demonstrates the great variability of clinical manifestations that these types of patients can suffer from, including bacterial and viral infections, autoimmune phenomena, and neoplasia. Notably, the patient suffered from recurrent gastrointestinal infection with macrolide-resistant Campylobacter jejuni and gastroduodenal disease and viraemia by cytomegalovirus (CMV). In addition, CMV was postulated as the main pro-oncogenic factor contributing to the development of early-onset intestinal-type gastric adenocarcinoma, for which the patient underwent gastrectomy. The patient's evolution was difficult, but finally, as a result of the multidisciplinary approach, clinical stabilization and improvement in his quality of life were achieved. Based on our brief literature review, this is the first reported case of this clinical complexity. Our experience could help with the management of future patients with CVID and may also update current epidemiological data on CVID.
C1 [Diaz-Alberola, Irene; Lopez-Nevot, Miguel angel] Hosp Univ Virgen Nieves, Serv Anal Clin Inmunol, Granada 18014, Spain.
   [Diaz-Alberola, Irene; Fernandez-Segovia, Francisco; Lopez-Nevot, Miguel angel] Inst Invest Biosanit Granada Ibs Granada, Granada 18016, Spain.
   [Espuch-Oliver, Andrea] Hosp Univ Torrecardenas, Serv Anal Clin, Almeria 04009, Spain.
   [Fernandez-Segovia, Francisco] Hosp Univ Clin San Cecilio, Serv Anat Patol, Granada 18016, Spain.
   [Lopez-Nevot, Miguel angel] Univ Granada, Dept Bioquim Biol Mol & Inmunol 3, Granada 18012, Spain.
C3 Hospital Universitario Virgen de las Nieves; Instituto de Investigacion
   Biosanitaria IBS Granada; Hospital Torrecardenas; University of Granada
RP López-Nevot, MA (corresponding author), Hosp Univ Virgen Nieves, Serv Anal Clin Inmunol, Granada 18014, Spain.; López-Nevot, MA (corresponding author), Inst Invest Biosanit Granada Ibs Granada, Granada 18016, Spain.; López-Nevot, MA (corresponding author), Univ Granada, Dept Bioquim Biol Mol & Inmunol 3, Granada 18012, Spain.
OI Fernandez Segovia, Francisco/0000-0001-7558-0116; DIAZ ALBEROLA,
   IRENE/0000-0002-8458-612X; Lopez Nevot, Miguel Angel/0000-0002-3465-6062
FU Palex Medical S.A
FX This study was partially financed by Palex Medical S.A.
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NR 57
TC 0
Z9 0
U1 2
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD JUN
PY 2024
VL 12
IS 6
AR 1078
DI 10.3390/microorganisms12061078
PG 11
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA WU1M8
UT WOS:001257296500001
PM 38930460
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Venerito, M
   Radünz, M
   Reschke, K
   Reinhold, D
   Frauenschläger, K
   Jechorek, D
   Di Mario, F
   Malfertheiner, P
AF Venerito, M.
   Raduenz, M.
   Reschke, K.
   Reinhold, D.
   Frauenschlaeger, K.
   Jechorek, D.
   Di Mario, F.
   Malfertheiner, P.
TI Autoimmune gastritis in autoimmune thyroid disease
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; PARIETAL-CELL ANTIBODIES; ATROPHIC BODY
   GASTRITIS; PERNICIOUS-ANEMIA; RISK-FACTORS; CANCER; PREVALENCE; OLGA;
   DIAGNOSIS; GERMANY
AB BackgroundAutoimmune gastritis leads to oxyntic gastric atrophy, a condition at increased risk for gastric cancer. Autoimmune gastritis in conjunction with autoimmune thyroid disease has been reported previously.
   AimIn a case-control study in patients with autoimmune thyroid disease to evaluate the usefulness of serum pepsinogens for the identification of oxyntic gastric atrophy, and to determine the relationship of Helicobacter pylori with oxyntic gastric atrophy.
   MethodsPatients with autoimmune thyroid disease (cases) and goitre (controls) were prospectively enrolled in the study. Pepsinogen (PG) I levels 25g/mL and PG I/II ratio 3 were indicative for oxyntic gastric atrophy. Antibodies against H.pylori, CagA and parietal cells were also determined. Esophagogastroduodenoscopy with biopsies was offered to patients with serological oxyntic gastric atrophy.
   ResultsIn total, 34 autoimmune thyroid disease patients and 30 controls were enrolled. Serological oxyntic gastric atrophy was present only in autoimmune thyroid disease patients (8/34, 23.5%, OR 8.3, 95% CI=1.9-36.2). In all eight patients oxyntic gastric atrophy was confirmed by histology. OLGA stage I, II, III and IV was described in 0%, 33%, 50% and 17% of the cases, respectively. About, 89% and 11% of oxyntic gastric atrophy patients were seropositive for antibodies against parietal cells or H.pylori infection, respectively. Gastric atrophy involved the angulus/antrum in 50% of patients with autoimmune gastritis.
   ConclusionsThe seroprevalence of oxyntic gastric atrophy is high in patients with autoimmune thyroid disease, and testing of serum pepsinogens should be included in the clinical assessment of these patients. H.pylori infection is unlikely to be a principal factor in the pathogenesis of oxyntic gastric atrophy in patients with autoimmune thyroid disease. In autoimmune gastritis, gastric atrophy can spread from the oxyntic towards the antral mucosa.
C1 [Venerito, M.; Raduenz, M.; Malfertheiner, P.] Otto Von Guericke Univ, Dept Gastroenterol Hepatol & Infect Dis, D-39120 Magdeburg, Germany.
   [Reschke, K.] Otto Von Guericke Univ, Dept Nephrol Hypertens Diabet & Endocrinol, D-39120 Magdeburg, Germany.
   [Reinhold, D.] Otto Von Guericke Univ, Inst Mol & Clin Immunol, D-39120 Magdeburg, Germany.
   [Frauenschlaeger, K.; Jechorek, D.] Otto Von Guericke Univ, Inst Pathol, D-39120 Magdeburg, Germany.
   [Di Mario, F.] Univ Parma, Dept Med, Gastroenterol Unit, I-43100 Parma, Italy.
C3 Otto von Guericke University; Otto von Guericke University; Otto von
   Guericke University; Otto von Guericke University; University of Parma
RP Malfertheiner, P (corresponding author), Otto Von Guericke Univ, Dept Gastroenterol Hepatol & Infect Dis, Leipziger Str 44, D-39120 Magdeburg, Germany.
EM peter.malfertheiner@med.ovgu.de
RI Malfertheiner, Peter/AEZ-6553-2022; Venerito, Marino/AAF-4493-2020;
   Jechorek, Doerthe/J-4716-2014
OI Malfertheiner, Peter/0000-0001-8439-9036; Jechorek,
   Doerthe/0000-0002-1480-5200; Venerito, Prof. Dr. med.
   Marino/0000-0001-8581-0974
FU Biohit Oyj
FX Prof. Malfertheiner has served as a speker for Takeda, AstraZeneca and
   Reckitt Benckiser. Prof. Di Mario received research support from Biohit
   Oyj. All other authors have no personal interests to disclose.
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NR 34
TC 31
Z9 35
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD APR
PY 2015
VL 41
IS 7
BP 686
EP 693
DI 10.1111/apt.13097
PG 8
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA CD4IO
UT WOS:000351046200008
PM 25648057
OA Bronze
DA 2025-06-01
ER

PT J
AU Dickman, R
   Shaklai, M
   Lapidot, M
   Okon, E
   Zandbank, J
   Fraser, GM
   Niv, Y
AF Dickman, R
   Shaklai, M
   Lapidot, M
   Okon, E
   Zandbank, J
   Fraser, GM
   Niv, Y
TI Pernicious anemia, gastric carcinoid, and autoimmune thrombocytopenia in
   a young woman
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE autoimmune thrombocytopenia; gastric carcinoid; atrophic gastritis;
   enterochromaffin cell
ID ENTEROCHROMAFFIN-LIKE CELL; TUMORS; MANAGEMENT; DISEASE; GROWTHS
AB The association between gastric carcinoid tumors and pernicious anemia is well recognized. Such turners occur in the presence of achlorhydria, chronic atrophic gastritis, hypergastrinemia, and enterochromaffin-like cell hyperplasia. In this case report, a 29-year-old woman with pernicious anemia and autoimmune thrombocytopenia who developed gastric carcinoid tumors of the gastric body is described. This is the second description of pernicious anemia associated with autoimmune thrombocytopenia. This association in a young woman together with the therapeutic options and decisions that were taken in the treatment of the patient are discussed.
C1 Tel Aviv Univ, Sackler Sch Med, Rabin Med Sch, Dept Gastroenterol, Petach Tikva, Israel.
   Tel Aviv Univ, Sackler Sch Med, Rabin Med Sch, Dept Hematol, Petach Tikva, Israel.
   Tel Aviv Univ, Sackler Sch Med, Rabin Med Sch, Dept Endocrinol, Petach Tikva, Israel.
   Tel Aviv Univ, Sackler Sch Med, Rabin Med Sch, Dept Pathol, Petach Tikva, Israel.
C3 Tel Aviv University; Sackler Faculty of Medicine; Tel Aviv University;
   Sackler Faculty of Medicine; Tel Aviv University; Sackler Faculty of
   Medicine; Tel Aviv University; Sackler Faculty of Medicine
RP Niv, Y (corresponding author), Tel Aviv Univ, Sackler Sch Med, Rabin Med Sch, Dept Gastroenterol, Belinson Campus, Petach Tikva, Israel.
RI Lapidot, Moshe/HDL-8093-2022
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NR 19
TC 5
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0192-0790
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD APR
PY 2000
VL 30
IS 3
BP 299
EP 302
DI 10.1097/00004836-200004000-00019
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 301XU
UT WOS:000086336500018
PM 10777192
DA 2025-06-01
ER

PT J
AU Song, MY
   Liang, J
   Wang, LY
   Li, W
   Jiang, SL
   Xu, S
   Tang, L
   Du, QC
   Liu, GX
   Meng, HN
   Zhai, DC
   Shi, SH
   Yang, YY
   Zhang, L
   Zhang, B
AF Song, Meiying
   Liang, Jie
   Wang, Luoyang
   Li, Wei
   Jiang, Suli
   Xu, Shuo
   Tang, Lei
   Du, Qiaochu
   Liu, Guixian
   Meng, Haining
   Zhai, Dongchang
   Shi, Shangheng
   Yang, Yanyan
   Zhang, Li
   Zhang, Bei
TI IL-17A functions and the therapeutic use of IL-17A and IL-17RA targeted
   antibodies for cancer treatment
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Interleukin-17A; Cancer; Secukinumab; Ixekizumab; Brodalumab
ID DELTA-T-CELLS; EPITHELIAL-MESENCHYMAL TRANSITION; INTERLEUKIN 17
   RECEPTOR; PROMOTES TUMOR-GROWTH; LUNG-CANCER; PLAQUE PSORIASIS;
   PROSTATE-CANCER; POOR-PROGNOSIS; TH17 CELLS; EXPRESSION
AB Interleukin 17A (IL-17A) is a major member of the IL-17 cytokine family and is produced mainly by T helper 17 (Th17) cells. Other cells such as CD8+ T cells, & gamma;& delta; T cells, natural killer T cells and innate lymphoid-like cells can also produce IL-17A. In healthy individuals, IL-17A has a host-protective capacity, but excessive elevation of IL17A is associated with the development of autoimmune diseases and cancer. Monoclonal antibodies (mAbs) targeting IL-17A (e.g., ixekizumab and secukinumab) or IL-17A receptor (IL-17RA) (e.g., brodalumab) would be investigated as potential treatments for these diseases. Currently, the application of IL-17A-targeted drugs in autoimmune diseases will provide new ideas for the treatment of tumors, and its combined application with immune checkpoint inhibitors has become a research hotspot. This article reviews the mechanism of action of IL17A and the application of anti-IL-17A antibodies, focusing on the research progress on the mechanism of action and therapeutic blockade of IL-17A in various tumors such as colorectal cancer (CRC), lung cancer, gastric cancer and breast cancer. Moreover, we also include the results of therapeutic blockade in the field of cancer as well as recent advances in the regulation of IL-17A signaling.
C1 [Song, Meiying; Liang, Jie; Wang, Luoyang; Li, Wei; Jiang, Suli; Xu, Shuo; Du, Qiaochu; Liu, Guixian; Yang, Yanyan; Zhang, Li; Zhang, Bei] Qingdao Univ, Med Coll, Dept Immunol, 308 Ningxia Rd, Qingdao 266071, Shandong, Peoples R China.
   [Meng, Haining] Qingdao Univ, Sch Emergency Med, Med Coll, Qingdao 266071, Shandong, Peoples R China.
   [Tang, Lei; Zhai, Dongchang] Qingdao Univ, Sch Basic Med Coll, Dept Special Med, Qingdao 266071, Shandong, Peoples R China.
   [Shi, Shangheng] Qingdao Univ, Sch Clin Med, Dept Liver Transplantat, Qingdao 266071, Shandong, Peoples R China.
C3 Qingdao University; Qingdao University; Qingdao University; Qingdao
   University
RP Zhang, B (corresponding author), Qingdao Univ, Med Coll, Dept Immunol, 308 Ningxia Rd, Qingdao 266071, Shandong, Peoples R China.
EM zhangbei124@aliyun.com
RI LIU, Guixian/ISB-0842-2023; tang, lei/JCO-4117-2023; li,
   tao/JVO-9006-2024; Wang, Luoyang/AAG-3348-2019
OI Wang, Luoyang/0000-0002-1396-0057
FU Natural Science Foundation of Shandong Province, China
   [22-3-7-smjk-7-nsh]; Natural Science Foundation of Qingdao, Shandong; 
   [ZR2022MH029]
FX This work was supported by the Natural Science Foundation of Shandong
   Province, China (grant number ZR2022MH029) and the Natural Science
   Foundation of Qingdao, Shandong (grant number 22-3-7-smjk-7-nsh) .
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NR 183
TC 21
Z9 23
U1 5
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2023
VL 123
AR 110757
DI 10.1016/j.intimp.2023.110757
EA AUG 2023
PG 17
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA Q5IG9
UT WOS:001057850200001
PM 37579542
DA 2025-06-01
ER

PT J
AU Wan, J
   Wu, YQ
   Ji, XY
   Huang, L
   Cai, W
   Su, ZL
   Wang, SJ
   Xu, HX
AF Wan, Jie
   Wu, Yinqiu
   Ji, Xiaoyun
   Huang, Lan
   Cai, Wei
   Su, Zhaoliang
   Wang, Shengjun
   Xu, Huaxi
TI IL-9 and IL-9-producing cells in tumor immunity
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Review
DE IL-9; Th9; Tc9; Mast cells; Tumor; Tumor diseases
ID CD8(+) T-CELLS; MAST-CELLS; TH9 CELLS; ANTITUMOR IMMUNITY;
   GASTRIC-CANCER; TC9 CELLS; TGF-BETA; DIFFERENTIATION; EXPRESSION;
   PROMOTES
AB Interleukin (IL)-9 belongs to the IL-2R gamma c chain family and is a multifunctional cytokine that can regulate the function of many kinds of cells. It was originally identified as a growth factor of T cells and mast cells. In previous studies, IL-9 was mainly involved in the development of allergic diseases, autoimmune diseases and parasite infections. Recently, IL-9, as a double-edged sword in the development of cancers, has attracted extensive attention. Since T-helper 9 (Th9) cell-derived IL-9 was verified to play a powerful antitumor role in solid tumors, an increasing number of researchers have started to pay attention to the role of IL-9-skewed CD8(+) T (Tc9) cells, mast cells and V delta 2 T cell-derived IL-9 in tumor immunity. Here, we review recent studies on IL-9 and several kinds of IL-9-producing cells in tumor immunity to provide useful insight into tumorigenesis and treatment.
C1 [Wan, Jie; Wu, Yinqiu; Ji, Xiaoyun; Huang, Lan; Cai, Wei; Su, Zhaoliang; Wang, Shengjun; Xu, Huaxi] Jiangsu Univ, Dept Immunol, Zhenjiang 212013, Jiangsu, Peoples R China.
   [Su, Zhaoliang] Jiangsu Univ, China Int Genom Res Ctr IGRC, Zhenjiang 212013, Jiangsu, Peoples R China.
   [Wang, Shengjun] Jiangsu Univ, Dept Lab Med, Affiliated Peoples Hosp, Zhenjiang 212001, Jiangsu, Peoples R China.
C3 Jiangsu University; Jiangsu University; Jiangsu University
RP Xu, HX (corresponding author), Jiangsu Univ, Dept Immunol, Zhenjiang 212013, Jiangsu, Peoples R China.
EM xuhx@ujs.edu.cn
RI SU, Zhaoliang/ABD-9062-2021; cai, wei/JPY-3260-2023
OI Huang, Lan/0009-0001-1533-6792; Xu, Huaxi/0000-0002-2568-7393
FU National Natural Science Foundation of China [81771756, 81871244];
   Social development project of Jiangsu Province [BE2016716]; Postdoctoral
   Foundation of Jiangsu Province [1601002C]
FX This work was supported by National Natural Science Foundation of China
   (grant nos. 81771756, 81871244), Social development project of Jiangsu
   Province (grant no. BE2016716), the Postdoctoral Foundation of Jiangsu
   Province (grant no.1601002C).
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NR 98
TC 60
Z9 66
U1 2
U2 17
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1478-811X
J9 CELL COMMUN SIGNAL
JI Cell Commun. Signal.
PD MAR 30
PY 2020
VL 18
IS 1
AR 50
DI 10.1186/s12964-020-00538-5
PG 11
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA KZ0EQ
UT WOS:000522945900002
PM 32228589
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Lahner, E
   Capasso, M
   Carabotti, M
   Annibale, B
AF Lahner, Edith
   Capasso, Marina
   Carabotti, Marilia
   Annibale, Bruno
TI Incidence of cancer (other than gastric cancer) in pernicious anaemia: A
   systematic review with meta-analysis
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Autoimmune gastritis; Biliary tract cancer; Cancer risk; Leukaemia;
   Lymphoma; Meta-analysis; Pernicious anaemia; Systematic review
ID UPPER GASTROINTESTINAL-TRACT; FOLLOW-UP; PROMOTER METHYLATION; POSSIBLE
   ASSOCIATION; AUTOIMMUNE-DISEASES; ATROPHIC GASTRITIS; COLORECTAL-CANCER;
   SERUM PEPSINOGENS; MULTIPLE-MYELOMA; FOLATE-DEFICIENT
AB Background: Pernicious anaemia (PA) is associated with increased gastric cancer risk, but the evidence is conflicting regarding the associated risk of other cancers.
   Aim: To systematically determine the incidence rates of gastro-intestinal cancers other than gastric cancers (GI-other-than-GC) and non-gastrointestinal cancers (non-GIC) in PA adults, globally and per tumour site, and the risk associated with PA for GI-other than GC and non-GIC. Methods: Studies of PA patients reporting the incidence of GI-other-than-GCs and non-GICs were identified with MEDLINE (PubMed)-EMBASE (from first date available to April 2017). A meta-analysis of annual cancer incidence rates was performed. The outcome was the cumulative incidence of GI-other-than-GCs and non-GICs (ratio between the numbers of new cancer cases identified during the follow-up period and the number of PA patients) and the incidence rate expressed as the rate of events-per-time-unit (person-years).
   Results: Of 82,257 PA patients, the pooled incidence rates/100 person-years for non-GCs and non-GICs of 0.27 (95% CI: 0.16-0.42) and 0.23 (95% CI: 0.22-0.25) were calculated by meta-analysis. Compared to the GLOBOCAN data for the general population from the countries of the included studies, the meta-analysis showed an overall relative risk (RR) of cancer in PA of 0.68 (95% CI: 0.48-0.95). PA patients had a lower RR of colorectal, breast, liver, oesophageal, lung, thyroid, ovary, non-melanoma skin and kidney cancers but had a higher RR of biliary tract cancer (1.81: 1.21-2.70), multiple myeloma (2.83: 1.76-4.55), Hodgkin's lymphoma (3.0: 1.35-6.68), non-Hodgkin's lymphoma (2.08: 1.58-2.75), and leukaemia (1.56: 1.16-2.12).
   Conclusion: An overall lower RR of cancers-other-than-gastric-cancer in PA patients but an increased RR of biliary tract cancers and haematological malignancies was observed. (c) 2018 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Lahner, Edith; Capasso, Marina; Carabotti, Marilia; Annibale, Bruno] Sapienza Univ Rome, Med Surg Dept Clin Sci & Translat Med, Rome, Italy.
C3 Sapienza University Rome
RP Lahner, E (corresponding author), Sapienza Univ Rome, Dept Med Surg Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM edith.lahner@uniroma1.it
RI Lahner, Edith/AAM-1039-2021; Annibale, Bruno/A-5372-2008
FU Sapienza University
FX This paper was funded in part by a grant from Sapienza University, funds
   of Oncology Doctorate 2016.
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NR 62
TC 19
Z9 23
U1 0
U2 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD AUG
PY 2018
VL 50
IS 8
BP 780
EP 786
DI 10.1016/j.dld.2018.05.012
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GN8GK
UT WOS:000439397500006
PM 29887343
DA 2025-06-01
ER

PT J
AU Song, M
   Camargo, MC
   Derkach, A
   Rabkin, CS
   Engels, EA
AF Song, Minkyo
   Camargo, M. Constanza
   Derkach, Andriy
   Rabkin, Charles S.
   Engels, Eric A.
TI Associations Between Autoimmune Conditions and Gastric Cancer Risk Among
   Elderly Adults in the United States
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID RED-CELL APLASIA
AB INTRODUCTION: Pernicious anemia (PA) is a risk factor for gastric cancer. Other autoimmune conditions may also contribute. METHODS: In a case-control study, we evaluated 47 autoimmune conditions among 39,125 gastric cancers and 200,000 cancer-free controls. RESULTS: Six conditions were associated with increased gastric cancer risk (range of adjusted odds ratios: 1.28-1.93, P < 0.05): PA, membranous nephropathy, primary biliary cirrhosis, pure red cell aplasia, primary sclerosing cholangitis, and Graves disease. PA was associated with 8 other autoimmune conditions (adjusted odds ratios: 1.57-4.54, P < 0.05). DISCUSSION: Autoimmune conditions associated with gastric cancer or PA may reflect effects of autoimmune gastritis or other carcinogenic pathways.
C1 [Song, Minkyo; Camargo, M. Constanza; Derkach, Andriy; Rabkin, Charles S.; Engels, Eric A.] US Dept HHS, Div Canc Epidemiol & Genet, NCI, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); NIH National Cancer Institute- Division of Cancer Epidemiology &
   Genetics
RP Song, M (corresponding author), US Dept HHS, Div Canc Epidemiol & Genet, NCI, NIH, Bethesda, MD 20892 USA.
EM minkyo.song@nih.gov
RI Camargo, M. Constanza/R-9891-2016; Song, Minkyo/AAE-9095-2020
OI Song, Minkyo/0000-0002-9412-2871; Derkach, Andriy/0000-0003-2178-8493
FU Intramural Research Program of the National Cancer Institute; National
   Cancer Institute [ZIACP010150] Funding Source: NIH RePORTER
FX This study was supported by the Intramural Research Program of the
   National Cancer Institute.
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NR 14
TC 10
Z9 10
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD MAR
PY 2022
VL 117
IS 3
BP 486
EP 490
DI 10.14309/ajg.0000000000001622
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA ZM1YE
UT WOS:000764159800026
PM 35029169
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Zhang, XJ
   Niu, MK
   Li, TY
   Wu, YZ
   Gao, JN
   Yi, M
   Wu, KM
AF Zhang, Xiaojun
   Niu, Mengke
   Li, Tianye
   Wu, Yuze
   Gao, Jinnan
   Yi, Ming
   Wu, Kongming
TI S100A8/A9 as a risk factor for breast cancer negatively regulated by
   DACH1
SO BIOMARKER RESEARCH
LA English
DT Article
DE S100A8; S100A9; DACH1; Breast cancer; Prognosis; Biomarker
ID FATE DETERMINATION FACTOR; INHIBITS CYCLIN D1; LUNG ADENOCARCINOMA;
   PROGNOSTIC BIOMARKER; BISPECIFIC ANTIBODY; EXPRESSION PROFILE;
   GASTRIC-CANCER; GENE NETWORK; TUMOR-GROWTH; 6 FAMILY
AB Background S100A8 and S100A9 are members of Ca2+-binding EF-hand superfamily, mainly expressed by macrophages and neutrophils. Limited by the poor stability of homodimers, they commonly exist as heterodimers. Beyond acting as antibacterial cytokines, S100A8/A9 is also associated with metabolic and autoimmune diseases such as obesity, diabetes, and rheumatoid arthritis. While the involvement of S100A8/A9 in breast cancer development has been documented, its prognostic significance and the precise regulatory mechanisms remain unclear.
   Methods S100A8/A9 protein in breast cancer samples was evaluated by immunohistochemistry staining with tumor tissue microarrays. The serum S100A8 concentration in patients was measured by enzyme-linked immunosorbent assay (ELISA). The S100A8 secreted by breast cancer cells was detected by ELISA as well. Pooled analyses were conducted to explore the relationships between S100A8/A9 mRNA level and clinicopathological features of breast cancer patients. Besides, the effects of S100A8/A9 and DACH1 on patient outcomes were analyzed by tissue assays. Finally, xenograft tumor assays were adopted to validate the effects of DACH1 on tumor growth and S100A8/A9 expression.
   Results The level of S100A8/A9 was higher in breast cancer, relative to normal tissue. Increased S100A8/A9 was related to poor differentiation grade, loss of hormone receptors, and Her2 positive. Moreover, elevated S100A8/A9 predicted a worse prognosis for breast cancer patients. Meanwhile, serum S100A8 concentration was upregulated in Grade 3, basal-like, and Her2-overexpressed subtypes. Additionally, the results of public databases showed S100A8/A9 mRNA level was negatively correlated to DACH1. Stable overexpressing DACH1 in breast cancer cells significantly decreased the generation of S100A8. The survival analysis demonstrated that patients with high S100A8/A9 and low DACH1 achieved the shortest overall survival. The xenograft models indicated that DACH1 expression significantly retarded tumor growth and downregulated S100A8/A9 protein abundance.
   Conclusion S100A8/A9 is remarkedly increased in basal-like and Her2-overexpressed subtypes, predicting poor prognosis of breast cancer patients. Tumor suppressor DACH1 inhibits S100A8/A9 expression. The combination of S100A8/A9 and DACH1 predicted the overall survival of breast cancer patients more preciously.
C1 [Zhang, Xiaojun; Gao, Jinnan; Wu, Kongming] Shanxi Med Univ, Tongji Shanxi Hosp, Shanxi Bethune Hosp, Hosp 3,Shanxi Acad Med Sci,Gen Surg Dept, Taiyuan, Peoples R China.
   [Niu, Mengke; Wu, Yuze; Wu, Kongming] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, Wuhan, Peoples R China.
   [Li, Tianye] Zhejiang Univ, Affiliated Hosp 2, Coll Med, Dept Gynecol, Hangzhou, Peoples R China.
   [Yi, Ming] Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Breast Surg, Hangzhou, Peoples R China.
C3 Shanxi Medical University; Huazhong University of Science & Technology;
   Zhejiang University; Zhejiang University
RP Wu, KM (corresponding author), Shanxi Med Univ, Tongji Shanxi Hosp, Shanxi Bethune Hosp, Hosp 3,Shanxi Acad Med Sci,Gen Surg Dept, Taiyuan, Peoples R China.; Wu, KM (corresponding author), Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Oncol, Wuhan, Peoples R China.; Yi, M (corresponding author), Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Breast Surg, Hangzhou, Peoples R China.
EM mingyi_onco@outlook.com; kmwu@tjh.tjmu.edu.cn
RI Li, Tianye/JZT-3021-2024; wu, Kongming/AET-0691-2022; Yi,
   Ming/AAN-4704-2020
OI Li, Tianye/0009-0003-6999-3020
FU Shanxi Province 136 Revitalization Medical Project Construction Funds
FX Not applicable.
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NR 72
TC 5
Z9 5
U1 2
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 2050-7771
J9 BIOMARK RES
JI Biomark. Res.
PD DEC 13
PY 2023
VL 11
IS 1
AR 106
DI 10.1186/s40364-023-00548-8
PG 18
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA CO7G6
UT WOS:001126248100001
PM 38093319
OA gold
DA 2025-06-01
ER

PT J
AU Hill, DG
   Ward, A
   Nicholson, LB
   Jones, GW
AF Hill, David G.
   Ward, Amy
   Nicholson, Lindsay B.
   Jones, Gareth W.
TI Emerging roles for IL-6 family cytokines as positive and negative
   regulators of ectopic lymphoid structures
SO CYTOKINE
LA English
DT Article
DE Interleukin-6; Interleukin-11; Interleukin-27; Oncostatin-M; Leukaemia
   inhibitory factor; Ectopic Lymphoid Structures; Tertiary Lymphoid
   Structures
ID TUMOR-INFILTRATING LYMPHOCYTES; CENTRAL-NERVOUS-SYSTEM; T-CELL
   INFILTRATION; ONCOSTATIN-M; B-CELLS; DENDRITIC CELLS; TH17 CELLS;
   IL-13-INDUCED INFLAMMATION; INTESTINAL INFLAMMATION; GASTRIC
   TUMORIGENESIS
AB IL-6 family cytokines display broad effects in haematopoietic and non-haematopoietic cells that regulate immune homeostasis, host defence, haematopoiesis, development, reproduction and wound healing. Dysregulation of these activities places this cytokine family as important mediators of autoimmunity, chronic inflammation and cancer. In this regard, ectopic lymphoid structures (ELS) are a pathological hallmark of many tissues affected by chronic disease. These inducible lymphoid aggregates form compartmentalised T cell and B cell zones, germinal centres, follicular dendritic cell networks and high endothelial venules, which are defining qualities of peripheral lymphoid organs. Accordingly, ELS can support local antigen-specific responses to self-antigens, alloantigens, pathogens and tumours. ELS often correlate with severe disease progression in autoimmune conditions, while tumour-associated ELS are associated with enhanced anti-tumour immunity and a favourable prognosis in cancer. Here, we discuss emerging roles for IL-6 family cytokines as regulators of ELS development, maintenance and activity and consider how modulation of these activities has the potential to aid the successful treatment of autoimmune conditions and cancers where ELS feature.
C1 [Hill, David G.; Ward, Amy; Nicholson, Lindsay B.; Jones, Gareth W.] Univ Bristol, Sch Cellular & Mol Med, Biomed Sci Bldg, Bristol BS8 1TD, Avon, England.
C3 University of Bristol
RP Jones, GW (corresponding author), Univ Bristol, Sch Cellular & Mol Med, Biomed Sci Bldg, Bristol BS8 1TD, Avon, England.
EM g.jones@bristol.ac.uk
OI Ward, Amy/0000-0002-4731-3333; Jones, Gareth/0000-0002-0125-4841
FU Versus Arthritis [20305, 22706]; National Eye Research Centre; James
   Tudor Foundation
FX GWJ and DGH are supported by grant funding from Versus Arthritis [grant
   numbers 20305, 22706] . LN and AW receive research funding from the
   National Eye Research Centre and the James Tudor Foundation.
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NR 221
TC 8
Z9 9
U1 0
U2 8
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD OCT
PY 2021
VL 146
AR 155650
DI 10.1016/j.cyto.2021.155650
EA JUL 2021
PG 14
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA TZ0YM
UT WOS:000684202400001
PM 34343865
OA Green Submitted
DA 2025-06-01
ER

PT J
AU Rao, H
   Guo, Z
   Wen, XJ
   Zeng, XL
   Wu, LQ
   Huang, L
AF Rao, Hui
   Guo, Zheng
   Wen, Xuejiao
   Zeng, Xiaoli
   Wu, Longqiu
   Huang, Li
TI Case Report: Immune checkpoint inhibitor-related vitiligo-like
   depigmentation in non-melanoma advanced cancer: A report of three cases
   and a pooled analysis of individual patient data
SO FRONTIERS IN ONCOLOGY
LA English
DT Article
DE immune checkpoint inhibitor; skin adverse events; immunotherapy;
   vitiligo-like depigmentation; case report
ID CELL LUNG-CANCER; OPEN-LABEL; STAGE-III; NIVOLUMAB; IMMUNOTHERAPY;
   MELANOMA; ATEZOLIZUMAB; AUTOIMMUNITY; CARCINOMA; THERAPY
AB BackgroundVitiligo-like depigmentation is a common skin adverse event in patients receiving immunotherapy for malignant melanoma, but has been rarely reported in patients with non-melanoma malignancies. To better understand this immune-related adverse event, we reviewed a series of cases of immunotherapy induced vitiligo-like depigmentation in patients with cancers other than malignant melanoma. Case presentationWe report three cases of vitiligo-like depigmentation after immune checkpoint inhibitor treatment in gastric adenocarcinoma, lung adenocarcinoma, and squamous cell carcinoma. The first case was treated with camrelizumab, the second was treated with QL1706 injection and sintilimab, and the third was treated with tislelizumab. Pembrolizumab, nivolumab, and ipilimumab caused the majority of vitiligo-like depigmentation, and all three of our patients experienced similar vitiligo-like depigmentation after taking other immune checkpoint inhibitors. MethodsThree patients who presented with vitiligo-like depigmentation after treatment with immune checkpoint inhibitors were selected. The clinical features, including radiological and histological examination, and the treatment process were reviewed. Eighteen previously published cases of vitiligo-like depigmentation were also used to analyze the results. The severity of vitiligo-like depigmentation in these cases was graded according to the Common Terminology Criteria for Adverse Events, version 5.0. ResultsVitiligo-like depigmentation occurred in 13 men (61.90%) and 8 women (38.10%), aged from 46 to 79 years, with an average age of 69.9 years. Of the 21 reviewed cases, vitiligo-like depigmentation was described in lung cancer (13/21, 61.90%), clear cell renal cell carcinoma (2/21, 9.52%), acute myeloid leukemia (1/21, 4.76%), cholangiocarcinoma (1/21, 4.76%), urothelial carcinoma (1/21, 4.76%), oral squamous cell carcinoma (1/21, 4.76%), esophageal squamous cell carcinoma (1/21, 4.76%), and gastric adenocarcinoma (1/21, 4.76%). The severity of vitiligo-like depigmentation after immunotherapy was unrelated to sex, age, cancer type, previous autoimmune diseases, and medication. ConclusionsVitiligo-like depigmentation is a non-specific skin adverse event in melanoma immunotherapy, but arises as a direct result of treatment with immune checkpoint inhibitors. Vitiligo-like depigmentation has an irregular location, is not limited to direct sunlight cracks, and has also been reported on hair on the head, eyelashes, and eyebrows. People without any skin or autoimmune diseases can also experience vitiligo-like depigmentation after immunotherapy; the incidence of which is irrespective of sex, age, cancer type, previous autoimmune diseases, and medication.
C1 [Rao, Hui; Wen, Xuejiao] Gannan Med Univ, Clin Med Coll 1, Ganzhou, Jiangxi, Peoples R China.
   [Guo, Zheng] Shenzhen Univ, Gen Hosp, Clin Med Acad, Int Canc Ctr,Dept Hematol & Oncol, Shenzhen, Guangdong, Peoples R China.
   [Zeng, Xiaoli; Wu, Longqiu; Huang, Li] Gannan Med Univ, Affiliated Hosp 1, Jiangxi Clin Med Res Ctr Canc, Dept Oncol, Ganzhou, Peoples R China.
C3 Gannan Medical University; Shenzhen University; Gannan Medical
   University
RP Huang, L (corresponding author), Gannan Med Univ, Affiliated Hosp 1, Jiangxi Clin Med Res Ctr Canc, Dept Oncol, Ganzhou, Peoples R China.
EM hlellen@gmu.edu.cn
RI Wang, Jinwu/AAG-4431-2021; huang, li/GXW-3191-2022
CR [Anonymous], 2017, Common terminology criteria for adverse events (ctcae) version 5.0
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NR 35
TC 4
Z9 5
U1 1
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 13
PY 2023
VL 12
AR 1099108
DI 10.3389/fonc.2022.1099108
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8D8NZ
UT WOS:000918545100001
PM 36713515
OA gold
DA 2025-06-01
ER

PT J
AU Krauth, MT
   Puthenparambil, J
   Lechner, K
AF Krauth, Maria-Theresa
   Puthenparambil, Joe
   Lechner, Klaus
TI Paraneoplastic autoimmune thrombocytopenia in solid tumors
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Autoimmune thrombocytopenia; Paraneoplastic syndrome; Solid tumors;
   Treatment; Surgery
ID RENAL-CELL CARCINOMA; PURPURA-LIKE SYNDROME; HEMOLYTIC-ANEMIA;
   BREAST-CANCER; IMMUNE THROMBOCYTOPENIA; LUNG-CANCER; GASTRIC-CANCER;
   EVANS-SYNDROME; HODGKIN LYMPHOMA; PATIENT
AB Immune-mediated hematological diseases are rare, but typical paraneoplastic syndromes. We have critically analyzed 68 published cases of an association of autoimmune thrombocytopenia (ITP) and solid cancers. Such cases occurred in a variety of cancers. They were most common in patients with lung and breast cancer, very rare in prostate cancer, but relatively common in renal cell and ovarian cancers. ITP occurred in about half of the patients concurrently with cancer, in about 25% prior to cancer and in others some time after diagnosis and treatment of cancer. In the latter patients ITP was either a sign of recurrence of cancer or had other causes. In most patients ITP responded to steroid treatment. There were only few patients who had a complete response of ITP after surgical removal or chemotherapy of the cancer and there was only one patient (ITP prior to cancer) in whom a long lasting complete remission of ITP after cancer resection could be ascribed solely to cancer resection. We believe that in patients with ITP a cancer-associated ITP has always to be considered, but an extensive search for a present or future cancer is not indicated unless there is laboratory or clinical suspicion of a malignant disease. In patients with cancer associated ITP cancer resection should be done in non-metastatic cases (after appropriate pretreatment). In metastatic cases steroids are probably the treatment of choice. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Krauth, Maria-Theresa; Puthenparambil, Joe; Lechner, Klaus] Med Univ Vienna, Div Hematol & Hemostaseol, Dept Internal Med 1, A-1090 Vienna, Austria.
C3 Medical University of Vienna
RP Krauth, MT (corresponding author), Med Univ Vienna, Div Hematol & Hemostaseol, Dept Internal Med 1, Wahringer Gurtel 18-20, A-1090 Vienna, Austria.
EM maria.krauth@meduniwien.ac.at
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NR 64
TC 64
Z9 67
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD JAN
PY 2012
VL 81
IS 1
BP 75
EP 81
DI 10.1016/j.critrevonc.2011.02.004
PG 7
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 882RG
UT WOS:000299581000007
PM 21515071
DA 2025-06-01
ER

PT J
AU Papakonstantinou, IP
   Karakousis, ND
   Andreadis, EA
AF Papakonstantinou, Ilias P.
   Karakousis, Nikolaos D.
   Andreadis, Emmanouel A.
TI Gastric neuroendocrine tumour, atrophic gastritis and autoimmune
   haemolytic anaemia: a case report and review
SO SCOTTISH MEDICAL JOURNAL
LA English
DT Review
DE Autoimmune haemolytic anaemia; gastric neuroendocrine; type-1 gastric
   carcinoid; atrophic gastritis; anti-cardiolipin antibodies
AB Gastric neuroendocrine tumours are rare. We describe a unique case of a 66-year-old male patient who presented with shortness of breath and malaise, eventually attributed to severe autoimmune haemolysis in the context of atrophic gastritis and multiple type-1 gastric neuroendocrine tumours. The patient had also positive anti-cardiolipin antibodies. A favourable outcome was attained with corticosteroids plus subtotal gastrectomy for the treatment of the underlying neoplastic disease. This case illustrates that the differential diagnosis of any associated causes of autoimmune haemolytic anaemia can be challenging, and may extend to unexpected conditions.
C1 [Papakonstantinou, Ilias P.; Karakousis, Nikolaos D.] Sismanoglio Gen Hosp Attica, Dept Internal Med 2, Athens, Greece.
   [Andreadis, Emmanouel A.] Evangelismos Gen Hosp Athens, Dept Internal Med 4, Athens, Greece.
RP Papakonstantinou, IP (corresponding author), Sismanoglio Gen Hosp Attica, Dept Internal Med 2, Athens, Greece.
EM iliaspapacon@yahoo.gr
RI Papakonstantinou, Ilias/AAC-5703-2022
OI Karakousis, Nikolaos D./0000-0003-4882-7042
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NR 21
TC 1
Z9 1
U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0036-9330
EI 2045-6441
J9 SCOT MED J
JI Scott. Med. J.
PD NOV
PY 2019
VL 64
IS 4
BP 154
EP 158
AR 0036933019867574
DI 10.1177/0036933019867574
EA AUG 2019
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA JH2IZ
UT WOS:000482370400001
PM 31403382
DA 2025-06-01
ER

PT J
AU Homma, S
   Sagawa, Y
   Ito, M
   Ohno, T
   Toda, G
AF Homma, S
   Sagawa, Y
   Ito, M
   Ohno, T
   Toda, G
TI Cancer immunotherapy using dendritic/tumour-fusion vaccine induces
   elevation of serum anti-nuclear antibody with better clinical responses
SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY
LA English
DT Article
DE anti-nuclear antibody; cancer vaccine; dendritic cell
ID ANTITUMOR-ACTIVITY; CARCINOMA-CELLS; AUTOIMMUNE-RESPONSE; TUMOR-CELLS;
   PHASE-I; MICE; DISEASE; ANTIGEN; IMMUNIZATION; INDUCTION
AB Dendritic cell (DC) vaccines might induce both anti-tumour immunity and autoimmunity. In this report, we demonstrate elevated levels of anti-nuclear antibody (ANA) in the sera of patients with cancer who had received immunotherapy with a dendritic/tumour-fusion vaccine. Twenty-two patients were treated with DC vaccine of fusion cells composed of autologous DCs and tumour cells (DC/tumour-fusion vaccine), which was generated by treating each cell type with polyethylene glycol. Nine of the 22 patients were treated with both the DC/tumour-fusion vaccine and systemic administration of recombinant human interleukin (rhIL)-12. Serum levels of ANA were examined with an enzyme-linked immunosorbent assay kit. One patient with gastric carcinoma (patient 1, DC/tumour-fusion vaccine alone), one patient with breast cancer (patient 2, DC/tumour-fusion vaccine alone) and one patient with ovarian cancer (patient 3, DC/tumour-fusion vaccine + rhIL-12) showed significant elevations of serum ANA levels during treatment. In patient 1 malignant ascitic effusion resolved and serum levels of tumour markers decreased. Patients 2 and 3 remained in good physical condition during treatment for 24 and 9 months, respectively. Immunoblot analysis indicated antibody responses to autologous tumour cells after vaccination in patient 2. None of the treated patients showed clinical symptoms suggesting autoimmune disease. Patients with elevated serum levels of ANA had significantly longer treatment periods than those without it. Elevated serum levels of ANA after DC/tumour-fusion cell vaccine might be associated with anti-tumour immune response induced by the vaccination.
C1 Jikei Univ, Sch Med, Inst DNA Med, Dept Oncol,Minato Ku, Tokyo 1058461, Japan.
   Jikei Univ, Sch Med, Inst DNA Med, Clin Data Bank, Tokyo 1058461, Japan.
   Senpo Takanawa Hosp, Tokyo, Japan.
C3 Jikei University; Jikei University
RP Jikei Univ, Sch Med, Inst DNA Med, Dept Oncol,Minato Ku, 3-25-8 Nishi Shimbashi, Tokyo 1058461, Japan.
EM sahya@jikei.ac.jp
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NR 37
TC 36
Z9 45
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0009-9104
EI 1365-2249
J9 CLIN EXP IMMUNOL
JI Clin. Exp. Immunol.
PD APR
PY 2006
VL 144
IS 1
BP 41
EP 47
DI 10.1111/j.1365-2249.2006.03029.x
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 021YT
UT WOS:000236022500006
PM 16542363
OA Green Published
DA 2025-06-01
ER

PT J
AU Watson, SA
   Gilliam, AD
AF Watson, SA
   Gilliam, AD
TI G17DT - a new weapon in the therapeutic armoury for gastrointestinal
   malignancy
SO EXPERT OPINION ON BIOLOGICAL THERAPY
LA English
DT Article
DE CCK-2 receptor; G17DT; gastrin; gastrin immunogen; gastrointestinal
   malignancy
ID HUMAN COLORECTAL TUMOR; GASTRIMMUNE INHIBIT; B/GASTRIN RECEPTOR;
   PANCREATIC-CANCER; GROWTH-FACTOR; ANTIBODIES; COEXPRESSION; GASTRIN-17;
   IMMUNOGEN; CARCINOMA
AB G17DT or Gastrimmune, as it was formally known, is an antigastrin 17 immunogen producing neutralising high affinity antibodies directed against gastrin-17 (G17). Preclinical studies, initiated to identify biological functionality of G17DT-induced antibodies, confirmed that the antibodies both reduced G17 stimulated gastric acid secretion and inhibited gastrin from interacting with the CCK-2 receptor. Therapeutic efficacy of both passive and active immunisation with G17DT has been established in a number of tumour systems including both primary and metastatic disease. Furthermore, additive effects with 5-fluorouracil (5-FU)/leucovorin have been confirmed in both colon and gastric turnout models. Phase I/II studies in advanced gastrointestinal (GI) malignancies have shown no systemic or autoimmune reactions to active immunisation with G17DT. Use of an optimised dose has yielded a high proportion of responders (> 80%), with minimal side effects and antibody titres measurable within 2 - 4 weeks. Taken together these results suggest that the G17DT immunogen is a promising agent for the treatment of GI cancer and Phase III trials, currently underway, will definitively evaluate this early promise.
C1 Univ Nottingham, QMC, Univ Hosp, Div GI Surg,Acad Unit Canc Studies, Nottingham NG7 2UH, England.
C3 University of Nottingham; Nottingham University Hospital NHS Trust
RP Univ Nottingham, QMC, Univ Hosp, Div GI Surg,Acad Unit Canc Studies, Nottingham NG7 2UH, England.
EM sue.watson@nottingham.ac.uk
RI Watson, Sarah/ABH-2848-2020
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NR 37
TC 31
Z9 38
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1471-2598
EI 1744-7682
J9 EXPERT OPIN BIOL TH
JI Expert Opin. Biol. Ther.
PD MAR
PY 2001
VL 1
IS 2
BP 309
EP 317
DI 10.1517/14712598.1.2.309
PG 9
WC Biotechnology & Applied Microbiology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Research & Experimental Medicine
GA 493XW
UT WOS:000172249600013
PM 11727538
DA 2025-06-01
ER

PT J
AU Nassereddine, H
   Chicaud, M
   Rebah, K
   Théou-Anton, N
   Sautet, A
   Dermer, J
   Couvelard, A
AF Nassereddine, Hussein
   Chicaud, Matthieu
   Rebah, Khedidja
   Theou-Anton, Nathalie
   Sautet, Anne
   Dermer, Jacques
   Couvelard, Anne
TI Pathogenic ATM Variant-Harbouring Well-Differentiated Aggressive
   Type 1 Gastric Neuroendocrine Tumour with High-grade Features (G3 NET):
   a New Addition to the Clinical and Pathological Spectrum of Gastric
   Neuroendocrine Neoplasms
SO ENDOCRINE PATHOLOGY
LA English
DT Article
DE Gastric; Neuroendocrine tumour; Type 1; Grade 3; Autoimmune gastritis
ID PROGNOSTIC-FACTORS; CLASSIFICATION; LANDSCAPE
AB Gastric type 1 neuroendocrine tumours are considered to have low rates of proliferation and a good prognosis. We report here a patient with an aggressive well-differentiated high-grade gastric neuroendocrine tumour (gastric grade 3 NET), in a context of autoimmune gastritis. Consistent with grade 3 disease, the tumour had a Ki-67 proliferation index of 30%. Targeted next-generation sequencing identified variants of four genes, including a pathogenic ATM variant underlying the differentiation and metastatic potential of the tumour. Liver metastasis was diagnosed during follow-up, and the patient died after 6 years, due to disease progression.
C1 [Nassereddine, Hussein; Chicaud, Matthieu; Couvelard, Anne] Hop Bichat Claude Bernard, AP HP, Dept Pathol, 46 Rue Henri Huchard, F-75018 Paris, France.
   [Chicaud, Matthieu] Sorbonne Univ, Paris, France.
   [Rebah, Khedidja; Theou-Anton, Nathalie] Hop Bichat Claude Bernard, AP HP, Dept Genet, 46 Rue Henri Huchard, F-75018 Paris, France.
   [Sautet, Anne] PRAXEA Diagnost, Massy, France.
   [Dermer, Jacques] Clin Estree, Serv Chirurg Viscerale & Cancerol, F-93245 Stains, France.
   [Couvelard, Anne] Univ Paris, Paris, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Bichat-Claude Bernard - APHP; Sorbonne Universite;
   Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Bichat-Claude Bernard - APHP; Universite Paris
   Cite
RP Nassereddine, H (corresponding author), Hop Bichat Claude Bernard, AP HP, Dept Pathol, 46 Rue Henri Huchard, F-75018 Paris, France.
EM hussein.nassereddine@hotmail.com
OI THEOU-ANTON, NATHALIE/0000-0002-5139-4260
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NR 23
TC 3
Z9 3
U1 0
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1046-3976
EI 1559-0097
J9 ENDOCR PATHOL
JI Endocr. Pathol.
PD DEC
PY 2021
VL 32
IS 4
BP 517
EP 523
DI 10.1007/s12022-021-09681-2
EA MAY 2021
PG 7
WC Endocrinology & Metabolism; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Pathology
GA XC4HI
UT WOS:000652923500002
PM 34019237
DA 2025-06-01
ER

PT J
AU Siddiqui, MS
   Shahi, MH
   Castresana, JS
AF Siddiqui, M. Sarim
   Shahi, Mehdi H.
   Castresana, Javier S.
TI The role of the adenylate kinase 5 gene in various diseases and cancer
SO JOURNAL OF CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Review
DE Adenylate kinase 5; adenylate kinases; cancer; diabetes;
   neurodegenerative diseases
ID K-ATP CHANNELS; LIMBIC ENCEPHALITIS; PURINE METABOLISM; PROTEIN-TAU;
   N-COPINE; IDENTIFICATION; EPILEPSY; LOCALIZATION; DEREGULATION;
   METHYLATION
AB Adenylate kinases (AKs) are important enzymes involved in cellular energy metabolism. Among AKs, AK5 (adenylate kinase 5), a cytosolic protein, is emerging as a significant contributor to various diseases and cellular processes. This comprehensive review integrates findings from various research groups on AK5 since its discovery, shedding light on its multifaceted roles in nucleotide metabolism, energy regulation, and cellular differentiation. We investigate its implications in a spectrum of diseases, including autoimmune encephalitis, epilepsy, neurodegenerative disorders such as Alzheimer's and Parkinson's, diabetes, lower extremity arterial disease, celiac disease, and various cancers. Notably, AK5's expression levels and methylation status have been associated with cancer progression and patient outcomes, indicating its potential as a prognostic indicator. Furthermore, AK5 is implicated in regulating cellular processes in breast cancer, gastric cancer, colorectal carcinoma, prostate cancer, and colon adenocarcinoma, suggesting its relevance across different cancer types. However, a limitation lies in the need for more robust clinical validation and a deeper understanding of AK5's precise mechanisms in disease pathogenesis, despite its association with various pathophysiological conditions. Nonetheless, AK5 holds promise as a therapeutic target, with emerging evidence suggesting its potential in therapy development.
C1 [Siddiqui, M. Sarim; Shahi, Mehdi H.] Aligarh Muslim Univ, Fac Med, Interdisciplinary Brain Res Ctr, Aligarh 202002, India.
   [Castresana, Javier S.] Univ Navarra, Sch Sci, Dept Biochem & Genet, Pamplona 31008, Spain.
C3 Aligarh Muslim University; University of Navarra
RP Castresana, JS (corresponding author), Univ Navarra, Sch Sci, Dept Biochem & Genet, Pamplona 31008, Spain.
EM jscastresana@unav.es
RI Shahi, Mehdi/HLG-7976-2023; Castresana, Javier/AFT-2167-2022
OI Castresana, Javier S./0000-0002-2373-482X
FU University of Navarra
FX Open access funding is provided by the University of Navarra.
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NR 80
TC 1
Z9 1
U1 0
U2 0
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
EI 2059-8661
J9 J CLIN TRANSL SCI
JI J. Clin. Transl. Sci.
PD AUG 19
PY 2024
VL 8
IS 1
AR e96
DI 10.1017/cts.2024.536
PG 9
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA D0B7Q
UT WOS:001292931800001
PM 39655021
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Ye, JH
   Li, JF
   Zhao, P
AF Ye, Junhong
   Li, Jifu
   Zhao, Ping
TI Roles of ncRNAs as ceRNAs in Gastric Cancer
SO GENES
LA English
DT Review
DE non-coding RNAs; competitive endogenous RNA; gastric cancer
ID LONG NONCODING RNA; COMPETING ENDOGENOUS RNA; TUMOR-SUPPRESSOR GENE;
   PROMOTES PROLIFERATION; CISPLATIN RESISTANCE; CELL-PROLIFERATION; MUSCLE
   DIFFERENTIATION; EXPRESSION PROFILE; INHIBITS APOPTOSIS; MICRORNA
   SPONGES
AB Although ignored in the past, with the recent deepening of research, significant progress has been made in the field of non-coding RNAs (ncRNAs). Accumulating evidence has revealed that microRNA (miRNA) response elements regulate RNA. Long ncRNAs, circular RNAs, pseudogenes, miRNAs, and messenger RNAs (mRNAs) form a competitive endogenous RNA (ceRNA) network that plays an essential role in cancer and cardiovascular, neurodegenerative, and autoimmune diseases. Gastric cancer (GC) is one of the most common cancers, with a high degree of malignancy. Considerable progress has been made in understanding the molecular mechanism and treatment of GC, but GC's mortality rate is still high. Studies have shown a complex ceRNA crosstalk mechanism in GC. lncRNAs, circRNAs, and pseudogenes can interact with miRNAs to affect mRNA transcription. The study of the involvement of ceRNA in GC could improve our understanding of GC and lead to the identification of potential effective therapeutic targets. The research strategy for ceRNA is mainly to screen the different miRNAs, lncRNAs, circRNAs, pseudogenes, and mRNAs in each sample through microarray or sequencing technology, predict the ceRNA regulatory network, and, finally, conduct functional research on ceRNA. In this review, we briefly discuss the proposal and development of the ceRNA hypothesis and the biological function and principle of ceRNAs in GC, and briefly introduce the role of ncRNAs in the GC's ceRNA network.
C1 [Ye, Junhong; Zhao, Ping] Southwest Univ, Biol Sci Res Ctr, State Key Lab Silkworm Genome Biol, Chongqing 400716, Peoples R China.
   [Li, Jifu] Southwest Univ, Coll Sericulture Text & Biomass Sci, Chongqing 400716, Peoples R China.
C3 Southwest University - China; Southwest University - China
RP Zhao, P (corresponding author), Southwest Univ, Biol Sci Res Ctr, State Key Lab Silkworm Genome Biol, Chongqing 400716, Peoples R China.
EM yejunhong0129@outlook.com; lijifu0103@163.com; zhaop@swu.edu.cn
RI jifu, li/LZH-0869-2025
OI Ye, Junhong/0000-0003-1501-0263
FU National Natural Science Foundation [31772532]
FX This study was funded by the National Natural Science Foundation, grant
   number 31772532.
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NR 200
TC 38
Z9 39
U1 1
U2 17
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD JUL
PY 2021
VL 12
IS 7
AR 1036
DI 10.3390/genes12071036
PG 22
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA TO3QS
UT WOS:000676831300001
PM 34356052
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Zádori, N
   Szakó, L
   Váncsa, S
   Vöerhendi, N
   Ostarijas, E
   Kiss, S
   Frim, L
   Hegyi, P
   Czimmer, J
AF Zadori, Noemi
   Szako, Lajos
   Vancsa, Szilard
   Voerhendi, Nora
   Ostarijas, Eduard
   Kiss, Szabolcs
   Frim, Levente
   Hegyi, Peter
   Czimmer, Jozsef
TI Six Autoimmune Disorders Are Associated With Increased Incidence of
   Gastric Cancer: A Systematic Review and Meta-Analysis of Half a Million
   Patients
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE autoimmune disease; gastric cancer; autoimmunity; risk; standardized
   incidence rate
ID POPULATION; RISK; MALIGNANCY; ANTIBODIES; DISEASE; EPIDEMIOLOGY; TRENDS;
   BIAS
AB Background: Gastric cancer is one of the most common cancers worldwide, with a high mortality rate. The potential etiological role of autoimmune (AI) disorders has been described in gastric cancer; however, the literature is controversial. This study aims to provide a comprehensive summary of the association between autoimmune disorders and the incidence of gastric cancer.Methods: This study was registered on PROSPERO under registration number CRD42021262875. The systematic literature search was conducted in four scientific databases up to May 17, 2021. Studies that reported standardized incidence rate (SIR) of gastric cancer in autoimmune disorders were eligible. We calculated pooled SIRs with 95% confidence intervals (CIs) in this meta-analysis.Results: We included 43 articles describing 36 AI disorders with data of 499,427 patients from four continents in our systematic review and meta-analysis. Significantly increased incidence of gastric cancer was observed in dermatomyositis (SIR = 3.71; CI: 2.04, 6.75), pernicious anemia (SIR = 3.28; CI: 2.71, 3.96), inflammatory myopathies (SIR = 2.68; CI:1.40; 5.12), systemic lupus erythematosus (SIR = 1.48; CI: 1.09, 2.01), diabetes mellitus type I (SIR = 1.29; CI:1.14, 1,47), and Graves' disease (SIR = 1.28; CI: 1.16, 1.41). No significant associations could be found regarding other AI disorders.Conclusions: Pernicious anemia, Graves' disease, dermatomyositis, diabetes mellitus type I, inflammatory myopathies, and systemic lupus erythematosus are associated with higher incidence rates of gastric cancer. Therefore, close gastroenterological follow-up or routinely performed gastroscopy and application of other diagnostic measures may be cost-effective and clinically helpful for patients diagnosed with these autoimmune diseases.
C1 [Zadori, Noemi; Szako, Lajos; Vancsa, Szilard; Voerhendi, Nora; Ostarijas, Eduard; Kiss, Szabolcs; Frim, Levente; Hegyi, Peter; Czimmer, Jozsef] Univ Pecs, Inst Translat Med, Sch Med, Pecs, Hungary.
   [Zadori, Noemi; Szako, Lajos; Vancsa, Szilard; Voerhendi, Nora; Hegyi, Peter] Univ Pecs, Janos Szentagothai Res Ctr, Pecs, Hungary.
   [Vancsa, Szilard; Hegyi, Peter] Semmelweis Univ, Ctr Translat Med, Budapest, Hungary.
   [Kiss, Szabolcs] Univ Szeged, Doctoral Sch Clin Med, Szeged, Hungary.
   [Kiss, Szabolcs] Heim Pal Natl Pediat Inst, Budapest, Hungary.
   [Hegyi, Peter] Semmelweis Univ, Div Pancreat Dis, Heart & Vasc Ctr, Budapest, Hungary.
   [Czimmer, Jozsef] Univ Pecs, Sch Med, Div Gastroenterol, Dept Med 1, Pecs, Hungary.
C3 University of Pecs; University of Pecs; Semmelweis University; Szeged
   University; Semmelweis University; University of Pecs
RP Czimmer, J (corresponding author), Univ Pecs, Inst Translat Med, Sch Med, Pecs, Hungary.
EM czimmer.jozsef@pte.hu
RI Hegyi, Péter/B-3163-2016; Ostarijas, Eduard/S-9447-2018
OI Ostarijas, Eduard/0000-0001-9999-9886; Frim, Levente/0000-0003-0097-6663
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NR 44
TC 16
Z9 19
U1 1
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD NOV 23
PY 2021
VL 12
AR 750533
DI 10.3389/fimmu.2021.750533
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA XL2UI
UT WOS:000728003900001
PM 34887857
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Solinas, C
   Pusole, G
   Demurtas, L
   Puzzoni, M
   Mascia, R
   Morgan, G
   Giampieri, R
   Scartozzi, M
AF Solinas, Cinzia
   Pusole, Grazia
   Demurtas, Laura
   Puzzoni, Marco
   Mascia, Roberta
   Morgan, Gilberto
   Giampieri, Riccardo
   Scartozzi, Mario
TI Tumor infiltrating lymphocytes in gastrointestinal tumors: Controversies
   and future clinical implications
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE Tumor infiltrating lymphocytes; Gastrointestinal tumors; Microsatellite
   instability; Prognosis; Immunotherapy
ID REGULATORY T-CELLS; HEPATOCELLULAR-CARCINOMA; GASTRIC-CANCER; FAVORABLE
   PROGNOSIS; COLORECTAL-CANCER; SUPPRESSOR-CELLS; PD-1 BLOCKADE; B-CELLS;
   MOLECULAR SUBTYPES; CTLA-4 BLOCKADE
AB Chronic inflammation following infections, autoimmune diseases or exposure to environmental irritants plays a crucial role in tumor development and influences the host immune response to neoplastic cells. The presence of an anti-tumor immune infiltrate is often associated with better outcomes in gastro-intestinal primary cancers, particularly in those with high microsatellite instability (MSI-H). Immunotherapeutic drugs inhibiting the PD-1 and PD-L1 pathway showed promising results in the treatment of these patients in the metastatic setting. The aim of this review is to resume the role tumor infiltrating lymphocytes (TILs) play in gastrointestinal tumors, underlining their potential value as a prognostic and predictive biomarker. TILs assessment could identify subsets of patients with high extent of TILs and better prognosis, that could be spared from adjuvant systemic treatments. Immune infiltration parameters might be additional predictors of a greater benefit from the immunotherapy with the immune checkpoint blockade. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
C1 [Solinas, Cinzia] Inst Jules Bordet, Mol Immunol Unit, Blvd Waterloo 127, B-1000 Brussels, Belgium.
   [Solinas, Cinzia] Univ Libre Bruxelles, Blvd Waterloo 127, B-1000 Brussels, Belgium.
   [Pusole, Grazia; Demurtas, Laura; Puzzoni, Marco; Mascia, Roberta; Scartozzi, Mario] Univ Cagliari, Med Oncol, Policlin Univ Ss 554 Bivio Sestu Km 4-5, Monserrato, CA, Italy.
   [Morgan, Gilberto] Skane Univ Hosp, Med Oncol, Lund, Sweden.
   [Giampieri, Riccardo] UNIVPM, Med Oncol, Ancona, Italy.
C3 Institut Jules Bordet; Universite Libre de Bruxelles; University of
   Cagliari; Lund University; Skane University Hospital; Marche Polytechnic
   University
RP Scartozzi, M (corresponding author), Policlin Univ Monserrato, AOU Cagliari, Oncol Med, Ss 554 Bivio Sestu Km 4500, I-09042 Cagliari, Italy.
EM czsolinas@gmail.com; grazia.pusole@gmail.com; lau.demi@tiscali.it;
   marcopuzzoni@gmail.com; roboa@hotmail.it; Gilberto.Morgan@Skane.se;
   riccardo.giampieri81@gmail.com; marioscartozzi@gmail.com
RI PUZZONI, MARCO/T-5453-2019; Solinas, Cinzia/AAC-2103-2020; Mascia,
   Roberta/ABD-8709-2020; Pusole, Grazia/G-4945-2018
OI SCARTOZZI, MARIO/0000-0001-5977-5546; Pusole,
   Grazia/0000-0002-1866-1371; puzzoni, marco/0000-0001-5880-4309;
   DEMURTAS, LAURA/0000-0002-9749-7628; mascia, roberta/0000-0002-7174-0220
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NR 100
TC 36
Z9 37
U1 0
U2 19
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD FEB
PY 2017
VL 110
BP 106
EP 116
DI 10.1016/j.critrevonc.2016.11.016
PG 11
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA EJ9GB
UT WOS:000393533500011
PM 28109400
DA 2025-06-01
ER

PT J
AU Rogosnitzky, M
   Danks, R
   Kardash, E
AF Rogosnitzky, Moshe
   Danks, Rachel
   Kardash, Elena
TI Therapeutic Potential of Tranilast, an Anti-allergy Drug, in
   Proliferative Disorders
SO ANTICANCER RESEARCH
LA English
DT Review
DE Tranilast; proliferative disorders; keloid tumors; tumor
   microenvironment; mast cells; TGF-beta signaling; cell cycle; apoptosis;
   review
ID N-(3,4-DIMETHOXYCINNAMOYL) ANTHRANILIC ACID; ARYL-HYDROCARBON RECEPTOR;
   BREAST-CANCER CELLS; PROSTATE-CANCER; IN-VITRO; INHIBITORY-ACTION;
   GASTRIC-CANCER; GROWTH; RELEASE; FIBROBLASTS
AB Tranilast (N-[3,4-dimethoxycinnamoyl]-anthranilic acid; Rizaben (R)) is an anti-allergy drug approved for use in Japan and South Korea, also used against asthma, autoimmune diseases, and atopic and fibrotic pathologies. The antitumor potential of tranilast is attracting considerable interest. This review summarizes recent evidence concerning the effect of tranilast on different tumor types and discusses the drug's possible mode of action in this area. In vivo and in vitro studies are covered, as well as evidence from clinical trials, in which tranilast was evaluated in various models of proliferative disorders. The findings presented in this report, demonstrate the excellent potential of tranilast in the management of certain types of tumor, and provide a strong rationale for the initiation of controlled clinical trials in this area.
C1 [Rogosnitzky, Moshe] MedInsight Res Inst, IL-90840 Telz Stone, Israel.
RP Rogosnitzky, M (corresponding author), MedInsight Res Inst, POB 386, IL-90840 Telz Stone, Israel.
EM moshe@medinsight.org
OI Kardash, Elena/0000-0002-7425-9862
CR [Anonymous], RIZABEN DATA SHEET
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NR 36
TC 64
Z9 66
U1 1
U2 10
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
J9 ANTICANCER RES
JI Anticancer Res.
PD JUL
PY 2012
VL 32
IS 7
SI SI
BP 2471
EP 2478
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 972CO
UT WOS:000306254300009
PM 22753703
DA 2025-06-01
ER

PT J
AU Calvete, O
   Reyes, J
   Benítez, J
AF Calvete, Oriol
   Reyes, Jose
   Benitez, Javier
TI Case Report: CMV Infection and Same Mechanism-Originated Intestinal
   Inflammation Compatible With Bowel/Crohn's Disease Is Suggested in ATP4A
   Mutated-Driven Gastric Neuroendocrine Tumors
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE gastric neuroendocrine tumor; ATP4A; co-occurring autoimmune disorders;
   cytomegalovirus; inflammatory bowel disease; Crohn&apos; s disease
AB Mutations in the ATP4A proton pump prevent gastric acidification and explain the chronic autoimmune gastritis scenario that conducts the gastric neuroendocrine tumor (gNET) formation. Here, we wanted to investigate the co-occurrence cytomegalovirus (CMV) infection and intestinal inflammation that presented all members of a family affected with gNET and carrying an ATP4A mutation. Intestinal inflammation persisted after CMV eradication and anemia treatment. The inflammation was compatible with a ileitis/Crohn's disease and was originated by the same autoimmune mechanism described in the tumorigenesis of gNETS. The same secondary disease but no the CMV infection was observed in all members affected with gNET and carrying the ATP4A mutation. Our results suggest that the ATP4A malfunction not only explained gNETs but also the co-occurring disease and opportunistic infections, which allowed to link autoimmune pathologies and gNETs in a unique mechanism. Our results open a new window to better understand not only gastric neoplasms formation but the co-occurring autoimmune disorders and the inflammatory mechanism that compose a premalignant scenario for other tumor formation. Our findings are important since contribute to describe the genetic landscape of the Inflammatory Bowel/Crohn's disease and alert clinicians to monitor patients with gastric neoplasms mediated by achlorhydria mechanisms for concomitant secondary pathologies.
C1 [Calvete, Oriol; Benitez, Javier] Spanish Natl Canc Res Ctr CNIO, Human Genet Grp, Madrid, Spain.
   [Calvete, Oriol; Benitez, Javier] Network Res Rare Dis CIBERER, Madrid, Spain.
   [Calvete, Oriol; Reyes, Jose] Grp Espanol Tumores Neuroendocrinos & Endocrinos, Madrid, Spain.
   [Reyes, Jose] Hosp Comarcal Inca, Balearic Isl Hlth Invest Inst IDISBA, Dept Gastroenterol, Mallorca, Spain.
C3 Centro Nacional de Investigaciones Oncologicas (CNIO); CIBER - Centro de
   Investigacion Biomedica en Red; CIBERER; Hospital Comarcal Inca
RP Calvete, O (corresponding author), Spanish Natl Canc Res Ctr CNIO, Human Genet Grp, Madrid, Spain.; Calvete, O (corresponding author), Network Res Rare Dis CIBERER, Madrid, Spain.; Calvete, O (corresponding author), Grp Espanol Tumores Neuroendocrinos & Endocrinos, Madrid, Spain.
EM ocalvete@cnio.es
RI ortiz, Javier/H-5232-2015; Moreno, José/H-9440-2017; Calvete,
   Oriol/ABH-6579-2020
OI Calvete, Oriol/0000-0002-2623-2876; Reyes Moreno,
   Jose/0000-0002-8894-8095
FU Instituto de Salud Carlos III; H2020 BRIDGES project [634935]; European
   Regional Development Fund (ERDF) [PI16/00440]; JB's lab
FX This work was supported by JB's lab and is partially funded by Instituto
   de Salud Carlos III, cofunded by European Regional Development Fund
   (ERDF) grant (PI16/00440). OC was granted by H2020 BRIDGES project
   (634935).
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NR 14
TC 3
Z9 3
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD APR 6
PY 2021
VL 8
AR 553110
DI 10.3389/fmed.2021.553110
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA RO6NM
UT WOS:000641160100001
PM 33889580
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Ge, Y
   Sun, FY
   Zhao, B
   Kong, FY
   Li, ZS
   Kong, XY
AF Ge, Yang
   Sun, Fengyuan
   Zhao, Bo
   Kong, Fanyang
   Li, Zhaoshen
   Kong, Xiangyu
TI Bacteria derived extracellular vesicles in the pathogenesis and
   treatment of gastrointestinal tumours
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE extracellular vesicles (EVs); cancer; immunotherapy; TLR; LPS; PAMP
ID OUTER-MEMBRANE VESICLES; TNF-ALPHA PRODUCTION; ESCHERICHIA-COLI;
   GENERALIZED MODULES; LIPID-A; PSEUDOMONAS-AERUGINOSA;
   SALMONELLA-TYPHIMURIUM; PERIODONTAL-DISEASE; MEDIATED TRANSFER;
   GASTRIC-CANCER
AB Extracellular vesicles are fundamentally significant in the communication between cells. Outer Membrane Vesicles(OMVs) are a special kind of EVs produced by Gram-negative bacteria, which are minute exosome-like particles budding from the outer membrane, which have been found to play essential roles in diverse bacterial life events, including regulation of microbial interactions, pathogenesis promotion, stress responses and biofilm formation. Recently, and more researches have explored the substantial potentials of EVs as natural functional nanoparticles in the bioengineering applications in infectious diseases, cardiovascular diseases, autoimmune diseases and neurological diseases, such as antibacterial therapy, cancer drugs and immunoadjuvants, with several candidates in clinical trials showing promising efficacy. However, due to the poor understanding of sources, membrane structures and biogenesis mechanisms of EVs, progress in clinical applications still remains timid. In this review, we summarize the latest findings of EVs, especially in gastrointestinal tract tumours, to provide a comprehensive introduction of EVs in tumorigenesis and therapeutics.
C1 [Ge, Yang; Sun, Fengyuan; Zhao, Bo; Kong, Fanyang; Li, Zhaoshen; Kong, Xiangyu] Naval Mil Med Univ, Changhai Hosp, Changhai Clin Res Unit, Shanghai, Peoples R China.
   [Ge, Yang; Kong, Fanyang; Kong, Xiangyu] Naval Mil Med Univ, Changhai Hosp, Dept Gastroenterol, Shanghai, Peoples R China.
   [Kong, Xiangyu] Second Mil Med Univ, Natl Key Lab Med Immunol, Shanghai, Peoples R China.
   [Kong, Xiangyu] Second Mil Med Univ, Inst Immunol, Shanghai, Peoples R China.
C3 Naval Medical University; Naval Medical University; Naval Medical
   University; Naval Medical University
RP Kong, FY; Li, ZS; Kong, XY (corresponding author), Naval Mil Med Univ, Changhai Hosp, Changhai Clin Res Unit, Shanghai, Peoples R China.; Kong, FY; Kong, XY (corresponding author), Naval Mil Med Univ, Changhai Hosp, Dept Gastroenterol, Shanghai, Peoples R China.; Kong, XY (corresponding author), Second Mil Med Univ, Natl Key Lab Med Immunol, Shanghai, Peoples R China.; Kong, XY (corresponding author), Second Mil Med Univ, Inst Immunol, Shanghai, Peoples R China.
EM kfy8195288@163.com; zhaoshenli.smmu.edu@hotmail.com;
   xiangyukong185@hotmail.com
RI Kong, Fanyang/GPX-5859-2022
OI Kong, Xiangyu/0000-0001-7515-2613
FU National Key R&D Program of China [2019YFC1315900, 2019YFC1315802];
   National Natural Science Foundation of China [82072760, 81902990]
FX Funding National Key R&D Program of China (2019YFC1315900,
   2019YFC1315802), and National Natural Science Foundation of China
   (82072760, 81902990).
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NR 136
TC 3
Z9 4
U1 4
U2 19
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD JAN 23
PY 2023
VL 12
AR 1103446
DI 10.3389/fonc.2022.1103446
PG 16
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 8S7NY
UT WOS:000928764700001
PM 36776356
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Waldum, H
   Fossmark, R
AF Waldum, Helge
   Fossmark, Reidar
TI Inflammation and Digestive Cancer
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE carcinogenesis; inflammation; chronic gastritis; gastric cancer; chronic
   hepatitis; hepatocellular carcinoma; inflammatory bowel disease; colon
   cancer; mechanism; hormonal carcinogenesis
ID HELICOBACTER-PYLORI INFECTION; MULTIPLE ENDOCRINE NEOPLASIA;
   ZOLLINGER-ELLISON-SYNDROME; GASTRIC CARCINOID-TUMORS; ECL-CELL
   CARCINOIDS; COLORECTAL-CANCER; PERNICIOUS-ANEMIA; BOWEL-DISEASE;
   ULCERATIVE-COLITIS; NEUROENDOCRINE DIFFERENTIATION
AB Chronic inflammation is linked to carcinogenesis, particularly in the digestive organs, i.e., the stomach, colon, and liver. The mechanism of this effect has, however, only partly been focused on. In this review, we focus on different forms of chronic hepatitis, chronic inflammatory bowel disease, and chronic gastritis, conditions predisposing individuals to the development of malignancy. Chronic inflammation may cause malignancy because (1) the cause of the chronic inflammation is itself genotoxic, (2) substances released from the inflammatory cells may be genotoxic, (3) the cell death induced by the inflammation induces a compensatory increase in proliferation with an inherent risk of mutation, (4) changes in cell composition due to inflammation may modify function, resulting in hormonal disturbances affecting cellular proliferation. The present review focuses on chronic gastritis (Helicobacter pylori or autoimmune type) since all four mechanisms may be relevant to this condition. Genotoxicity due to the hepatitis B virus is an important factor in hepatocellular cancer and viral infection can similarly be central in the etiology and malignancy of inflammatory bowel diseases. Helicobacter pylori (H. pylori) is the dominating cause of chronic gastritis and has not been shown to be genotoxic, so its carcinogenic effect is most probably due to the induction of atrophic oxyntic gastritis leading to hypergastrinemia.
C1 [Waldum, Helge; Fossmark, Reidar] Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
C3 Norwegian University of Science & Technology (NTNU)
RP Waldum, H (corresponding author), Norwegian Univ Sci & Technol, Fac Med & Hlth Sci, Dept Clin & Mol Med, N-7030 Trondheim, Norway.
EM helge.waldum@ntnu.com; reidar.fossmark@ntnu.no
RI Fossmark, Reidar/AAP-6442-2021
OI Waldum, Helge/0000-0002-3137-0843
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NR 133
TC 10
Z9 10
U1 9
U2 19
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2023
VL 24
IS 17
AR 13503
DI 10.3390/ijms241713503
PG 14
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA R0EW5
UT WOS:001061166700001
PM 37686307
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Song, M
   Latorre, G
   Ivanovic-Zuvic, D
   CamargO, MC
   Rabkin, CS
AF Song, Minkyo
   Latorre, Gonzalo
   Ivanovic-Zuvic, Danisa
   CamargO, M. Constanza
   Rabkin, Charles S.
TI Autoimmune Diseases and Gastric Cancer Risk: A Systematic Review and
   Meta-Analysis
SO CANCER RESEARCH AND TREATMENT
LA English
DT Review
DE Stomach neoplasms; Autoimmune diseases; Epidemiology; Risk
ID PERNICIOUS-ANEMIA; DIABETES-MELLITUS; FOLLOW-UP; CARCINOMA; MORTALITY;
   BIAS; TYPE-1; LUPUS
AB Purpose
   Autoimmunity is an alternative etiology of gastric inflammation, the initiating event in the gastric carcinogenic cascade. This mechanism may be an increasingly important cause of gastric cancer with the waning prevalence of its primary etiologic factor, chronic Helicobacter pylori infection.
   Materials and Methods
   PubMed and EMBASE were searched up to September 2018. Autoimmunity and 96 specific manifestations were considered for associations with gastric cancer risk. Random effects analysis was used to calculate pooled relative risk estimates (RR) and 95% confidence intervals (CI).
   Results
   We found a total of 52 observational studies representing 30 different autoimmune diseases. Overall, the presence of an autoimmune condition was associated with a gastric cancer pooled RR of 1.37 (95% CI, 1.24 to 1.52). Among the 24 autoimmune conditions with two or more independent reports, nine were significantly associated with increased gastric cancer risk: dermatomyositis (RR, 3.69; 95% CI, 1.74 to 7.79), pernicious anemia (RR, 2.84; 95% CI, 2.30 to 3.50), Addison disease (RR, 2.11; 95% CI, 1.26 to 3.53), dermatitis herpetiformis (RR, 1.74; 95% CI, 1.02 to 2.97; n=3), IgG4-related disease (RR, 1.69; 95% CI, 1.00 to 2.87), primary biliary cirrhosis (RR, 1.64; 95% CI, 1.13 to 2.37), diabetes mellitus type 1 (RR, 1.41; 95% CI, 1.20 to 1.67), systemic lupus erythematosus (RR, 1.37; 95% CI, 1.01 to 1.84), and Graves disease (RR, 1.27; 95% CI, 1.06 to 1.52).
   Conclusion
   Our analysis documents the wide range of autoimmune diseases associated with gastric cancer. These associations may reflect unreported links between these conditions and autoimmune gastritis. Further studies are warranted to investigate potential causal mechanisms.
C1 [Song, Minkyo; CamargO, M. Constanza; Rabkin, Charles S.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
   [Latorre, Gonzalo; Ivanovic-Zuvic, Danisa] Pontificia Univ Catolica Chile, Dept Internal Med, Santiago, Chile.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); NIH National Cancer Institute- Division of Cancer Epidemiology &
   Genetics; Pontificia Universidad Catolica de Chile
RP Song, M (corresponding author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E204, Bethesda, MD 20892 USA.
EM minkyo.song@nih.gov
RI Camargo, M. Constanza/R-9891-2016; Latorre, Gonzalo/JNT-4534-2023; SONG,
   MINKYO/AAE-9095-2020
FU Intramural Research Program, Division of Cancer Epidemiology and
   Genetics, US National Cancer Institute, National Institutes of Health,
   Department of Health and Human Services; National Cancer Institute
   [ZIACP010212] Funding Source: NIH RePORTER
FX This study was supported by the Intramural Research Program, Division of
   Cancer Epidemiology and Genetics, US National Cancer Institute, National
   Institutes of Health, Department of Health and Human Services. The
   authors thank Nancy Terry, Biomedical Librarian at the U.S. NIH Library
   for her help with reviewing the search strategies.
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NR 41
TC 53
Z9 57
U1 0
U2 17
PU KOREAN CANCER ASSOCIATION
PI SEOUL
PA RM 1824, GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 110-999,
   SOUTH KOREA
SN 1598-2998
EI 2005-9256
J9 CANCER RES TREAT
JI Cancer Res. Treat.
PD JUL
PY 2019
VL 51
IS 3
BP 841
EP 850
DI 10.4143/crt.2019.151
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IK6OE
UT WOS:000476707300001
PM 31048663
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Piemonti, L
   Vettor, L
   Contro, E
AF Piemonti, Linda
   Vettor, Laura
   Contro, Elena
TI A Case Report of Metastatic Gastric Cancer Treated with Pembrolizumab
   during Pregnancy
SO FETAL DIAGNOSIS AND THERAPY
LA English
DT Article
DE Immunotherapy; Immune checkpoint inhibitors; Pembrolizumab; Bowel
   dilation; Prenatal diagnosis
ID PROGRAMMED CELL-DEATH-1; T-CELLS; BLOCKADE; CTLA-4; TUMOR; MELANOMA;
   PATIENT
AB Introduction: Immune checkpoint inhibitors are extensively used in present-day clinical practice for treating many types of cancers at different stages. To date, there are scarce data on the use of immunotherapy in pregnancy. Immune-related adverse events are a typical consequence of this therapy miming autoimmune diseases. Case Presentation: A 35-year-old woman (G1P0) diagnosed with gastric carcinoma underwent neoadjuvant chemotherapy followed by surgery. During follow-up, axillary metastasis was discovered, radiotherapy failed, and consequently immunotherapy was started. Concurrently, pregnancy ensued. Despite potential risks, the patient opted to continue immunotherapy and the pregnancy. At 31 weeks, fetal bowel dilation was noted. Subsequently, the fetus also developed fetal growth restriction. A cesarean section was performed at 35 weeks. The newborn required repeated bowel resections for necrotizing enterocolitis, necessitating extensive medical intervention. The mother continues pembrolizumab treatment with a positive response. Conclusion: To the best of our knowledge, this might constitute a possible case of a fetal immune-related adverse event after immunotherapy in utero exposure.
C1 [Piemonti, Linda; Contro, Elena] Univ Bologna, Obstet Unit, IRCCS Azienda Osped, Bologna, Italy.
   [Vettor, Laura] Univ Padua, Dept Womens & Childrens Hlth, Obstet & Gynecol Clin, Padua, Italy.
C3 University of Bologna; University of Padua
RP Vettor, L (corresponding author), Univ Padua, Dept Womens & Childrens Hlth, Obstet & Gynecol Clin, Padua, Italy.
EM laura.vettor@studenti.unipd.com
RI Piemonti, Lorenzo/P-7605-2017
OI Piemonti, Lorenzo/0000-0002-2172-2198
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NR 33
TC 1
Z9 1
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1015-3837
EI 1421-9964
J9 FETAL DIAGN THER
JI Fetal Diagn. Ther.
PD OCT
PY 2024
VL 51
IS 5
BP 493
EP 499
DI 10.1159/000540000
PG 7
WC Obstetrics & Gynecology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Obstetrics & Gynecology
GA I2R5T
UT WOS:001328781600010
PM 38934141
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Miceli, E
   Lenti, MV
   Gentile, A
   Gambini, G
   Petrucci, C
   Pitotti, L
   Mengoli, C
   Di Stefano, M
   Vanoli, A
   Luinetti, O
   Brondino, N
   Paulli, M
   Anderloni, A
   Klersy, C
   Corazza, GR
   Di Sabatino, A
AF Miceli, Emanuela
   Lenti, Marco Vincenzo
   Gentile, Antonella
   Gambini, Giulia
   Petrucci, Clarissa
   Pitotti, Lavinia
   Mengoli, Caterina
   Di Stefano, Michele
   Vanoli, Alessandro
   Luinetti, Ombretta
   Brondino, Natascia
   Paulli, Marco
   Anderloni, Andrea
   Klersy, Catherine
   Corazza, Gino Roberto
   Di Sabatino, Antonio
TI Long-Term Natural History of Autoimmune Gastritis: Results From a
   Prospective Monocentric Series
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE anemia; dysplasia; gastric atrophy; neuroendocrine tumor; potential;
   vitamin B-12
ID ATROPHIC GASTRITIS; DIAGNOSIS; CLASSIFICATION
AB INTRODUCTION: The natural history of autoimmune gastritis (AIG) has been poorly described. In this study, we report the long-term natural history and clinical clustering of the full spectrum of AIG, from the potential to the complicated stage. METHODS: Prospective single-center study conducted in a tertiary referral center. Patients with AIG at any stage (0 = potential; 1 = early; 2 = florid; 3 = severe; and 4 = complicated) were enrolled (January 2000-December 2022). The histopathological evolution, the clinical presentation, and the correlates of evolution of potential AIG were assessed. RESULTS: Four hundred ninety-eight patients with AIG (mean age 56.7 +/- 15.2 years, F:M ratio 2.5:1) were included, of whom 93 experienced potential AIG. The maximum disease duration was 27 years (median 18, interquartile range 14-23), while the overall median follow-up was 52 months (interquartile range 12-95). Age was significantly lower in stage 0 compared with that in the other stages. Accidental histologic evidence and hematologic findings were the most common clusters of diagnosis. The overall median rate of progression was 7.29 per 100 persons/yr (95% confidence interval [CI] 6.19-8.59), while the stage-specific rates of progression were 10.85 (stage 0; 95% CI 7.75-15.18), 14.83 (stages 1-2; 95% CI 11.89-18.49), and 2.68 (stage 3; 95% CI 1.88-3.84). Newly onset neoplastic complications at follow-up occurred in 41/483 patients (8.5%; 23 neuroendocrine tumors and 18 epithelial dysplasia). No cases of adenocarcinoma were noticed. Male sex was associated with a greater likelihood of evolving from potential AIG to overt AIG. DISCUSSION: AIG is a progressive disorder, with a virtually absent risk of gastric adenocarcinoma. Patients with potential AIG should be monitored because they carry a high risk of evolving into overt AIG.
C1 [Miceli, Emanuela; Lenti, Marco Vincenzo; Mengoli, Caterina; Di Stefano, Michele; Corazza, Gino Roberto; Di Sabatino, Antonio] Fdn IRCCS Policlin, Dept Internal Med 1, Pavia, Italy.
   [Lenti, Marco Vincenzo; Gentile, Antonella; Petrucci, Clarissa; Pitotti, Lavinia; Corazza, Gino Roberto; Di Sabatino, Antonio] Univ Pavia, Dept Internal Med & Med Therapeut, Pavia, Italy.
   [Gambini, Giulia; Klersy, Catherine] Fdn IRCCS Policlin San Matteo, Clin Epidemiol & Biometry Serv, Pavia, Italy.
   [Vanoli, Alessandro; Luinetti, Ombretta; Paulli, Marco] Univ Pavia, Dept Mol Med, Unit Anat Pathol, Pavia, Italy.
   [Vanoli, Alessandro; Luinetti, Ombretta; Paulli, Marco] IRCCS San Matteo Hosp Fdn, Pavia, Italy.
   [Brondino, Natascia] Univ Pavia, Dept Brain & Behav Sci, Pavia, Italy.
   [Anderloni, Andrea] Fdn IRCCS Policlin San Matteo, Gastroenterol & Digest Endoscopy, Pavia, Italy.
C3 IRCCS Fondazione San Matteo; University of Pavia; IRCCS Fondazione San
   Matteo; University of Pavia; IRCCS Fondazione San Matteo; University of
   Pavia; IRCCS Fondazione San Matteo
RP Di Sabatino, A (corresponding author), Fdn IRCCS Policlin, Dept Internal Med 1, Pavia, Italy.; Di Sabatino, A (corresponding author), Univ Pavia, Dept Internal Med & Med Therapeut, Pavia, Italy.
EM e.miceli@smatteo.pv.it; marco.lenti@unipv.it;
   antonella.gentile01@universitadipavia.it; g.gambini@smatteo.pv.it;
   clarissa.petrucci01@universitadipavia.it; pitotti@gmail.com;
   c.mengoli@smatteo.pv.it; m.distefano@smatteo.pv.it;
   alessandro.vanoli@unipv.it; o.luinetti@smatteo.pv.it;
   natascia.brondino@unipv.it; marco.paulli@unipv.it;
   a.anderloni@smatteo.pv.it; klersy@smatteo.pv.it;
   gr.corazza@smatteo.pv.it; a.disabatino@smatteo.pv.it
RI Corazza, Gino/K-8500-2016; di stefano, michele/AAC-2205-2019; Anderloni,
   Andrea/ABE-9139-2020; Brondino, Natascia/ABG-6512-2021; klersy,
   catherine/AAA-3003-2019; Di Sabatino, Antonio/K-8015-2016; Vanoli,
   Alessandro/J-4469-2016; Lenti, Marco Vincenzo/F-9044-2018
OI Vanoli, Alessandro/0000-0002-2976-7032; Mengoli,
   Caterina/0000-0002-2253-7795; di stefano, michele/0000-0002-6971-6854;
   Gambini, Giulia/0009-0003-0795-7972; Lenti, Marco
   Vincenzo/0000-0002-6654-4911; PETRUCCI, CLARISSA/0000-0003-2448-4217
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NR 34
TC 21
Z9 21
U1 6
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD MAY
PY 2024
VL 119
IS 5
BP 837
EP 845
DI 10.14309/ajg.0000000000002619
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA C0Z4N
UT WOS:001286731000010
PM 38050966
DA 2025-06-01
ER

PT J
AU Ji, K
   Zhang, LY
   Zhang, MX
   Chu, Q
   Li, X
   Wang, W
AF Ji, Kun
   Zhang, Liyan
   Zhang, Mingxuan
   Chu, Qi
   Li, Xin
   Wang, Wei
TI Prognostic Value and Clinicopathological Significance of p-stat3 Among
   Gastric Carcinoma Patients A Systematic Review and Meta-Analysis
SO MEDICINE
LA English
DT Review
ID ACTIVATED SIGNAL TRANSDUCER; LYMPH-NODE METASTASIS; PHOSPHO-STAT3
   EXPRESSION; CONSTITUTIVE ACTIVATION; AUTOIMMUNE-DISEASES; STAT3
   ACTIVATION; POOR-PROGNOSIS; GROWTH-FACTOR; CANCER; SURVIVAL
AB The overexpression of phosphorylated signal transducer and activator of transcription 3 (p-stat3) was detected in a variety of human tumors. The published studies on p-stat3 expression among gastric carcinoma patients remain controversial.
   In order to clarify the prognosis value of p-stat3 with overall survival and its association with clinicopathological characteristics in gastric carcinoma, we performed a systematic review and meta-analysis.
   Eligible studies were retrieved by searching PubMed, Embase, Cochrane library, and Chinese biomedical literature service system databases.
   Studies described the association between p-stat3 expression and clinicopathological characteristics and overall survival in gastric carcinoma patients; p-stat3 expression was detected by immunohistochemistry (IHC).
   Odds ratio (OR) and hazard ratio (HR) were considered as a measure of evaluating the association in meta-analysis; I-2 was used to assess the heterogeneity across studies; publication bias was assessed with funnel plot, Egger test, and Begg test.
   Twenty-three studies including 2872 patients which evaluated the p-stat3 expression by IHC in gastric carcinoma were included. The pooled HR (HR = 2.02, 95% CI: 1.49-2.73, P < 0.00001) indicated that the increased p-stat3 expression was significantly associated with poor overall survival. In addition, when we investigated the association between p-stat3 overexpression and clinicopathological characteristics of gastric carcinoma, we found that the increased p-stat3 expression was significantly associated with tumor differentiation (poorly vs well-moderately: OR = 3.70, 95% CI: 1.98-6.93, P < 0.0001) and lymph node metastasis (present vs absent: OR = 2.40, 95% CI: 1.28-4.50, P = 0.007).
   The different type of primary antibody was used; the assessment methods of p-stat3 positive expression were defined differently; the locations of p-stat3 expression were different; the method of extrapolating HR from Kaplan-Meier survival curves did seem to be less reliable than when HR was extracted directly from literatures; sample sizes, the age of patients, and the follow-up durations are different.
   In conclusion, our meta-analysis indicates that the increased p-stat3 expression may be not only predict poor prognosis, but also be associated with worse tumor differentiation and lymph node metastasis in patients with gastric carcinoma.
C1 [Ji, Kun; Zhang, Liyan] Shenyang Med Coll, Dept Pathophysiol, Shenyang 110034, Peoples R China.
   [Zhang, Mingxuan; Chu, Qi] Shenyang Med Coll, Grade Clin Med 2012, Shenyang 110034, Peoples R China.
   [Li, Xin] Jilin Univ, Hosp 2, Dept Jilin Prov Key Lab Mol & Chem Genet, Changchun 130023, Peoples R China.
   [Wang, Wei] Inner Mongolia Univ Nationalities, Inner Mongolia Gen Forestry Hosp, Sch Clin Med 2, Dept Neurosurg, Yakeshi 022150, Inner Mongolia, Peoples R China.
C3 Shenyang Medical College; Shenyang Medical College; Jilin University;
   Inner Mongolia Minzu University
RP Ji, K (corresponding author), Shenyang Med Coll, Dept Pathophysiol, Shenyang 110034, Peoples R China.; Wang, W (corresponding author), Inner Mongolia Univ Nationalities, Inner Mongolia Gen Forestry Hosp, Sch Clin Med 2, Dept Neurosurg, Yakeshi 022150, Inner Mongolia, Peoples R China.
EM jikun200907@163.com; ww_nmgmd@163.com
FU Program for Liaoning Excellent Talents in University [LJQ2014113]
FX This paper was supported by Program for Liaoning Excellent Talents in
   University (LJQ2014113).
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NR 58
TC 22
Z9 23
U1 0
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD FEB
PY 2016
VL 95
IS 5
BP 1
EP 11
AR e2641
DI 10.1097/MD.0000000000002641
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DE3BV
UT WOS:000370502700001
PM 26844481
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Dinakar, P
   Höke, A
AF Dinakar, Pradeep
   Hoeke, Ahmet
TI Paraneoplastic fasciitis-panniculitis syndrome: a neurological point of
   view
SO NATURE CLINICAL PRACTICE NEUROLOGY
LA English
DT Article
DE eosinophilic fasciitis; fasciitis-panniculitis syndrome; gastric
   adenocarcinoma; paraneoplastic; stiff-person syndrome
ID CLINICAL SPECTRUM; MUSCLE
AB Background A 54-year-old woman who had undergone gastrectomy to treat gastric adenocarcinoma 5 years previously and had since been in remission presented to a neuromuscular clinic complaining of stiffening and painful spasms of the legs and abdomen. Repeat pan-CT scans and gastric biopsy confirmed the recurrence of poorly differentiated signet ring gastric adenocarcinoma. Her symptoms improved remarkably on initiation of chemotherapy and worsened on discontinuation of chemotherapy.
   Investigations Neurological examination, MRI of the abdomen and lower extremities, whole-body fluorodeoxyglucose PET, pan-CT scan, electromyography, muscle biopsy, upper gastrointestinal tract radiography, esophagogastroduodenoscopy, and immunophenotyping ( paraneoplastic, rheumatological and autoimmune diseases panels).
   Diagnosis Paraneoplastic fasciitis-panniculitis syndrome associated with the recurrence of poorly differentiated signet ring gastric adenocarcinoma.
   Management Chemotherapy of recurrent gastric adenocarcinoma and symptomatic management of painful spasms.
C1 [Dinakar, Pradeep] Harvard Univ, Pain Management Ctr, Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med,Sch Med, Chestnut Hill, MA 02467 USA.
   [Hoeke, Ahmet] Johns Hopkins Univ Hosp, Dept Neurol, Neuromuscular Div, Baltimore, MD 21287 USA.
C3 Harvard University; Harvard University Medical Affiliates; Brigham &
   Women's Hospital; Johns Hopkins University; Johns Hopkins Medicine
RP Dinakar, P (corresponding author), Harvard Univ, Pain Management Ctr, Brigham & Womens Hosp, Dept Anesthesiol Perioperat & Pain Med,Sch Med, Chestnut Hill, MA 02467 USA.
EM pdinakar@partners.org
RI Hoke, Ahmet/NJR-6098-2025
OI Hoke, Ahmet/0000-0003-1215-3373
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NR 16
TC 5
Z9 5
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1745-834X
J9 NAT CLIN PRACT NEURO
JI Nat. Clin. Pract. Neurol.
PD FEB
PY 2009
VL 5
IS 2
BP 113
EP 117
DI 10.1038/ncpneuro0999
PG 5
WC Clinical Neurology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA 403OB
UT WOS:000263090800012
PM 19194391
DA 2025-06-01
ER

PT J
AU Li, M
   Zhou, Q
   Yang, K
   Brigstock, DR
   Zhang, L
   Xiu, M
   Sun, L
   Gao, RP
AF Li, Min
   Zhou, Qiang
   Yang, Kun
   Brigstock, David R.
   Zhang, Lu
   Xiu, Ming
   Sun, Li
   Gao, Run-Ping
TI Rare case of Helicobacter pylori-positive multiorgan IgG4-related
   disease and gastric cancer
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE IgG4-related disease; Helicobacter pylori; Type 1 autoimmune
   pancreatitis; Sclerosing cholecystocholangitis; Gastric cancer
ID AUTOIMMUNE PANCREATITIS; CARBONIC-ANHYDRASE; SERUM IGG4; PATHOGENESIS;
   DIAGNOSIS; INFECTION
AB A 61-year-old male from Northeast China presented with a 2-mo history of abdominal distension, pruritus and jaundice. Laboratory testing revealed an elevated showed a typical feature of autoimmune pancreatitis (AIP) and cholecystocholangitis. Early gastric cancer was incidentally discovered when endoscopic untrasound-guided fine needle aspiration (EUSFNA) of the pancreas was carried out. The patient underwent radical subtotal gastrectomy for gastric cancer combined with cholecystectomy. Helicobacter pylori (H. pylori) and IgG4-positive plasmacytes were detected in gastric cancer tissue, pancreatic EUSFNA sample and resected gallbladder specimen by immunohistochemistry. The patient was diagnosed with H. pylori-positive IgG4-related AIP and sclerosing cholecystocholangitis as well as H. pylori-positive gastric cancer. He responded well to steroid therapy and remains healthy with no signs of recurrence at one year follow-up. We speculate that H. pylori might act as a trigger via direct or indirect action in the initiation of onset of gastric cancer and multiorgan IgG4-related disease.
C1 [Li, Min; Zhou, Qiang; Yang, Kun; Zhang, Lu; Xiu, Ming; Sun, Li; Gao, Run-Ping] Jilin Univ, Hosp 1, Dept Hepat Biliary Pancreat Med, Changchun 130021, Jilin Province, Peoples R China.
   [Brigstock, David R.] Nationwide Childrens Hosp, Res Inst, Columbus, OH 43205 USA.
   [Brigstock, David R.] Ohio State Univ, Div Pediat Surg, Dept Surg, Columbus, OH 43205 USA.
C3 Jilin University; University System of Ohio; Ohio State University;
   Nationwide Childrens Hospital; Research Institute at Nationwide
   Children's Hospital; University System of Ohio; Ohio State University
RP Gao, RP (corresponding author), Jilin Univ, Hosp 1, Dept Hepat Biliary Pancreat Med, 71 Xinmin Ave, Changchun 130021, Jilin Province, Peoples R China.
EM gao_runping@yahoo.com
OI Brigstock, David/0000-0001-8651-6486
FU National Natural Scientific Foundation of China [81070370, 81270544]
FX Supported by National Natural Scientific Foundation of China (to Gao
   RP), No. 81070370 and No. 81270544.
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NR 21
TC 9
Z9 11
U1 0
U2 12
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD MAR 21
PY 2015
VL 21
IS 11
BP 3429
EP 3434
DI 10.3748/wjg.v21.i11.3429
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CD5YQ
UT WOS:000351165100037
PM 25805956
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Mooney, CJ
   Dunphy, EJ
   Stone, B
   McNeel, DG
AF Mooney, CJ
   Dunphy, EJ
   Stone, B
   McNeel, DG
TI Identification of autoantibodies elicited in a patient with prostate
   cancer presenting as dermatomyositis
SO INTERNATIONAL JOURNAL OF UROLOGY
LA English
DT Article
DE autoantibody; dermatomyositis; prostate cancer; SEREX
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; ANTIGEN-SPECIFIC IGG; DENDRITIC CELLS;
   EXPRESSION; CARCINOMA; TRIAL; ADENOCARCINOMA; AUTOANTIGEN; RESPONSES;
   IMMUNITY
AB Objectives: Dermatomyositis is an uncommon autoimmune disease distinguished by proximal muscle weakness and a characteristic skin rash. Dermatomyositis has also frequently been associated with malignancy, typically heralding the diagnosis of ovarian, lung, gastric, or colorectal cancer. We report an unusual case of prostate adenocarcinoma preceded by a diagnosis of dermatomyositis. We hypothesized that in this particular patient, proteins produced by the neoplastic prostatic tissue, which might be normally expressed in muscle tissue, were immunologically recognized as autoantigens.
   Methods: Serum from this patient was used to screen a cDNA lambda phage expression library from normal prostate tissue for prostate protein-specific IgG.
   Results: We identified several immunoreactive plaques encoding known autoantigens, and several encoding known muscle-related proteins, including aldolase C, eukaryotic translation elongation factor 1 alpha 1, transgelin, and acetyl-coenzyme A acyltransferase 1. IgG specific for these proteins were not specifically recognized in sera from other patients with prostate cancer compared with male control blood donors, and were not specifically recognized in a small panel of sera from patients with breast or ovarian cancer and dermatomyositis.
   Conclusions: Our results demonstrate that this patient with prostate cancer presenting as dermatomyositis had autoantibodies to specific proteins, possibly associated with his autoimmune myopathy. Moreover, given this patient's history and the multiple treatment options for prostate cancer, the identification of dermatomyositis in men should prompt an evaluation to exclude a concurrent diagnosis of prostate cancer.
C1 Univ Wisconsin, Dept Med, Madison, WI USA.
   Virginia Mason Med Ctr, Benaroya Res Inst, Seattle, MA USA.
   Univ Wisconsin, Ctr Clin Sci, Sect Med Oncol, Madison, WI USA.
C3 University of Wisconsin System; University of Wisconsin Madison;
   Benaroya Research Institute; Virginia Mason Medical Center; University
   of Wisconsin System; University of Wisconsin Madison
RP K4 518 Clin Sci Ctr, Sect Med Oncol, 600 Highland Ave, Madison, WI 53792 USA.
EM dm3@medicine.wisc.edu
OI McNeel, Douglas/0000-0003-1471-6723
FU NCRR NIH HHS [K23 RR16489] Funding Source: Medline
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NR 36
TC 19
Z9 21
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0919-8172
EI 1442-2042
J9 INT J UROL
JI Int. J. Urol.
PD MAR
PY 2006
VL 13
IS 3
BP 211
EP 217
DI 10.1111/j.1442-2042.2006.01263.x
PG 7
WC Urology & Nephrology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Urology & Nephrology
GA 027ZX
UT WOS:000236456100004
PM 16643611
DA 2025-06-01
ER

PT J
AU Zhang, HJ
   Jin, Z
   Ding, SG
AF Zhang, Hejun
   Jin, Zhu
   Ding, Shigang
TI Gastric Calcifying Fibrous Tumor: A Case of Suspected Immunoglobulin
   G4-related Gastric Disease
SO SAUDI JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Calcifying fibrous tumor; IgG4-related disease; IgG4-related
   pseudotumor; stomach
ID STOMACH; PSEUDOTUMOR; CELLS
AB Gastrointestinal lesions resulting from immunoglobulin G4-related disease are classified into two types: One is a gastrointestinal lesion showing marked thickening of the wall, and the other is an IgG4-related pseudotumor. We report the case of a woman with gastric calcifying fibrous tumor undergoing endoscopic resection that contained 62 IgG4+ plasma cells per high-power field and an IgG4-to-IgG ratio of 41% in lesional plasma cells, which shared clinical and histopathological features associated with gastric IgG4-related pseudotumor. So, we postulate that calcifying fibrous tumor as part of the spectrum of IgG4-related disease might be the unifying concept with IgG4-related pseudotumor. Meanwhile, the patient had coexistent autoimmune diseases, including autoimmune atrophic gastritis, Hashimoto's thyroiditis, and possible primary biliary cirrhosis. The clinical follow-up evaluation was uneventful.
C1 [Zhang, Hejun; Jin, Zhu; Ding, Shigang] Peking Univ, Dept Gastroenterol, Hosp 3, Beijing 100871, Peoples R China.
C3 Peking University
RP Ding, SG (corresponding author), 49 Rd Huayuan, Beijing 100191, Peoples R China.
EM dingshigang222@163.com
CR Agaimy A, 2010, AM J SURG PATHOL, V34, P271, DOI 10.1097/PAS.0b013e3181ccb172
   [Anonymous], ISRN GASTROENTEROL
   Bedeir AS, 2010, J CLIN PATHOL, V63, P999, DOI 10.1136/jcp.2010.081232
   Chetty R, 2011, PATHOLOGY, V43, P31, DOI 10.1097/PAT.0b013e328340e450
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NR 10
TC 22
Z9 23
U1 0
U2 6
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 1319-3767
EI 1998-4049
J9 SAUDI J GASTROENTERO
JI Saudi J. Gastroenterol.
PD NOV-DEC
PY 2015
VL 21
IS 6
BP 423
EP 426
DI 10.4103/1319-3767.170950
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CZ4RB
UT WOS:000367089300014
PM 26655140
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Freeman, HJ
AF Freeman, HJ
TI Lymphoproliferative and intestinal malignancies in 214 patients with
   biopsy-defined celiac disease
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
ID T-CELL LYMPHOMA; DERMATITIS-HERPETIFORMIS; PRESENTING MANIFESTATION;
   SPRUE; POPULATION; ANTIBODY
AB Prior studies have suggested that the incidence of some neoplastic disorders, particularly malignant lymphoma, is increased in celiac disease. In the present study, lymphoproliferative and intestinal cancers in 214 consecutive biopsy-defined celiac disease patients, including 148 females (69.2%) and 66 males (30.8%), seen by a single clinician over more than 20 years were tabulated. Of the 214 patients, 151 were diagnosed with celiac disease before age 60 and 63 at or after age 60. In total, 18 malignant lymphomas and 3 small intestinal adenocarcinomas were detected. While the overall incidence of malignant lymphoma was 8.4%, similar to other European centers, the incidence in elderly celiacs in this study was 22.2%. Celiac disease was detected before or even after the diagnoses of lymphoma or small intestinal adenocarcinoma were established. In some, epithelial lymphocytosis was evident in gastric, colonic, or biliary ductal epithelium. In addition, other immune-mediated disorders, dermatitis herpetiformis, and autoimmune thyroid disease were common, suggesting a distinct clinical and pathologic phenotype in celiac disease that may predispose to malignant complications. Finally, except for a single hypopharyngeal carcinoma in a celiac disease patient with a malignant lymphoma, other malignant disorders of esophagus, stomach, and colon were not detected.
C1 Univ British Columbia, Dept Med Gastroenterol, Vancouver, BC V5Z 1M9, Canada.
C3 University of British Columbia
RP Univ British Columbia Hosp, 2211 Westbrook Mall, Vancouver, BC V6T 1W5, Canada.
EM hugfree@shaw.ca
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NR 36
TC 56
Z9 59
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAY-JUN
PY 2004
VL 38
IS 5
BP 429
EP 434
DI 10.1097/00004836-200405000-00008
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 817KT
UT WOS:000221177100009
PM 15100523
DA 2025-06-01
ER

PT J
AU Izawa, N
   Shiokawa, H
   Onuki, R
   Hamaji, K
   Morikawa, K
   Saji, H
   Ohashi, H
   Kasugai, S
   Hayakawa, N
   Ohara, T
   Sunakawa, Y
AF Izawa, N.
   Shiokawa, H.
   Onuki, R.
   Hamaji, K.
   Morikawa, K.
   Saji, H.
   Ohashi, H.
   Kasugai, S.
   Hayakawa, N.
   Ohara, T.
   Sunakawa, Y.
TI The clinical utility of comprehensive measurement of autoimmune
   disease-related antibodies in patients with advanced solid tumors
   receiving immune checkpoint inhibitors: a retrospective study
SO ESMO OPEN
LA English
DT Article
DE immune checkpoint inhibitors; immune-related adverse events; autoimmune
   disease-related antibodies
ID THYROIDITIS; NIVOLUMAB; MELANOMA
AB Background: The comprehensive measurement of autoimmune disease-related antibodies (Abs) before immune checkpoint inhibitor (ICI) treatment may be useful for predicting the development of immune-related adverse events (irAEs); however, the clinical utility is not well known.
   Materials and methods: We retrospectively analyzed patients with advanced solid tumors treated with ICI monotherapy or doublet combination therapy between July 2014 and December 2020 at single institute. Antinuclear antibody (ANA), anti-thyroglobulin (Tg) Ab, anti-thyroid peroxidase (TPO) Ab, anti-glutamic acid decarboxylase (GAD) Ab, anti-acetylcholine esterase receptor (AchR) Ab, and platelet-associated immunoglobulin G (PA-IgG) Ab were comprehensively measured for the screening before ICI therapy.
   Results: Of 275 registered patients (median age, 70 years; male, 64.4%; Eastern Cooperative Oncology Group performance status of 0 or 1, 88.7%; and prior regimen of 0-1/>= 2, 88.7%/11.3%), 128 non-small-cell lung cancer, 35 gastric cancer, 33 head and neck cancer, 24 melanoma, 19 renal cell carcinoma, 13 urothelial carcinoma, 12 esophageal cancer, 5 malignant mesothelioma of pleura, 2 endometrial cancer, and 4 other cancer were included. The number of patients with positive ANA, Tg, TPO, PA-IgG, GAD, and AchR Abs was 52 (24.9%), 38 (14.5%), 11 (10.1%), 6 (3.5%), 5 (2.0%), and 1 (0.5%), respectively. There was no association between the development of any irAEs and Abs positivity, while thyroid dysfunction developed more frequently among patients with than without Tg Ab or TPO Ab (39.5% versus 12.5%, P < 0.01; 45.5% versus 14.3%, P = 0.02).
   Conclusions: The clinical utility of comprehensive measurement of autoimmune disease-related Abs before introduction of ICI therapy was limited for predicting irAE. However, Tg and TPO Abs were risk factors as regards the development of ICI-induced thyroid dysfunction.
C1 [Izawa, N.; Sunakawa, Y.] St Marianna Univ, Sch Med, Dept Clin Oncol, Kawasaki, Kanagawa, Japan.
   [Shiokawa, H.; Onuki, R.; Hamaji, K.] St Marianna Univ Hosp, Dept Pharm, Kawasaki, Kanagawa, Japan.
   [Morikawa, K.] St Marianna Univ, Sch Med, Dept Internal Med, Div Resp Med, Kawasaki, Kanagawa, Japan.
   [Saji, H.] St Marianna Univ, Sch Med, Dept Chest Surg, Kawasaki, Kanagawa, Japan.
   [Ohashi, H.] St Marianna Univ, Sch Med, Dept Dermatol, Kawasaki, Kanagawa, Japan.
   [Kasugai, S.] St Marianna Univ, Sch Med, Dept Otorhinolaryngol, Kawasaki, Kanagawa, Japan.
   [Hayakawa, N.] St Marianna Univ, Sch Med, Dept Urol, Kawasaki, Kanagawa, Japan.
   [Ohara, T.] St Marianna Univ, Sch Med, Dept Obstet & Gynecol, Kawasaki, Kanagawa, Japan.
C3 Saint Marianna University; Saint Marianna University; Saint Marianna
   University; Saint Marianna University; Saint Marianna University; Saint
   Marianna University; Saint Marianna University; Saint Marianna
   University
RP Sunakawa, Y (corresponding author), St Marianna Univ, Sch Med, Dept Clin Oncol, Miyamae Ku, 2-16-1 Sugao, Kawasaki, Kanagawa 2168511, Japan.
EM y.sunakawa@marianna-u.ac.jp
RI Sunakawa, Yu/AGW-7031-2022; Morikawa, Kei/AAG-8086-2019
CR Ansari MJI, 2003, J EXP MED, V198, P63, DOI 10.1084/jem.20022125
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NR 17
TC 10
Z9 13
U1 1
U2 3
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
EI 2059-7029
J9 ESMO OPEN
JI ESMO Open
PD APR
PY 2022
VL 7
IS 2
AR 100415
DI 10.1016/j.esmoop.2022.100415
EA MAR 2022
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 2P7NB
UT WOS:000819921700011
PM 35247869
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Kandemir, EG
   Yonem, A
   Narin, Y
AF Kandemir, EG
   Yonem, A
   Narin, Y
TI Gastric carcinoma and thyroid status
SO JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
LA English
DT Article
DE gastric carcinoma; autoimmune thyroid disease; thyroid
ID HELICOBACTER-PYLORI; IODINE; EXPRESSION; INFECTION
AB Gastric carcinoma is reported to be more frequent in geographical areas where diets are either iodine-deficient or iodine-excessive. Reports have also shown an association between thyroid diseases and some of the risk factors for gastric carcinoma. We investigated the frequency of thyroid disorders in 61 patients with gastric carcinoma compared with 55 healthy control subjects. Thyroid health was evaluated by physical examination and by measuring the serum levels of thyroid hormones and thyroid autoantibodies. More patients with gastric cancer had goitre compared with healthy controls (49.1% versus 20%, respectively). Significantly more patients with gastric cancer had non-toxic goitre compared with control subjects. There was also a significant difference in the incidence of autoimmune thyroid disease - 27.8% of patients with gastric cancer versus 10.9% of control subjects were affected. These results indicate that there is a significant association between gastric cancer and thyroid disorders.
C1 GATA Haydarpasa Egitim Hastansei, Onkoloji Klingi, Dept Med Oncol, TR-81020 Istanbul, Turkey.
   GATA Haydarpasa Egitim Hastansei, Dept Endocrinol, TR-81020 Istanbul, Turkey.
   GATA Haydarpasa Egitim Hastansei, Dept Nucl Med, TR-81020 Istanbul, Turkey.
C3 Gulhane Military Medical Academy; Istanbul Haydarpasa Sultan Abdulhamid
   Training & Research Hospital; Istanbul Haydarpasa Sultan Abdulhamid
   Training & Research Hospital; Gulhane Military Medical Academy; Gulhane
   Military Medical Academy; Istanbul Haydarpasa Sultan Abdulhamid Training
   & Research Hospital
RP GATA Haydarpasa Egitim Hastansei, Onkoloji Klingi, Dept Med Oncol, TR-81020 Istanbul, Turkey.
EM egkondemir@yahoo.com
OI Yonem, Arif/0000-0003-1517-9376
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NR 27
TC 19
Z9 21
U1 0
U2 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0300-0605
EI 1473-2300
J9 J INT MED RES
JI J. Int. Med. Res.
PD MAR-APR
PY 2005
VL 33
IS 2
BP 222
EP 227
DI 10.1177/147323000503300210
PG 6
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA 905PK
UT WOS:000227581200010
PM 15790134
DA 2025-06-01
ER

PT J
AU Honan, AM
   Chen, ZB
AF Honan, Amanda M.
   Chen, Zhibin
TI Stromal Cells Underlining the Paths From Autoimmunity, Inflammation to
   Cancer With Roles Beyond Structural and Nutritional Support
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE stromal cells; secondary lymphoid organs; autoimmunity; cancer;
   non-lymphoid tissues
ID LYMPH-NODE; T-CELLS; DENDRITIC CELLS; GASTRIC-CANCER; CONTROL POINTS;
   CD8; ANTIGEN; MECHANISMS; EXPRESSION; ENDOTHELIUM
AB Stromal cells provide structural support and nutrients in secondary lymphoid organs and non-lymphoid tissues. However, accumulating evidence suggests that a complex relationship exists between stromal cells and immune cells. Interactions between immune cells and stromal cells have been shown to influence the pathology of both autoimmunity and cancer. This review examines the heterogeneity of stromal cells within the lymph node and non-lymphoid tissues during both homeostatic and inflammatory conditions, in particular autoimmunity and cancer, with the goal of better understanding the complex and apparently paradoxical relationship between these two classes of diseases. The review surveys potential novel mechanisms involving the interactions between stromal cells and immune cells which may contribute to the development, pathology and underlying connection between autoimmunity and cancer, including potential pathways from autoimmune inflammation to either "hot" or "cold" tumors. These interactions may provide some insights to explain the rising incidence of both autoimmunity and cancer in young women in industrialized countries and have the potential to be exploited in the development of new interventions for preventions and treatments of both autoimmune diseases and cancer.
C1 [Honan, Amanda M.; Chen, Zhibin] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.
   [Chen, Zhibin] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
C3 University of Miami; University of Miami
RP Chen, ZB (corresponding author), Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.; Chen, ZB (corresponding author), Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
EM zchen@med.miami.edu
FU National Institutes of Health [R01AI134903, R01CA245673]
FX This work is supported in part by grants from the National Institutes of
   Health R01AI134903 and R01CA245673.
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NR 117
TC 11
Z9 12
U1 0
U2 0
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD MAY 25
PY 2021
VL 9
AR 658984
DI 10.3389/fcell.2021.658984
PG 14
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA SO0PA
UT WOS:000658682500001
PM 34113615
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Calvete, O
   Reyes, J
   Valdés-Socin, H
   Martin, P
   Marazuela, M
   Barroso, A
   Escalada, J
   Castells, A
   Torres-Ruiz, R
   Rodríguez-Perales, S
   Currás-Freixes, M
   Benítez, J
AF Calvete, Oriol
   Reyes, Jose
   Valdes-Socin, Hernan
   Martin, Paloma
   Marazuela, Monica
   Barroso, Alicia
   Escalada, Javier
   Castells, Antoni
   Torres-Ruiz, Raul
   Rodriguez-Perales, Sandra
   Curras-Freixes, Maria
   Benitez, Javier
TI Alterations in SLC4A2, SLC26A7 and SLC26A9 Drive Acid-Base Imbalance in
   Gastric Neuroendocrine Tumors and Uncover a Novel Mechanism for a
   Co-Occurring Polyautoimmune Scenario
SO CELLS
LA English
DT Article
DE gastric neuroendocrine tumors (gNETS); autoimmune thyrogastric syndrome;
   autoimmune polyendocrine syndrome (APS); achlorhydria; solute carriers
   (SLCs); immunodeficiencies
ID AUTOIMMUNE-DISEASES; PERNICIOUS-ANEMIA; GENES
AB Autoimmune polyendocrine syndrome (APS) is assumed to involve an immune system malfunction and entails several autoimmune diseases co-occurring in different tissues of the same patient; however, they are orphans of its accurate diagnosis, as its genetic basis and pathogenic mechanism are not understood. Our previous studies uncovered alterations in the ATPase H+/K+ Transporting Subunit Alpha (ATP4A) proton pump that triggered an internal cell acid-base imbalance, offering an autoimmune scenario for atrophic gastritis and gastric neuroendocrine tumors with secondary autoimmune pathologies. Here, we propose the genetic exploration of APS involving gastric disease to understand the underlying pathogenic mechanism of the polyautoimmune scenario. The whole exome sequencing (WES) study of five autoimmune thyrogastric families uncovered different pathogenic variants in SLC4A2, SLC26A7 and SLC26A9, which cotransport together with ATP4A. Exploratory in vitro studies suggested that the uncovered genes were involved in a pathogenic mechanism based on the alteration of the acid-base balance. Thus, we built a custom gene panel with 12 genes based on the suggested mechanism to evaluate a new series of 69 APS patients. In total, 64 filtered putatively damaging variants in the 12 genes of the panel were found in 54.17% of the studied patients and none of the healthy controls. Our studies reveal a constellation of solute carriers that co-express in the tissues affected with different autoimmune diseases, proposing a unique genetic origin for co-occurring pathologies. These results settle a new-fangled genetics-based mechanism for polyautoimmunity that explains not only gastric disease, but also thyrogastric pathology and disease co-occurrence in APS that are different from clinical incidental findings. This opens a new window leading to the prediction and diagnosis of co-occurring autoimmune diseases and clinical management of patients.
C1 [Calvete, Oriol; Martin, Paloma; Barroso, Alicia; Benitez, Javier] Spanish Natl Canc Res Ctr CNIO, Human Genet Grp, Madrid 28029, Spain.
   [Calvete, Oriol; Martin, Paloma; Benitez, Javier] Network Res Rare Dis CIBERER, Madrid 28029, Spain.
   [Calvete, Oriol; Reyes, Jose] Grp Espanol Tumores Neuroendocrinos & Endocrinos, Madrid 28054, Spain.
   [Reyes, Jose] Hosp Comarcal Inca, Dept Gastroenterol, Inca 07300, Spain.
   [Reyes, Jose] Hlth Invest Inst IDISBA, Palma De Mallorca 07120, Spain.
   [Valdes-Socin, Hernan] Ctr Hosp Univ Liege, Dept Endocrinol, B-4000 Liege, Belgium.
   [Marazuela, Monica] Univ Autonoma Madrid, Hosp Princesa, Inst Invest Princesa, Madrid 28006, Spain.
   [Escalada, Javier] Clin Univ Navarra, Endocrinol & Nutr Dept, Pamplona 31008, Spain.
   [Escalada, Javier] Navarra Inst Hlth Res, IdiSNA, Pamplona 31008, Spain.
   [Escalada, Javier] Inst Salud Carlos III, CIBER Fisiopatol Obesidad & Nutr CIBEROBN, Madrid 28009, Spain.
   [Castells, Antoni] Univ Barcelona, Hosp Clin Barcelona, IDIBAPS, CIBEREHD, Barcelona 08036, Spain.
   [Torres-Ruiz, Raul; Rodriguez-Perales, Sandra] Spanish Natl Canc Res Ctr CNIO, Mol Cytogenet & Genome Editing Unit, Madrid 28029, Spain.
   [Curras-Freixes, Maria] Clin Univ Navarra, Endocrinol & Nutr Dept, Madrid 28027, Spain.
   [Calvete, Oriol] Inst Recerca Leucemia Josep Carreras, MDS Grp, Badalona 08916, Spain.
C3 Centro Nacional de Investigaciones Oncologicas (CNIO); CIBER - Centro de
   Investigacion Biomedica en Red; CIBERER; Hospital Comarcal Inca;
   University of Liege; Autonomous University of Madrid; Hospital de La
   Princesa; University of Navarra; Instituto de Salud Carlos III; CIBER -
   Centro de Investigacion Biomedica en Red; CIBEROBN; University of
   Barcelona; Hospital Clinic de Barcelona; IDIBAPS; CIBER - Centro de
   Investigacion Biomedica en Red; CIBEREHD; Centro Nacional de
   Investigaciones Oncologicas (CNIO); University of Navarra; Institut de
   Recerca Contra la Leucemia Josep Carreras (IJC)
RP Calvete, O; Benítez, J (corresponding author), Spanish Natl Canc Res Ctr CNIO, Human Genet Grp, Madrid 28029, Spain.; Calvete, O; Benítez, J (corresponding author), Network Res Rare Dis CIBERER, Madrid 28029, Spain.; Calvete, O (corresponding author), Grp Espanol Tumores Neuroendocrinos & Endocrinos, Madrid 28054, Spain.; Calvete, O (corresponding author), Inst Recerca Leucemia Josep Carreras, MDS Grp, Badalona 08916, Spain.
EM oriolcalvete@gmail.com; jose.reyes@hcin.es; hg.valdessocin@chuliege.be;
   p.martingimeno@hotmail.com; monica.marazuela@gmail.com;
   monica.marazuela@gmail.com; fescalada@unav.es; castells@clinic.cat;
   rtorresr@cnio.es; srodriguezp@cnio.es; mcurras@unav.es; jenitez@cnio.es
RI ortiz, Javier/H-5232-2015; Castells, Antoni/ABC-1002-2021; Moreno,
   José/H-9440-2017; marazuela, monica/D-8385-2016; Calvete,
   Oriol/ABH-6579-2020; Rodriguez-Perales, Sandra/T-7667-2017; Torres,
   Raul/J-1649-2018; Escalada, Javier/E-6330-2013
OI Rodriguez-Perales, Sandra/0000-0001-7221-3636; Calvete,
   Oriol/0000-0002-2623-2876; Torres, Raul/0000-0001-9606-0398; Reyes
   Moreno, Jose/0000-0002-8894-8095; Marazuela, Monica/0000-0003-1158-9618;
   Escalada, Javier/0000-0001-5877-9465; Castells,
   Antoni/0000-0001-8431-2033
FU H2020 BRIDGES project [634935]; 2017 BBMRI-LPC Whole Exome Sequencing
   Call and Instituto de Salud Carlos III; European Regional Development
   Fund (ERDF) [PI16/00440]
FX This research was funded by the H2020 BRIDGES project, grant number
   634935, and by the 2017 BBMRI-LPC Whole Exome Sequencing Call and
   Instituto de Salud Carlos III, co-funded by the European Regional
   Development Fund (ERDF), grant number (PI16/00440).
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NR 37
TC 5
Z9 6
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD DEC
PY 2021
VL 10
IS 12
AR 3500
DI 10.3390/cells10123500
PG 20
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA XX5CM
UT WOS:000736313500001
PM 34944008
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Friedrich, M
   Pracht, K
   Mashreghi, MF
   Jäck, HM
   Radbruch, A
   Seliger, B
AF Friedrich, Michael
   Pracht, Katharina
   Mashreghi, Mir-Farzin
   Jaeck, Hans-Martin
   Radbruch, Andreas
   Seliger, Barbara
TI The role of the miR-148/-152 family in physiology and disease
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Review
DE Cancer; Diseases; Epigenetic; Lymphocytes; MicroRNA-148/-152 family;
   miRNA regulation; Post-transcriptional regulation
ID HLA-G EXPRESSION; INHIBITS CELL-PROLIFERATION; GLIOBLASTOMA STEM-CELLS;
   GASTRIC-CANCER; TUMOR-SUPPRESSOR; MICRORNA-148A SUPPRESSES; DNA
   METHYLATION; POSTTRANSCRIPTIONAL REGULATION; HEPATOCELLULAR-CARCINOMA;
   MESENCHYMAL TRANSITION
AB MicroRNAs (miRNAs) are endogenously encoded similar to 22 nt small non-coding RNAs. They function as key players of many cellular processes by base pairing with target mRNAs and thereby impairing gene expression at the post-transcriptional level. Recent findings demonstrate a critical role of many miRNAs in immune cell differentiation and immune responses, which is also associated with the development and progression of many tumor and non-tumor diseases. Here we review the multifaceted miRNA-148/-152 family members consisting of miR-148a, miR-148b and miR-152. Next to regulation mechanisms that control the expression of this miRNA family, we will focus on (i) the role of miR-148a in regulating B and T lymphocyte function and its role in associated diseases and (ii) the importance of miR-148/-152 family members for cancer initiation, tumor growth and metastasis formation. In addition, this review aims to highlight some selected targets of the miRNA-148/-152 family members, which are involved in the biology of cancer and maintenance of epigenetic patterns. In conclusion, members of the miR-148/-152 family might represent prognostic markers and/or potential therapeutic targets for treatment of autoimmune disorders, chronic inflammatory diseases and multiple types of cancer.
C1 [Friedrich, Michael; Seliger, Barbara] Martin Luther Univ Halle Wittenberg, Inst Med Immunol, Halle, Germany.
   [Pracht, Katharina; Jaeck, Hans-Martin] Univ Erlangen Nurnberg, Dept Internal Med 3, Nikolaus Fiebiger Ctr, Div Mol Immunol, Erlangen, Germany.
   [Mashreghi, Mir-Farzin; Radbruch, Andreas] Deutsch Rheuma Forsch Zentrum DRFZ, Berlin, Germany.
C3 Martin Luther University Halle Wittenberg; University of Erlangen
   Nuremberg
RP Seliger, B (corresponding author), Martin Luther Univ Halle Wittenberg, Inst Med Immunol, Halle, Germany.
EM Barbara.Seliger@uk-halle.de
RI Pracht, Katharina/KCX-8352-2024; Mashreghi, Mir-Farzin/AFL-8690-2022;
   Radbruch, Andreas/ADI-4973-2022
OI Pracht, Katharina/0000-0002-8943-4897; Mashreghi,
   Mir-Farzin/0000-0002-8015-6907; Jack, Hans-Martin/0000-0002-6332-8463;
   Radbruch, Andreas/0000-0001-5753-0000; Seliger,
   Barbara/0000-0002-5544-4958
FU Deutsche Forschungsgemeinschaft [Se581-23, GRK1591/BS, TRR130, GRK1660];
   European Research Council Advanced Grant IMMEMO [ERC-2010-AdG.20100317,
   268987]; state of Berlin; European Regional Development Fund (ERDF)
   [EFRE 1.8/11]
FX Part of this work was funded by the Deutsche Forschungsgemeinschaft to
   B.S. (Se581-23) GRK1591/BS, H.-M.J (TRR130 and GRK1660). This work was
   supported by a European Research Council Advanced Grant IMMEMO
   (ERC-2010-AdG.20100317 Grant 268987 awarded to A.R.). M.F.M is supported
   by the state of Berlin and the "European Regional Development Fund"
   (ERDF 2014-2020, EFRE 1.8/11, Deutsches Rheuma-Forschungszentrum).
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NR 136
TC 98
Z9 111
U1 1
U2 25
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD DEC
PY 2017
VL 47
IS 12
BP 2026
EP 2038
DI 10.1002/eji.201747132
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FP0FC
UT WOS:000417273800003
PM 28880997
OA Bronze
DA 2025-06-01
ER

PT J
AU Kanamaru, R
   Ohzawa, H
   Miyato, H
   Yamaguchi, H
   Hosoya, Y
   Lefor, AK
   Sata, N
   Kitayama, J
AF Kanamaru, Rihito
   Ohzawa, Hideyuki
   Miyato, Hideyo
   Yamaguchi, Hironori
   Hosoya, Yoshinori
   Lefor, Alan Kawarai
   Sata, Naohiro
   Kitayama, Joji
TI Neutrophil Extracellular Traps Generated by Low Density Neutrophils
   Obtained from Peritoneal Lavage Fluid Mediate Tumor Cell Growth and
   Attachment
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Cancer Research; Issue 138; Low density neutrophils (LDN); neutrophil
   extracellular traps (NETs); DNase; peritoneal metastases; adhesion;
   microenvironment
ID GRANULOCYTES
AB Activated neutrophils release neutrophil extracellular traps (NETs), which can capture and destroy microbes. Recent studies suggest that NETs are involved in various disease processes, such as autoimmune disease, thrombosis, and tumor metastases. Here, we show a detailed in vitro technique to detect NET activity during the trapping of free tumor cells, which grow after attachment to NETs. First, we collected low density neutrophils (LDN) from postoperative peritoneal lavage fluid from patients who underwent laparotomies. Short-term culturing of LDN resulted in massive NET formation that was visualized with green fluorescent nuclear and chromosome counterstain. After co-incubation of human gastric cancer cell lines MKN45, OCUM-1, and NUGC-4 with the NETs, many tumor cells were trapped by the NETs. Subsequently, the attachment was completely abrogated by the degradation of NETs with DNase I. Time-lapse video revealed that tumor cells trapped by the NETs did not die but instead grew vigorously in a continuous culture. These methods may be applied to the detection of adhesive interactions between NETs and various types of cells and materials.
C1 [Kanamaru, Rihito; Ohzawa, Hideyuki; Miyato, Hideyo; Yamaguchi, Hironori; Hosoya, Yoshinori; Lefor, Alan Kawarai; Sata, Naohiro; Kitayama, Joji] Jichi Med Univ, Dept Gastrointestinal Surg, Shimotsuke, Tochigi, Japan.
C3 Jichi Medical University
RP Kitayama, J (corresponding author), Jichi Med Univ, Dept Gastrointestinal Surg, Shimotsuke, Tochigi, Japan.
EM kitayama@jichi.ac.jp
RI Yamaguchi, Hironori/AAA-3642-2022; Lefor, Alan/E-9979-2012
FU Ministry of Education, Science, Sports, and Culture of Japan; Japan
   Society for the Promotion of Science [17K10606]; Grants-in-Aid for
   Scientific Research [17K10606] Funding Source: KAKEN
FX We thank Ms. J. Shinohara and I. Nieda for technical and clerical work.
   Also, we thank Drs. Shiro Matsumoto, Hidenori Haruta, Kentaro Kurashina,
   and Kazuya Takahashi for their cooperation for sample acquisition in
   operating room. This work was supported by a Grant-in-Aid for Scientific
   Research from the Ministry of Education, Science, Sports, and Culture of
   Japan and the Japan Society for the Promotion of Science (17K10606).
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NR 17
TC 27
Z9 27
U1 0
U2 5
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD AUG
PY 2018
IS 138
AR e58201
DI 10.3791/58201
PG 6
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GU0BQ
UT WOS:000444913100133
PM 30124642
OA Green Published
DA 2025-06-01
ER

PT J
AU Neumann, WL
   Coss, E
   Rugge, M
   Genta, RM
AF Neumann, William L.
   Coss, Elizabeth
   Rugge, Massimo
   Genta, Robert M.
TI Autoimmune atrophic gastritis-pathogenesis, pathology and management
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID HELICOBACTER-PYLORI INFECTION; SERUM PEPSINOGEN-I; PERNICIOUS-ANEMIA;
   FOLLOW-UP; GLAND ADENOMA; ANTIGASTRIC AUTOANTIBODIES; CHANGING
   EPIDEMIOLOGY; 1ST-DEGREE RELATIVES; COBALAMIN DEFICIENCY;
   CARCINOID-TUMORS
AB Autoimmune gastritis is a chronic progressive inflammatory condition that results in the replacement of the parietal cell mass by atrophic and metaplastic mucosa. A complex interaction of autoantibodies against the parietal cell proton pump and sensitized T cells progressively destroy the parietal cells, inducing hypochlorhydria and then achlorhydria, while autoantibodies against the intrinsic factor impair the absorption of vitamin B-12. The resulting cobalamin deficiency manifests with megaloblastic anaemia and neurological and systemic signs and symptoms collectively known as pernicious anaemia. Previously believed to be predominantly a disease of elderly women of Northern European ancestry, autoimmune gastritis has now been recognized in all populations and ethnic groups, but because of the complexity of the diagnosis no reliable prevalence data are available. For similar reasons, as well as the frequent and often unknown overlap with Helicobacter pylori infection, the risk of gastric cancer has not been adequately assessed in these patients. This Review summarizes the epidemiology, pathogenesis and pathological aspects of autoimmune metaplastic atrophic gastritis. We also provide practical advice for the diagnosis and management of patients with this disease.
C1 [Neumann, William L.; Genta, Robert M.] Miraca Life Sci Res Inst, Irving, TX 75039 USA.
   [Coss, Elizabeth] Univ Texas SW Med Ctr Dallas, Dept Med, Div Gastroenterol, VAMC, Dallas, TX 75216 USA.
   [Rugge, Massimo] Univ Padua, Dept Med DIMED, Pathol & Cytopathol Unit, I-35128 Padua, Italy.
C3 University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Padua
RP Genta, RM (corresponding author), Miraca Life Sci Res Inst, 6655 North MacArthur Blvd, Irving, TX 75039 USA.
EM robert.genta@utsouthwestern.edu
RI Rugge, Massimo/K-7525-2016
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NR 149
TC 270
Z9 285
U1 5
U2 81
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD SEP
PY 2013
VL 10
IS 9
BP 529
EP 541
DI 10.1038/nrgastro.2013.101
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 214HZ
UT WOS:000324124300008
PM 23774773
DA 2025-06-01
ER

PT J
AU Rugge, M
   Bricca, L
   Guzzinati, S
   Sacchi, D
   Pizzi, M
   Savarino, E
   Farinati, F
   Zorzi, M
   Fassan, M
   Dei Tos, AP
   Malfertheiner, P
   Genta, RM
   Graham, DY
AF Rugge, Massimo
   Bricca, Ludovica
   Guzzinati, Stefano
   Sacchi, Diana
   Pizzi, Marco
   Savarino, Edoardo
   Farinati, Fabio
   Zorzi, Manuel
   Fassan, Matteo
   Dei Tos, Angelo Paolo
   Malfertheiner, Peter
   Genta, Robert M.
   Graham, David Y.
TI Autoimmune gastritis: long-term natural history in naive Helicobacter
   pylori-negative patients
SO GUT
LA English
DT Article
DE gastritis; autoimmune disease; neuroendocrine tumors; gastric
   metaplasia; staging
ID ATROPHIC GASTRITIS; INCREASED RISK; SYDNEY SYSTEM; METAPLASIA; CANCER;
   CLASSIFICATION; DIAGNOSIS; PATHOLOGY; STOMACH; DYSPLASIA
AB Objective Autoimmune gastritis (AIG) is an immunomediated disease targeting parietal cells, eventually resulting in oxyntic-restricted atrophy. This long-term follow-up study aimed at elucidating the natural history, histological phenotype(s), and associated cancer risk of patients with AIG consistently tested H. pylori-negative (naive H. pylori-negative subjects). Design Two-hundred eleven naive H. pylori-negative patients (tested by serology, histology, molecular biology) with AIG (F:M=3.15:1; p<0.001) were prospectively followed up with paired biopsies (T1 vs T2; mean follow-up years:7.5 (SD:4.4); median:7). Histology distinguished non-atrophic versus atrophic AIG. Atrophy was further subtyped/scored as non-metaplastic versus metaplastic (pseudopyloric (PPM) and intestinal (IM)). Enterochromaffin-like-cell (ECL) status was categorised as diffuse versus adenomatoid hyperplasia/dysplasia, and type 1 neuroendocrine tumours (Type1-NETs). Results Over the long-term histological follow-up, AIG consistently featured oxyntic-predominant-mononuclear inflammation. At T1, PPM-score was greater than IM (200/211 vs 160/211, respectively); IM scores increased from T1 to T2 (160/211 to 179/211), with no changes in the PPM prevalence (T1=200/211; T2=201/211). At both T1/T2, the prevalence of OLGA-III-stage was <5%; no Operative Link on Gastritis Assessment (OLGA)-IV-stage occurred. ECL-cell-status progressed from diffuse to adenomatoid hyperplasia/dysplasia (T1=167/14 vs T2=151/25). Type1-NETs (T1=10; T2=11) always coexisted with extensive oxyntic-atrophy, and ECL adenomatoid-hyperplasia/dysplasia. No excess risk of gastric or other malignancies was found over a cumulative follow-up time of 10 541 person years, except for (marginally significant) thyroid cancer (SIR=3.09; 95% CI 1.001 to 7.20). Conclusions Oxyntic-restricted inflammation, PPM (more than IM), and ECL-cell hyperplasia/neoplasia are the histological AIG hallmarks. Compared with the general population, corpus-restricted inflammation/atrophy does not increase the GC risk. The excess of GC risk reported in patients with AIG could plausibly result from unrecognised previous/current H. pylori comorbidity.
C1 [Rugge, Massimo; Bricca, Ludovica; Pizzi, Marco; Fassan, Matteo; Dei Tos, Angelo Paolo] Dept Med DIMED, Ringgold ID 9308, Padua, Veneto, Italy.
   [Rugge, Massimo; Guzzinati, Stefano; Zorzi, Manuel] Azienda Zero, Veneto Tumor Registry, Padua, Veneto, Italy.
   [Sacchi, Diana; Savarino, Edoardo; Farinati, Fabio] Univ Padua, Dept Surg Oncol & Gastroenterol, Ringgold ID 9308, Padua, Italy.
   [Fassan, Matteo] Veneto Inst Oncol IOV IRCCS, Padua, Italy.
   [Malfertheiner, Peter] Ludwig Maximilians Univ Munchen, Radiol, Munich, Germany.
   [Genta, Robert M.] Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA.
   [Genta, Robert M.; Graham, David Y.] Baylor Coll Med, Dept Med, Michael E De Bakey VA Med Ctr, Houston, TX 77030 USA.
C3 Azienda Zero; University of Padua; IRCCS Istituto Oncologico Veneto
   (IOV); University of Munich; Baylor College of Medicine; Baylor College
   of Medicine; US Department of Veterans Affairs; Veterans Health
   Administration (VHA); Michael E DeBakey VA Medical Center
RP Rugge, M (corresponding author), Univ Padua, Dept Med DIMED, I-35121 Padua, Veneto, Italy.
EM massimo.rugge@unipd.it
RI Guzzinati, Stefano/K-4987-2012; Graham, David/AAL-2165-2021; Farinati,
   Fabio/A-8267-2012; Dei Tos, Angelo/AAN-3244-2020; Savarino,
   Edoardo/AAC-7510-2022; Zorzi, Manuel/HPD-1873-2023; Malfertheiner,
   Peter/AEZ-6553-2022; Pizzi, Marco/LIA-7766-2024; Pizzi,
   Marco/H-6273-2016; Zorzi, Manuel/J-7029-2016; Fassan, Matteo/F-5152-2012
OI Pizzi, Marco/0000-0003-4006-7317; RUGGE, MASSIMO/0000-0002-0679-0563;
   Savarino, Edoardo/0000-0002-3187-2894; Zorzi,
   Manuel/0000-0001-6025-5214; FARINATI, FABIO/0000-0002-2944-1374; DEI
   TOS, ANGELO/0000-0002-1228-8940; Fassan, Matteo/0000-0001-6515-5482
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NR 72
TC 74
Z9 78
U1 1
U2 13
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0017-5749
EI 1468-3288
J9 GUT
JI Gut
PD JAN
PY 2023
VL 72
IS 1
BP 30
EP 38
DI 10.1136/gutjnl-2022-327827
EA JUN 2022
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 8H5IJ
UT WOS:000820347100001
PM 35772926
DA 2025-06-01
ER

PT J
AU Zhang, SY
   Shi, D
   Li, MR
   Li, YR
   Wang, XM
   Li, W
AF Zhang, Shuyi
   Shi, Dan
   Li, Muran
   Li, Yanru
   Wang, Ximo
   Li, Wen
TI The relationship between gastric microbiota and gastric disease
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Gastric microbiota; Helicobacter pylori; chronic atrophic gastritis;
   autoimmune gastritis; gastric cancer
ID HELICOBACTER-PYLORI INFECTION; PROTON PUMP INHIBITORS; NITRIC-OXIDE
   SYNTHASE; ATROPHIC GASTRITIS; GUT MICROBIOTA; INTESTINAL METAPLASIA;
   AUTOIMMUNE GASTRITIS; BACTERIAL-FLORA; INCREASED RISK; CANCER
AB Traditionally, the stomach was believed to be a sterile organ unsuitable for microbiota growth. However, the discovery of H. pylori subverted this conception. With the development of molecular techniques, an abundance of microbiota of great diversity was found in the stomach. In addition, various lines of evidence suggest that the gastric microbiota plays a critical role in the development and progression of the gastric disease.The gastrointestinal microbiome plays an important role in various physiologic and pathologic processes.
C1 [Zhang, Shuyi; Li, Yanru; Li, Wen] Tianjin Union Med Ctr, Endoscopy Ctr, 190 Jieyuan Rd, Tianjin 300121, Peoples R China.
   [Shi, Dan; Li, Wen] Tianjin Med Univ, Grad Sch, Tianjin, Peoples R China.
   [Li, Muran] Tianjin Union Med Ctr, Dept Gastroenterol, Tianjin, Peoples R China.
   [Wang, Ximo] ITCWM Nankai Hosp, ITCWM Acute Abdomen Tianjin Hosp, Tianjin Clin Med Res Ctr, Tianjin, Peoples R China.
C3 Tianjin Medical University
RP Li, W (corresponding author), Tianjin Union Med Ctr, Endoscopy Ctr, 190 Jieyuan Rd, Tianjin 300121, Peoples R China.
EM zhangshuyi1973@126.com
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NR 88
TC 37
Z9 40
U1 1
U2 36
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD APR 3
PY 2019
VL 54
IS 4
BP 391
EP 396
DI 10.1080/00365521.2019.1591499
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IK9WR
UT WOS:000476948200001
PM 30945954
DA 2025-06-01
ER

PT J
AU Li, CM
   Chen, ZB
AF Li, Chris M.
   Chen, Zhibin
TI Autoimmunity as an Etiological Factor of Cancer: The Transformative
   Potential of Chronic Type 2 Inflammation
SO FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE autoimmunity; type 2 immunity; interleukin-4; interleukin-13; chronic
   inflammation; tumorigenesis; metaplasia; cancer
ID TUMOR-ASSOCIATED MACROPHAGES; INTERLEUKIN-4 RECEPTOR-ALPHA; SINONASAL
   TRACT INFLAMMATION; NONCARDIA GASTRIC-CANCER; ATOPIC-DERMATITIS;
   T-CELLS; NASOPHARYNGEAL CARCINOMA; IMMUNE DYSREGULATION; CTLA4
   INSUFFICIENCY; COLORECTAL-CANCER
AB Recent epidemiological studies have found an alarming trend of increased cancer incidence in adults younger than 50 years of age and projected a substantial rise in cancer incidence over the next 10 years in this age group. This trend was exemplified in the incidence of non-cardia gastric cancer and its disproportionate impact on non-Hispanic white females under the age of 50. The trend is concurrent with the increasing incidence of autoimmune diseases in industrialized countries, suggesting a causal link between the two. While autoimmunity has been suspected to be a risk factor for some cancers, the exact mechanisms underlying the connection between autoimmunity and cancer remain unclear and are often controversial. The link has been attributed to several mediators such as immune suppression, infection, diet, environment, or, perhaps most plausibly, chronic inflammation because of its well-recognized role in tumorigenesis. In that regard, autoimmune conditions are common causes of chronic inflammation and may trigger repetitive cycles of antigen-specific cell damage, tissue regeneration, and wound healing. Illustrating the connection between autoimmune diseases and cancer are patients who have an increased risk of cancer development associated with genetically predisposed insufficiency of cytotoxic T lymphocyte-associated protein 4 (CTLA4), a prototypical immune checkpoint against autoimmunity and one of the main targets of cancer immune therapy. The tumorigenic process triggered by CTLA4 insufficiency has been shown in a mouse model to be dependent on the type 2 cytokines interleukin-4 (IL4) and interleukin-13 (IL13). In this type 2 inflammatory milieu, crosstalk with type 2 immune cells may initiate epigenetic reprogramming of epithelial cells, leading to a metaplastic differentiation and eventually malignant transformation even in the absence of classical oncogenic mutations. Those findings complement a large body of evidence for type 1, type 3, or other inflammatory mediators in inflammatory tumorigenesis. This review addresses the potential of autoimmunity as a causal factor for tumorigenesis, the underlying inflammatory mechanisms that may vary depending on host-environment variations, and implications to cancer prevention and immunotherapy.
C1 [Li, Chris M.; Chen, Zhibin] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.
   [Chen, Zhibin] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
C3 University of Miami; University of Miami
RP Chen, ZB (corresponding author), Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33136 USA.; Chen, ZB (corresponding author), Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Miami, FL 33136 USA.
EM zchen@med.miami.edu
FU National Cancer Institute (NCI) of National Institutes of Health (NIH)
   [R01CA245673]
FX This work is supported in part by a grant from the National Cancer
   Institute (NCI) of National Institutes of Health (NIH) R01CA245673.
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NR 177
TC 22
Z9 26
U1 0
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-634X
J9 FRONT CELL DEV BIOL
JI Front. Cell. Dev. Biol.
PD JUN 21
PY 2021
VL 9
AR 664305
DI 10.3389/fcell.2021.664305
PG 16
WC Cell Biology; Developmental Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Developmental Biology
GA TD6VO
UT WOS:000669462200001
PM 34235145
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Eslinger, C
   Walden, D
   Barry, T
   Shah, S
   Samadder, NJ
   Bekaii-Saab, TS
AF Eslinger, Cody
   Walden, Daniel
   Barry, Timothy
   Shah, Shimoli
   Samadder, Niloy Jewel
   Bekaii-Saab, Tanios S.
TI Rechallenge With Switching Immune Checkpoint Inhibitors Following
   Autoimmune Myocarditis in a Patient With Lynch Syndrome
SO JOURNAL OF THE NATIONAL COMPREHENSIVE CANCER NETWORK
LA English
DT Article
ID MICROSATELLITE INSTABILITY; CANCER; CHEMOTHERAPY; SURVIVAL; GENES
AB Immune checkpoint inhibitors (ICIs) induce profound benefits in cancer patients with mismatch repair gene mutations or high levels of microsatellite instability. Herein, we present a case of a patient with history of Muir-Torre/Lynch syndrome and metastatic gastric adenocarcinoma in the presence of an MSH2 gene mutation. The patient was initially treated with a PD-1 inhibitor, pembrolizumab, but developed grade 4 myocarditis requiring treatment with infliximab and a prolonged steroid taper. Following discontinuation of pembrolizumab, surveillance testing showed no radiographic or endoscopic evidence of progression for 7 months, until biopsy results from a repeat upper endoscopy indicated local disease recurrence. The patient was subsequently rechallenged with another PD-1 inhibitor, nivolumab, at a 50% dose reduction without recurrent adverse events and eventually achieved a complete response after 13 cycles. This case highlights the relative importance of considering careful rechallenge with ICI therapy in patients with microsatellite instability-high malignancies and a high risk of severe adverse events.
C1 [Eslinger, Cody] Mayo Clin, Dept Internal Med, Phoenix, AZ 85054 USA.
   [Walden, Daniel; Bekaii-Saab, Tanios S.] Mayo Clin, Dept Hematol & Oncol, 5881 East Mayo Blvd, Phoenix, AZ 85054 USA.
   [Barry, Timothy; Shah, Shimoli] Mayo Clin, Dept Cardiovasc Med, Phoenix, AZ 85054 USA.
   [Samadder, Niloy Jewel] Mayo Clin, Dept Gastroenterol & Hepatol, Phoenix, AZ 85054 USA.
C3 Mayo Clinic; Mayo Clinic Phoenix; Mayo Clinic; Mayo Clinic Phoenix; Mayo
   Clinic; Mayo Clinic Phoenix; Mayo Clinic; Mayo Clinic Phoenix
RP Bekaii-Saab, TS (corresponding author), Mayo Clin, Dept Hematol & Oncol, 5881 East Mayo Blvd, Phoenix, AZ 85054 USA.
EM bekaii-saab.tanios@mayo.edu
RI Bekaii-Saab, Tanios/AGD-6851-2022
OI Bekaii-Saab, Tanios/0000-0001-7721-1699
CR Ajani JA, 2023, NCCN Clinical Practice Guidelines in Oncology: Esophageal and Esophagogastric Junction Cancers
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PI HUNTINGTON
PA 94 NORTH WOODHULL RD, HUNTINGTON, NY 11743 USA
SN 1540-1405
EI 1540-1413
J9 J NATL COMPR CANC NE
JI J. Natl. Compr. Cancer Netw.
PD SEP
PY 2023
VL 21
IS 9
BP 894
EP 899
DI 10.6004/jnccn.2023.7029
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA T7LZ3
UT WOS:001079774300002
PM 37673116
OA Bronze
DA 2025-06-01
ER

PT J
AU La Placa, M
   Balestri, R
   Tartari, F
   Sechi, A
   Ferrara, F
   Loi, C
   Patrizi, A
   Bardazzi, F
AF La Placa, Michelangelo
   Balestri, Riccardo
   Tartari, Federico
   Sechi, Andrea
   Ferrara, Francesca
   Loi, Camilla
   Patrizi, Annalisa
   Bardazzi, Federico
TI Mucous Membrane Pemphigoid-Associated Malignancies: Case Series and a
   Brief Overview of the Literature
SO DERMATOLOGY PRACTICAL & CONCEPTUAL
LA English
DT Article
DE mucous membrane pemphigoid; malignancy; autoimmune bullous disorders;
   paraneoplastic pemphigus; laminin-332; blistering diseases; laminin-5;
   anti-epiligrin; cicatricial pemphigoid; adenocarcinoma
ID PARANEOPLASTIC PEMPHIGUS; ANTIEPILIGRIN LAMININ-5; LARYNGEAL STENOSIS;
   GASTRIC-CARCINOMA; BETA-4 INTEGRIN; LUNG-CARCINOMA; RELATIVE RISK;
   AUTOANTIBODIES; DISEASE; REMISSION
AB Background: Mucous membrane pemphigoid (MMP) is a heterogeneous group of blistering disorders affecting the mucosae with or without skin involvement, characterized by the presence of autoantibodies to components of the basement membrane zone, including the bullous pemphigoid antigen BP180 and beta 4 integrin. Current literature has shown that a minority of patients present circulating antibodies to laminin-332 and this population seems to be associated with a relatively high risk of malignancy.
   Objective: To present our personal case series of patients with MMP-associated malignancy from a dermatology university hospital.
   Methods: Twenty-two patients affected by MMP were seen in the period between 2001 and 2016; in 4 patients (18%) an associated cancer was detected.
   Results: These patients were 2 men and 2 women, with a mean age of 69.7 years (range, 48-83). The associated malignancies included a breast cancer, a pancreatic adenocarcinoma, a metastatic laryngeal carcinoma, and a hepatic carcinoma. All patients had negative results for both BP180 and laminin-332 autoantibodies.
   Conclusion: We confirm that MMP patients have a relatively high possibility of developing a solid cancer, but the autoantibody detection is not mandatory and is probably correlated with the severity of the disease.
C1 [La Placa, Michelangelo; Balestri, Riccardo; Tartari, Federico; Sechi, Andrea; Ferrara, Francesca; Loi, Camilla; Patrizi, Annalisa; Bardazzi, Federico] Univ Bologna, Dept Expt Diagnost & Specialty Med, Dermatol Div, Via Massarenti 1, I-40138 Bologna, Italy.
C3 University of Bologna
RP La Placa, M (corresponding author), Univ Bologna, Dept Expt Diagnost & Specialty Med, Dermatol Div, Via Massarenti 1, I-40138 Bologna, Italy.
EM michelangelo.laplaca@unibo.it
RI Sechi, Andrea/GLT-1493-2022; La Placa, Michelangelo/U-7723-2018;
   Bardazzi, Federico/HKE-8187-2023; Balestri, Riccardo/AGK-9827-2022
OI Balestri, Riccardo/0000-0002-0885-054X; LA PLACA,
   MICHELANGELO/0000-0002-6894-3350
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   Young AL, 2011, EUR J DERMATOL, V21, P401, DOI 10.1684/ejd.2011.1360
NR 38
TC 14
Z9 14
U1 1
U2 7
PU INT DERMOSCOPY SOCIETY
PI GRAZ
PA AUENBRUGGERPLATZ 8, GRAZ, A-8036, AUSTRIA
SN 2160-9381
J9 DERMATOL PRACT CONCE
JI Dermatol. Pract. Concept.
PD APR
PY 2019
VL 9
IS 2
BP 119
EP 125
DI 10.5826/dpc.0902a07
PG 7
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA OE9UK
UT WOS:000580866500007
PM 31106014
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Oshima, T
   Okugawa, T
   Hori, K
   Kim, Y
   Tanaka, J
   Watari, J
   Miwa, H
AF Oshima, Tadayuki
   Okugawa, Takuya
   Hori, Kazutoshi
   Kim, Yongmin
   Tanaka, Junji
   Watari, Jiro
   Miwa, Hiroto
TI Successful Endoscopic Submucosal Dissection of Gastric Carcinoid in a
   Patient with Autoimmune Gastritis and Systemic Lupus Erythematosus
SO INTERNAL MEDICINE
LA English
DT Article
DE carcinoid; SLE; autoimmune gastritis; ESD
ID YOUNG WOMAN; TUMORS
AB A 41-year-old woman was referred with epigastric discomfort. She had a 20-year history of SLE. Esophagogastroduodenoscopy (EGD) examination showed severe atrophic gastritis in the stomach and a protruding lesion was detected. Histological examination showed a carcinoid tumor with cytoplasmic staining with chromogranin-A. Using an endoscopic submucosal dissection (ESD) technique, en bloc resection of the tumor was performed. No recurrence has been found for 3 years after the treatment. Type I gastric carcinoid can occur at an earlier age with AIG and autoimmune diseases such as systemic lupus erythematosus (SLE). This is the first report of gastric carcinoid that was treated by ESD.
C1 [Oshima, Tadayuki; Okugawa, Takuya; Hori, Kazutoshi; Kim, Yongmin; Tanaka, Junji; Watari, Jiro; Miwa, Hiroto] Hyogo Coll Med, Dept Internal Med, Div Upper Gastroenterol, Nishinomiya, Hyogo, Japan.
C3 Hyogo Medical University
RP Oshima, T (corresponding author), Hyogo Coll Med, Dept Internal Med, Div Upper Gastroenterol, Nishinomiya, Hyogo, Japan.
EM t-oshima@hyo-med.ac.jp
RI Oshima, Tadayuki/KLY-4234-2024
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NR 10
TC 10
Z9 10
U1 0
U2 0
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2012
VL 51
IS 10
BP 1211
EP 1213
DI 10.2169/internalmedicine.51.7077
PG 3
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 949VP
UT WOS:000304604600011
PM 22687792
OA hybrid
DA 2025-06-01
ER

PT J
AU Alexandraki, KI
   Spyroglou, A
   Xekouki, P
   Bramis, KI
   Kyriakopoulos, G
   Barkas, K
   Papanikolaou, IS
   Mastorakos, G
   Konstadoulakis, M
AF Alexandraki, Krystallenia I.
   Spyroglou, Ariadni
   Xekouki, Paraskevi
   Bramis, Konstantinos I.
   Kyriakopoulos, Georgios
   Barkas, Konstantinos
   Papanikolaou, Ioannis S.
   Mastorakos, George
   Konstadoulakis, Manousos
TI When rare diseases crisscross within the same patient: von Hippel-Lindau
   and type 1 gastric neuroendocrine tumor
SO HORMONES-INTERNATIONAL JOURNAL OF ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE Von-Hippel-Lindau; Gastric neuroendocrine neoplasm; Chronic autoimmune
   gastritis; Clear cells
AB Von-Hippel-Lindau (VHL) is a genetic multisystem disorder characterized by visceral cysts and benign and malignant tumors in various organs. Herein, we present the case of a 23-year-old woman with VHL presenting with multiple gastric neuroendocrine neoplasms (gNENs) type 1 in the context of chronic autoimmune gastritis (CAG). Although gNENs are not acknowledged as a typical entity in VHL patients, in the present case, gNENs were composed of neoplastic cells with clear cytoplasm usually seen in tumors related to VHL disease. We additionally performed a literature review on the presence of neuroendocrine clear cell tumors and report on further cases of clear cell NENs. The present case illustrates that clear-cell transformation in gNENs may be due to the dual genetic background of the patient; the real oncogenic stimulus may be more closely related to CAG than to VHL disease accompanied by an interplay between neoplastic and autoimmune processes. Therefore, close monitoring of patients with clear cell NENs appears to be important before excluding VHL disease, even in the context of phenotypically unrelated diseases.
C1 [Alexandraki, Krystallenia I.; Spyroglou, Ariadni; Bramis, Konstantinos I.; Papanikolaou, Ioannis S.; Mastorakos, George; Konstadoulakis, Manousos] Natl & Kapodistrian Univ Athens, Med Sch, Dept Surg 2, Athens, Greece.
   [Xekouki, Paraskevi] Univ Crete, Univ Hosp Heraklion, Sch Med, Endocrinol & Diabet Clin, Voutes, Greece.
   [Kyriakopoulos, Georgios] Evangelismos Med Ctr, Dept Pathol, Athens, Greece.
   [Barkas, Konstantinos] Gen Hosp Nikaia Peiraia, Dept Neurosurg, Athens, Greece.
   [Papanikolaou, Ioannis S.] Natl & Kapodistrian Univ Athens, Attikon Univ Gen Hosp, Dept Internal Med Propaedeut 2, Hepatogastroenterol Unit, Athens, Greece.
C3 National & Kapodistrian University of Athens; University Hospital of
   Heraklion; University of Crete; Evangelismos Hospital; University
   Hospital Attikon; National & Kapodistrian University of Athens
RP Alexandraki, KI (corresponding author), Natl & Kapodistrian Univ Athens, Med Sch, Dept Surg 2, Athens, Greece.
EM alexandrakik@gmail.com
RI Papanikolaou, Ioannis/AAA-8261-2022; Alexandraki,
   Krystallenia/S-4058-2019; Xekouki, Paraskevi/AAM-2485-2021; Spyroglou,
   Ariadni/KTI-5377-2024
OI Alexandraki, Krystallenia/0000-0003-2398-6768
FU University of Athens
FX No Statement Available
CR Alexandraki KI, 2014, CLIN ENDOCRINOL, V80, P685, DOI 10.1111/cen.12346
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NR 18
TC 1
Z9 1
U1 2
U2 3
PU SPRINGER INT PUBL AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 1109-3099
EI 2520-8721
J9 HORM-INT J ENDOCRINO
JI Horm.-Int. J. Endocrinol. Metab.
PD SEP
PY 2024
VL 23
IS 3
BP 585
EP 590
DI 10.1007/s42000-024-00556-9
EA APR 2024
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA H2S4U
UT WOS:001204674700001
PM 38619811
OA hybrid, Green Accepted
DA 2025-06-01
ER

PT J
AU Rugge, M
   Savarino, E
   Sbaraglia, M
   Bricca, L
   Malfertheiner, P
AF Rugge, Massimo
   Savarino, Edoardo
   Sbaraglia, Marta
   Bricca, Ludovica
   Malfertheiner, Peter
TI Gastritis: The clinico-pathological spectrum
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Review
DE Atrophic gastritis; Atrophic border; Autoimmune gastritis; Gastric
   biopsy protocol; Gastric cancer; Gastric metaplasia; Intestinal
   Metaplasia; OLGA staging; SPEM
ID HELICOBACTER-PYLORI INFECTION; FOCALLY ENHANCED GASTRITIS; INTESTINAL
   METAPLASIA; ATROPHIC GASTRITIS; EPITHELIAL DYSPLASIA; OPERATIVE LINK;
   CANCER; STOMACH; DIAGNOSIS; PATHOLOGY
AB The inflammatory spectrum of gastric diseases includes different clinico-pathological entities, the etiology of which was recently established in the international Kyoto classification. A diagnosis of gastritis combines the information resulting form the gross examination (endoscopy) and histology (microscopy). It is important to consider the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative mucosal biopsy samples. Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory diseases, and the latter are epidemiologically, biologically and clinically linked to the onset of gastric cancer (i.e. "inflammation-associated cancer"). Different biological models of inflammation-associated gastric oncogenesis have been proposed. Helicobacter pylori ( H. pylori ) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis may also be triggered by the immune mediated destruction of gastric parietal cells, resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term follow-up studies consistently demonstrate the prognostic impact of the histological staging of gastritis in gastric cancer secondary prevention strategies. (c) 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Rugge, Massimo; Sbaraglia, Marta; Bricca, Ludovica] Padova Univ, Dept Med DIMED, Surg Pathol & Cytopathol Unit, Padua, Italy.
   [Rugge, Massimo] Azienda Zero, Veneto Tumor Registry RTV, Padua, Italy.
   [Savarino, Edoardo; Bricca, Ludovica] Padova Univ, Dept Surg Ontol Gastroenterol Sci DiSCOG, Gastroenterol Unit, Padua, Italy.
   [Malfertheiner, Peter] Ludwig Maximilian Univ Hosp, Dept Internal Med 2, Munich, Germany.
C3 University of Padua; Azienda Zero; University of Padua; University of
   Munich
RP Rugge, M (corresponding author), Padova Univ, Dept Med DIMED, Surg Pathol & Cytopathol Unit, Padua, Italy.; Rugge, M (corresponding author), Azienda Zero, Veneto Tumor Registry RTV, Padua, Italy.
EM massimo.rugge@unipd.it
RI Savarino, Edoardo/AAC-7510-2022; Malfertheiner, Peter/AEZ-6553-2022;
   Sbaraglia, Marta/AAC-4996-2022
OI Savarino, Edoardo/0000-0002-3187-2894; Malfertheiner,
   Peter/0000-0001-8439-9036; RUGGE, MASSIMO/0000-0002-0679-0563;
   Sbaraglia, Marta/0000-0002-7116-6513
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NR 126
TC 35
Z9 37
U1 3
U2 31
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD OCT
PY 2021
VL 53
IS 10
BP 1237
EP 1246
DI 10.1016/j.dld.2021.03.007
EA SEP 2021
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WH0QU
UT WOS:000707394700005
PM 33785282
DA 2025-06-01
ER

PT J
AU Liu, SH
   Deng, ZL
   Zhu, JX
   Ma, ZY
   Tuo, B
   Li, TL
   Liu, XM
AF Liu, Shuhui
   Deng, Zilin
   Zhu, Jiaxing
   Ma, Zhiyuan
   Tuo, Biguang
   Li, Taolang
   Liu, Xuemei
TI Gastric immune homeostasis imbalance: An important factor in the
   development of gastric mucosal diseases
SO BIOMEDICINE & PHARMACOTHERAPY
LA English
DT Review
DE Gastric mucosal immunity; Gastric immune disorder; Multiple gastric
   mucosa diseases
ID HELICOBACTER-PYLORI INFECTION; POLYPEPTIDE-EXPRESSING METAPLASIA;
   EPSTEIN-BARR-VIRUS; NF-KAPPA-B; EPITHELIAL-CELLS; PARIETAL-CELL;
   AUTOIMMUNE GASTRITIS; T-CELLS; SONIC HEDGEHOG; STEM-CELLS
AB The gastric mucosal immune system is a unique immune organ independent of systemic immunity that not only maintains nutrient absorption but also plays a role in resisting the external environment. Gastric mucosal im-mune disorder leads to a series of gastric mucosal diseases, including autoimmune gastritis (AIG)-related dis-eases, Helicobacter pylori (H. pylori)-induced diseases, and various types of gastric cancer (GC). Therefore, understanding the role of gastric mucosal immune homeostasis in gastric mucosal protection and the relationship between mucosal immunity and gastric mucosal diseases is very important. This review focuses on the protective effect of gastric mucosal immune homeostasis on the gastric mucosa, as well as multiple gastric mucosal diseases caused by gastric immune disorders. We hope to offer new prospects for the prevention and treatment of gastric mucosal diseases.
C1 [Liu, Shuhui; Deng, Zilin; Zhu, Jiaxing; Ma, Zhiyuan; Tuo, Biguang] Zunyi Med Univ, Digest Dis Hosp, Dept Gastroenterol, Affiliated Hosp, Zunyi, Guizhou Provinc, Peoples R China.
   [Li, Taolang] Zunyi Med Univ, Dept Gen Surg, Affiliated Hosp, Zunyi, Peoples R China.
   [Li, Taolang] Zunyi Med Univ, Dept Gen Surg, Affiliated Hosp, Zunyi 563003, Peoples R China.
   [Liu, Xuemei] Zunyi Med Univ, Digest Dis Hosp, Dept Gastroenterol, Affiliated Hosp, Zunyi 563003, Peoples R China.
C3 Zunyi Medical University; Zunyi Medical University; Zunyi Medical
   University; Zunyi Medical University
RP Li, TL (corresponding author), Zunyi Med Univ, Dept Gen Surg, Affiliated Hosp, Zunyi 563003, Peoples R China.; Liu, XM (corresponding author), Zunyi Med Univ, Digest Dis Hosp, Dept Gastroenterol, Affiliated Hosp, Zunyi 563003, Peoples R China.
EM 0078029@sina.com; onlyoneliuxuemei@163.com
RI Ma, Zhi-Yuan/AAC-4453-2020; Liu, Xuemei/AAE-1768-2020; LIU,
   SHUHUI/IYS-9738-2023
FU National Natural Science Foundation of China [82070536, 81860103,
   82160505, 81660098, 82073087]; Guizhou Province Interna-tional Science
   and Technology Cooperation (Gastroenterology) Base;  [059];  [HZJD
   [2021] 001]
FX This research was supported by the National Natural Science Foundation
   of China (82070536 and 81860103 to X.L., 82160505 and 81660098 to T.L.,
   and 82073087 to B.T.) , Guizhou Province Interna-tional Science and
   Technology Cooperation (Gastroenterology) Base (Qian Ke He Platform
   Talents-HZJD [2021] 001 and Qian Ke He basic research-ZK [2023] major
   project 059 to X.L.) .
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NR 184
TC 10
Z9 10
U1 4
U2 26
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0753-3322
EI 1950-6007
J9 BIOMED PHARMACOTHER
JI Biomed. Pharmacother.
PD MAY
PY 2023
VL 161
AR 114338
DI 10.1016/j.biopha.2023.114338
EA MAR 2023
PG 11
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA E0MW1
UT WOS:000972588900001
PM 36905807
OA gold
DA 2025-06-01
ER

PT J
AU de Jonge, H
   Iamele, L
   Maggi, M
   Pessino, G
   Scotti, C
AF de Jonge, Hugo
   Iamele, Luisa
   Maggi, Maristella
   Pessino, Greta
   Scotti, Claudia
TI Anti-Cancer Auto-Antibodies: Roles, Applications and Open Issues
SO CANCERS
LA English
DT Review
DE auto-antibodies; cancer; tumor-associated antigens; tumor-specific
   antigens
ID TUMOR-ASSOCIATED ANTIGENS; BREAST-CANCER RISK; T-CELL THERAPY;
   OVARIAN-CANCER; SERUM AUTOANTIBODIES; POTENTIAL BIOMARKER;
   COLORECTAL-CANCER; ESOPHAGEAL CANCER; CLINICAL UTILITY; GASTRIC-CANCER
AB Simple Summary
   Cancer is one of the main causes of death worldwide and early detection is crucial for effective treatment. Scientists have therefore focused on the identification of circulating cancer-specific molecules, so-called markers, that can be detected with non- or less-invasive techniques. One attractive emerging marker is represented by circulating antibodies against molecules that are specific for the tumor cells and not produced by normal cells. Many such auto-antibodies have been discovered, but still not much is known about their significance and role in either promoting or inhibiting tumor growth. The aim of this review is to summarize the current knowledge on auto-antibodies in different cancer types and on their current or possible utilization for effective cancer management. Reference to autoimmune diseases will also be made, as they share with cancer the presence of such auto-antibodies.
   Auto-antibodies are classically associated with autoimmune diseases, where they are an integral part of diagnostic panels. However, recent evidence is accumulating on the presence of auto-antibodies against single or selected panels of auto-antigens in many types of cancer. Auto-antibodies might initially represent an epiphenomenon derived from the inflammatory environment induced by the tumor. However, their effect on tumor evolution can be crucial, as is discussed in this paper. It has been demonstrated that some of these auto-antibodies can be used for early detection and cancer staging, as well as for monitoring of cancer regression during treatment and follow up. Interestingly, certain auto-antibodies were found to promote cancer progression and metastasis, while others contribute to the body's defense against it. Moreover, auto-antibodies are of a polyclonal nature, which means that often several antibodies are involved in the response to a single tumor antigen. Dissection of these antibody specificities is now possible, allowing their identification at the genetic, structural, and epitope levels. In this review, we report the evidence available on the presence of auto-antibodies in the main cancer types and discuss some of the open issues that still need to be addressed by the research community.
C1 [de Jonge, Hugo; Iamele, Luisa; Maggi, Maristella; Pessino, Greta; Scotti, Claudia] Univ Pavia, Dept Mol Med, Unit Immunol & Gen Pathol, I-27100 Pavia, Italy.
C3 University of Pavia
RP Scotti, C (corresponding author), Univ Pavia, Dept Mol Med, Unit Immunol & Gen Pathol, I-27100 Pavia, Italy.
EM hugo.dejonge@unipv.it; luisa.iamele@unipv.it; maristella.maggi@unipv.it;
   greta.pessino01@universitadipavia.it; claudia.scotti@unipv.it
RI de Jonge, Hugo/AAI-1861-2019; de Jonge, Hugo/D-4036-2018; Maggi,
   Maristella/O-6759-2014; Scotti, Claudia/A-7126-2012
OI de Jonge, Hugo/0000-0003-2777-4084; Maggi,
   Maristella/0000-0002-9075-8143; Pessino, Greta/0000-0001-6504-9882;
   Scotti, Claudia/0000-0002-5790-1833
FU Italian Ministry of Education, University and Research (MIUR);
   Associazione Gianfranco Lupo - Un sorriso alla vita
FX This research was supported by a grant from the Italian Ministry of
   Education, University and Research (MIUR) to the Department of Molecular
   Medicine of the University of Pavia under the "Dipartimenti di
   Eccellenza (2018-2022)" initiative, and by "Associazione Gianfranco Lupo
   - Un sorriso alla vita".
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NR 149
TC 24
Z9 24
U1 0
U2 21
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD FEB
PY 2021
VL 13
IS 4
AR 813
DI 10.3390/cancers13040813
PG 33
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA QO7VZ
UT WOS:000623349000001
PM 33672007
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Katoh, M
AF Katoh, Masaru
TI Mutation spectra of histone methyltransferases with canonical SET
   domains and EZH2-targeted therapy
SO EPIGENOMICS
LA English
DT Review
DE breast cancer; chronic inflammation; epigenetics; gastric cancer;
   immune-checkpoint blocker; lung cancer; melanoma; MYC; prostate cancer;
   synthetic lethality
ID ACUTE MYELOID-LEUKEMIA; NF-KAPPA-B; PROTEIN LYSINE METHYLTRANSFERASES;
   CHROMATIN REMODELING GENES; RESISTANT PROSTATE-CANCER;
   WOLF-HIRSCHHORN-SYNDROME; BREAST-CANCER; SELECTIVE-INHIBITION; REGULATES
   EZH2; PHARMACOLOGICAL DISRUPTION
AB Germline mutations in canonical SET-methyltransferases have been identified in autism and intellectual disability syndromes and gain-of-function somatic alterations in EZH2, MLL3, NSD1, WHSC1 (NSD2) and WHSC1L1 (NSD3) in cancer. EZH2 interacts with AR, ERa, beta-catenin, FOXP3, NF-.B, PRC2, REST and SNAI2, resulting in context-dependent transcriptional activation and repression. Pharmacological EZH2 inhibitors are currently in clinical trials for the treatment of B-cell lymphomas and solid tumors. EZH2 inhibitors might also be applicable in the treatment of SWI/SNF-mutant cancers, reflecting the reciprocal expression of and functional overlap between EZH2 and SMARCA4. Because of the risks for autoimmune diseases, cognitive impairment, cardiomyopathy and myelodysplastic syndrome, EZH2 inhibitors should be utilized for cancer treatment in patients receiving long-term surveillance but not for cancer chemoprevention.
C1 [Katoh, Masaru] Natl Canc Ctr, Dept Omics Network, Chuo Ward, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
C3 National Cancer Center - Japan
RP Katoh, M (corresponding author), Natl Canc Ctr, Dept Omics Network, Chuo Ward, 5-1-1 Tsukiji, Tokyo 1040045, Japan.
EM mkatoh-kkr@umin.ac.jp
FU M Katoh's Fund
FX This study was financially supported in part by a grant-in-aid for the
   Knowledgebase Project from the M Katoh's Fund. The author has no other
   relevant affiliations or financial involvement with any organization or
   entity with a financial interest in or financial conflict with the
   subject matter or materials discussed in the manuscript apart from those
   disclosed.
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NR 143
TC 25
Z9 30
U1 0
U2 22
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1750-1911
EI 1750-192X
J9 EPIGENOMICS-UK
JI Epigenomics
PY 2016
VL 8
IS 2
BP 285
EP 305
DI 10.2217/epi.15.89
PG 21
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA DF1GF
UT WOS:000371086900011
PM 26411517
DA 2025-06-01
ER

PT J
AU Jubel, JM
   Barbati, ZR
   Burger, C
   Wirtz, DC
   Schildberg, FA
AF Jubel, Jil M.
   Barbati, Zachary R.
   Burger, Christof
   Wirtz, Dieter C.
   Schildberg, Frank A.
TI The Role of PD-1 in Acute and Chronic Infection
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE PD-1; PD-L1; PD-L2; T cell exhaustion; acute infection; chronic
   infection; checkpoint inhibitor; infectious disease
ID REGULATORY T-CELLS; HUMAN-IMMUNODEFICIENCY-VIRUS; GASTRIC
   EPITHELIAL-CELLS; PROGRAMMED DEATH-1; EXPRESSION CHARACTERISTICS;
   COINHIBITORY PATHWAYS; IMMUNE DYSFUNCTION; VIRAL PERSISTENCE;
   TUMOR-CELLS; HEPATITIS-C
AB PD-1 as an immune checkpoint molecule down-regulates T cell activity during immune responses in order to prevent autoimmune tissue damage. In chronic infections or tumors, lasting antigen-exposure leads to permanent PD-1 expression that can limit immune-mediated clearance of pathogens or degenerated cells. Blocking PD-1 can enhance T cell function; in cancer treatment PD-1 blockade is already used as a successful therapy. However, the role of PD-1 expression and blocking in the context of acute and chronic infections is less defined. Building on its success in cancer therapy leads to the hypothesis that blocking PD-1 in infectious diseases is also beneficial in acute or chronic infections. This review will focus on the role of PD-1 expression in acute and chronic infections with virus, bacteria, and parasites, with a particular focus on recent studies regarding PD-1 blockade in infectious diseases.
C1 [Jubel, Jil M.; Burger, Christof; Wirtz, Dieter C.; Schildberg, Frank A.] Univ Hosp Bonn, Clin Orthoped & Trauma Surg, Bonn, Germany.
   [Barbati, Zachary R.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
C3 University of Bonn; Tufts University
RP Schildberg, FA (corresponding author), Univ Hosp Bonn, Clin Orthoped & Trauma Surg, Bonn, Germany.
EM frank.schildberg@ukbonn.de
FU National Multiple Sclerosis Society [RG 1809-32591]
FX This work was supported by a grant from the National Multiple Sclerosis
   Society (RG 1809-32591 to FS) and is part of the doctoral thesis of JJ.
   Because of space restrictions, we were able to cite only a fraction of
   the relevant literature and apologize to colleagues whose contributions
   might not be appropriately acknowledged in this review.
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NR 129
TC 191
Z9 218
U1 2
U2 12
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAR 24
PY 2020
VL 11
AR 487
DI 10.3389/fimmu.2020.00487
PG 15
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA PC3HU
UT WOS:000596897400001
PM 32265932
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Iwamoto, M
   Kato, K
   Kusumi, Y
   Masuda, S
   Nakayama, T
   Moriyama, M
AF Iwamoto, Maho
   Kato, Kimitoshi
   Kusumi, Yoshiaki
   Masuda, Shinobu
   Nakayama, Tomohiro
   Moriyama, Mitsuhiko
TI Celiac Disease Diagnosed after Gastrectomy for Gastric Cancer
SO INTERNAL MEDICINE
LA English
DT Article
DE celiac disease; gastric cancer; post-gastrectomy; small bowel capsule
   endoscopy; diarrhea
ID CAPSULE ENDOSCOPY; SMALL-INTESTINE; GLUTEN; SYMPTOMS; SOCIETY; COMPLEX
AB Celiac disease is a systemic autoimmune disorder leading to manifestations of malabsorption syndrome. A 47-year-old Japanese man developed severe diarrhea after surgery for gastric cancer. The diarrhea persisted for seven months, leading to a state of malabsorption. Celiac disease was suspected based on small bowel capsule endoscopy findings. The duodenal findings observed during gastric cancer surgery were reassessed, and Marsh-Oberhuber classification type 3c celiac disease was diagnosed. The anti-tissue glutaminase antibody test results were positive. The patient was started on a gluten-free diet, following which the diarrhea resolved, and the nutritional status improved. Adjuvant therapy after gastric cancer surgery was initiated.
C1 [Iwamoto, Maho; Moriyama, Mitsuhiko] Nihon Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Sch Med, Tokyo, Japan.
   [Kato, Kimitoshi] Nihon Univ, Div Res Planning & Dev, Sch Med, Tokyo, Japan.
   [Kusumi, Yoshiaki; Masuda, Shinobu] Nihon Univ, Dept Pathol, Sch Med, Tokyo, Japan.
   [Nakayama, Tomohiro] Nihon Univ, Dept Pathol & Microbiol, Div Lab Med, Sch Med, Tokyo, Japan.
C3 Nihon University; Nihon University; Nihon University; Nihon University
RP Iwamoto, M (corresponding author), Nihon Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Sch Med, Tokyo, Japan.
EM maho_9245@yahoo.co.jp
RI Nakayama, Tomohiro/GYU-0303-2022
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NR 22
TC 3
Z9 3
U1 0
U2 1
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2022
VL 61
IS 3
BP 323
EP 328
DI 10.2169/internalmedicine.7901-21
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA YV5SI
UT WOS:000752787300005
PM 34334571
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Sadler, E
   Lazarova, Z
   Sarasombath, P
   Yancey, KB
AF Sadler, Elke
   Lazarova, Zelmira
   Sarasombath, Pichaya
   Yancey, Kim B.
TI A widening perspective regarding the relationship between anti-epiligrin
   cicatricial pemphigoid and cancer
SO JOURNAL OF DERMATOLOGICAL SCIENCE
LA English
DT Review
DE laminin 5; anti-epiligrin cicatricial pemphigoid (AECP); cancer
ID INDUCE SUBEPIDERMAL BLISTERS; LAMININ-5 GAMMA-2 CHAIN; DIFFERENTIAL
   EXPRESSION; GASTRIC-CARCINOMA; BASEMENT-MEMBRANE; CELL-ADHESION;
   EPIDERMOLYSIS-BULLOSA; BIOLOGICAL-ACTIVITY; LAMA3 GENE; SHORT ARM
AB Anti-epiligrin cicatricial pemphigoid (AECP) is a chronic, autoimmune, subepidermal blistering disease characterized by circulating anti-basement membrane autoantibodies to laminin 5. Recent studies have shown that patients with this form of cicatricial pemphigoid have an increased relative risk for malignant solid tumors. The mechanism underlying this association of AECP and cancer is unknown, but there is accumulating evidence that laminin 5 plays a central role. In this article we report a patient with AECP and co-associated cutaneous T cell lymphoma and summarize at[ to date reported cases of AECP associated with malignancies. In addition we provide a review of the biology of laminin 5 and its potential rote in cancer development. (c) 2007 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
C1 Univ Texas, SW Med Ctr, Dept Dermatol, Dallas, TX 75390 USA.
   Med Coll Wisconsin, Dept Dermatol, Milwaukee, WI 53226 USA.
C3 University of Texas System; University of Texas Southwestern Medical
   Center Dallas; University of Texas Dallas; Medical College of Wisconsin
RP Yancey, KB (corresponding author), Univ Texas, SW Med Ctr, Dept Dermatol, 5323 Harry Hines Blvd, Dallas, TX 75390 USA.
EM kim.yancey@utsouthwestern.edu
RI Yancey, Kim/AIC-0005-2022
OI Yancey, Kim/0000-0001-6101-4690
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U1 0
U2 4
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0923-1811
EI 1873-569X
J9 J DERMATOL SCI
JI J. Dermatol. Sci.
PD JUL
PY 2007
VL 47
IS 1
BP 1
EP 7
DI 10.1016/j.jdermsci.2007.02.012
PG 7
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA 188UD
UT WOS:000247943900001
PM 17467241
DA 2025-06-01
ER

PT J
AU Ramakrishna, B
   Yewale, R
   Vijayakumar, K
   Radhakrishna, P
   Ramakrishna, BS
AF Ramakrishna, Banumathi
   Yewale, Roban
   Vijayakumar, Kavita
   Radhakrishna, Patta
   Ramakrishna, Balakrishnan Siddartha
TI Gastric IgG4-related disease presenting as a mass lesion and
   masquerading as a gastrointestinal stromal tumor
SO JOURNAL OF PATHOLOGY AND TRANSLATIONAL MEDICINE
LA English
DT Article
DE IgG4-related disease; Stomach; Autoimmune diseases; Gastrointestinal
   stromal tumors
ID G4-RELATED INFLAMMATORY PSEUDOTUMOR; AUTOIMMUNE PANCREATITIS
AB IgG4-related disease of the stomach is a rare disorder, and only a few cases have been reported. We present two cases that were identified over a 2-month period in our center. Two male patients aged 52 and 48 years presented with mass lesion in the stomach, which were clinically thought to be gastrointestinal stromal tumor, and they underwent excision of the lesion. Microscopic examination revealed marked fibrosis, which was storiform in one case, associated with diffuse lymphoplasmacytic infiltration and an increase in IgG4positive plasma cells on immunohistochemistry. Serum IgG4 level was markedly elevated. Although rare, IgG4-related disease should be considered in the differential diagnosis of gastric submucosal mass lesions.
C1 [Ramakrishna, Banumathi; Vijayakumar, Kavita] SRM Inst Med Sci, Dept Pathol, Vadapalani, India.
   [Yewale, Roban; Ramakrishna, Balakrishnan Siddartha] SRM Inst Med Sci, Dept Med Gastroenterol, Vadapalani, India.
   [Radhakrishna, Patta] SRM Inst Med Sci, Dept Surg Gastroenterol, Vadapalani, India.
C3 SRM Institute of Science & Technology Chennai; SRM Institute of Science
   & Technology Chennai; SRM Institute of Science & Technology Chennai
RP Ramakrishna, B (corresponding author), SRM Inst Med Sci, Dept Pathol, 1 Jawaharlal Nehru Rd, Chennai 600026, Tamil Nadu, India.
EM banu_ramakrishna@hotmail.com
RI Ramakrishna, Balakrishnan/D-6808-2015
CR [Anonymous], ISRN GASTROENTEROL
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NR 20
TC 8
Z9 9
U1 0
U2 0
PU KOREAN SOC PATHOLOGISTS
PI SEOUL
PA 1209 GWANGHWAMUN OFFICIA, 92 SAEMUNAN-RO, JONGNO-GU, SEOUL, 03186, SOUTH
   KOREA
SN 2383-7837
EI 2383-7845
J9 J PATHOL TRANSL MED
JI J. Pathol. Transl. Med.
PD MAY
PY 2020
VL 54
IS 3
BP 258
EP 262
DI 10.4132/jptm.2020.02.10
PG 5
WC Pathology
WE Emerging Sources Citation Index (ESCI)
SC Pathology
GA LO5HH
UT WOS:000533658200009
PM 32126738
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Kaushik, P
   Kumar, A
AF Kaushik, Pankhuri
   Kumar, Arun
TI Emerging role and function of miR-198 in human health and diseases
SO PATHOLOGY RESEARCH AND PRACTICE
LA English
DT Review
DE MicroRNAs; MiRNAs; MiR-198; LncRNAs; Circular RNAs; Cancer
ID MICRORNA EXPRESSION PROFILES; SQUAMOUS-CELL CARCINOMA;
   COLORECTAL-CANCER; LUNG-CANCER; HEPATOCELLULAR-CARCINOMA;
   OVARIAN-CANCER; PROSTATE-CANCER; DOWN-REGULATION; GASTRIC-CANCER;
   PROLIFERATION
AB Ever since their discovery, microRNAs (miRNAs/miRs) have astonished us by the plethora of processes they regulate, and thus adding another dimension to the gene regulation. They have been implicated in several diseases affecting cardiovascular, neurodegenerative, hepatic, autoimmune and inflammatory functions. A primate specific exonic miRNA, miR-198 has been vastly studied during the past decade, and shown to have a critical role in wound healing. The aberrant expression of miR-198 was first reported in schizophrenia, linking it to neural development. Later, its dysregulation and tumor suppressive role was reported in hepatocellular carcinoma. However, this was just a beginning, and after which there was an explosion of reports linking miR-198 deregulation to cancers and other ailments. The first target to be identified for miR-198 was Cyclin T1 in monocytes affecting HIV1 replication. Depending on the type of cancer, miR-198 has been shown to function either as a tumor suppressor or an oncomir. Interestingly, miR-198 is not only known to regulate multiple targets and pathways, but also is itself regulated by several circular RNAs and long-non-coding RNAs, highlighting a complex regulatory network. This review highlights the currently understood mechanism and regulation of miR198 in different diseases, and its possible diagnostic and therapeutic potential.
C1 [Kaushik, Pankhuri; Kumar, Arun] Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India.
C3 Indian Institute of Science (IISC) - Bangalore
RP Kumar, A (corresponding author), Indian Inst Sci, Dept Mol Reprod Dev & Genet, Bangalore 560012, Karnataka, India.
EM arunk@iisc.ac.in
FU Department of Biotechnology, New Delhi [BT/PR33054/MED/30/2210/2020]
FX The financial support from Department of Biotechnology
   (BT/PR33054/MED/30/2210/2020) , New Delhi is gratefully acknowledged.
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NR 135
TC 5
Z9 5
U1 0
U2 7
PU ELSEVIER GMBH
PI MUNICH
PA HACKERBRUCKE 6, 80335 MUNICH, GERMANY
SN 0344-0338
EI 1618-0631
J9 PATHOL RES PRACT
JI Pathol. Res. Pract.
PD JAN
PY 2022
VL 229
AR 153741
DI 10.1016/j.prp.2021.153741
EA DEC 2021
PG 13
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA XW0UA
UT WOS:000735344000003
PM 34952425
DA 2025-06-01
ER

PT J
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TI <hr>Unveiling Cancer-Related Metaplastic Cells in Both Helicobacter
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SO GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune Gastritis; Helicobacter pylori Infection; Gastric Metaplasia;
   Gastric Cancer; Gastric Inflammation
ID EXPRESSION; PROMOTES
AB BACKGROUND & AIMS: Gastric metaplasia may arise as a consequence of chronic inflammation and is associated with an increased risk of gastric cancer development. Although Helicobacter pylori (Hp) infection and autoimmune gastritis (AIG) both induce gastric metaplasia, possible distinctions in resulting metaplastic cells and their respective cancer risks requires further investigation. METHODS: Using both mouse models and human participants, we scrutinized the metaplasia originating from Hp infection and AIG. Gastric pathology and metaplasia were examined through histopathologic assessment. Molecular features of metaplastic cells were defined using single-cell transcriptomics in murine models of Hp infection and AIG, as well as in human biopsy specimens from patients with Hp infection and AIG. Expression of a newly defined cancer-related metaplastic biomarker was confirmed through immunofluorescence. RESULTS: Metaplasia in Hp infection and AIG displayed comparable histopathologic and transcriptional features. Diverse metaplastic subtypes were identified across both disease settings, with subtle differences in the prevalence of certain subtypes between inflammatory contexts. Notably, Hp infection did not drive a unique metaplastic cell phenotype. One metaplastic subtype, which resembled incomplete intestinal metaplasia and shared transcriptional features with gastric cancer, was identified in both diseases. This cancer-like metaplastic subtype was characterized by expression of the cancer-associated biomarker ANPEP/CD13. CONCLUSION: Both Hp infection and AIG trigger a diverse array of metaplastic cell types. Identification of a cancer-related metaplastic cell uniquely expressing ANPEP/CD13, present in both Hp- and AIG-induced gastritis, indicates the carcinogenic capacity of both diseases. This discovery can guide early detection and risk stratification for patients with chronic gastritis.
C1 [Hoft, Stella G.; Carrero, Javier A.; Jackson, Nicholas M.; Dipaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, 1100 South Grand Blvd DRC707, St Louis, MO 63104 USA.
   [Brennan, Michelle] St Louis Univ, Sch Med, Dept Biochem & Mol Biol, St Louis, MO USA.
   [Bigley, Tarin M.] Washington Univ St Louis, Sch Med, Dept Pediat, Div Rheumatol Immunol, St Louis, MO USA.
   [Saenz, Jose B.] Washington Univ St Louis, Sch Med, Dept Med, Div Gastroenterol, St Louis, MO USA.
   [Saenz, Jose B.] Washington Univ St Louis, Sch Med, Dept Mol Cell Biol, Div Gastroenterol, St Louis, MO USA.
C3 Saint Louis University; Saint Louis University; Washington University
   (WUSTL); Washington University (WUSTL); Washington University (WUSTL)
RP Dipaolo, RJ (corresponding author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, 1100 South Grand Blvd DRC707, St Louis, MO 63104 USA.
EM richard.dipaolo@health.slu.edu
OI Hoft, Stella/0000-0003-1783-7790; DiPaolo, Richard/0000-0002-2191-6689
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
   [2R56DK110406-06A1, R01DK134531, F30DK134124, 1K08DK122116,
   R03DK133243]; Children's Discovery Institute of Washington University
   [MI-FR-2022-990]; St. Louis Children's Hospital Scholar's Award
FX This work was supported by the National Institute of Diabetes and
   Digestive and Kidney Diseases (NIDDK) under 2R56DK110406-06A1,
   R01DK134531, F30DK134124, 1K08DK122116, and R03DK133243. Funding for
   Tarin Bigley for this project was provided by the Children's Discovery
   Institute of Washington University (MI-FR-2022-990) and St. Louis
   Children's Hospital Scholar's Award.
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NR 60
TC 7
Z9 7
U1 4
U2 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD JAN
PY 2025
VL 168
IS 1
BP 53
EP 67
DI 10.1053/j.gastro.2024.08.032
EA DEC 2024
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA R5S7Z
UT WOS:001392052800001
PM 39236896
DA 2025-06-01
ER

PT J
AU Fu, JX
   Guo, Q
   Feng, Y
   Cheng, P
   Wu, AH
AF Fu, Jinxing
   Guo, Qing
   Feng, Yuan
   Cheng, Peng
   Wu, Anhua
TI Dual role of fucosidase in cancers and its clinical potential
SO JOURNAL OF CANCER
LA English
DT Review
DE Fucosidase; defucosylation; cancer; microenvironment; signaling pathway
ID ALPHA-L-FUCOSIDASE; ORAL PRECANCEROUS CONDITIONS; FUCOSYL-TRANSFERASE;
   HEPATOCELLULAR-CARCINOMA; CORE FUCOSYLATION; DOWN-REGULATION; GENE
   FUCA1; EXPRESSION; SERUM; GLYCOSYLATION
AB Glycosidases and glycosyltransferases greatly impact malignant phenotype of tumors though genetics and epigenetics mechanisms. As the member of glycoside hydrolase (GH) families 29A, alpha-L-fucosidases (AFUs) are involved in the hydrolysis of terminal L-fucose residues linked via alpha-1,2, alpha-1,3, alpha-1,4 or alpha-1,6 to the reducing end of N-acetyl glucosamine (GlcNAc) of oligosaccharide chains. The defucosylation process mediated by AFUs contributes to the development of various diseases, such as chronic inflammatory diseases, immune disorders, and autoimmune diseases by reducing the interaction between fucosylated adhesion molecules supporting leukocyte extravasation. AFUs also impair crucial cell-extracellular matrix (ECM) interactions and presumably subsequent cell signaling pathways, which lead to changes in tumor function and behavior. There are two isoforms of AFUs in human, namely alpha-L-fucosidase 1 (FUCA1) and alpha-L-fucosidase 2 (FUCA2), respectively. FUCA1 is a p53 target gene and can hydrolyze different fucosylation sites on epidermal growth factor receptor (EGFR), thereby determining the activation of EGFR. FUCA2 mediates the adhesion between Helicobacter pylori and gastric mucosa and is upregulated in 24 tumor types. Besides, based on the participation of AFU in signaling pathways and tumor progression, we discuss the prospect of AFU as a therapeutic target.
C1 [Fu, Jinxing; Guo, Qing; Feng, Yuan; Cheng, Peng; Wu, Anhua] China Med Univ, Dept Neurosurg, First Hosp, Shenyang, Peoples R China.
   [Cheng, Peng; Wu, Anhua] China Med Univ, First Hosp, 155 Nanjingbei St, Shenyang 110001, Liaoning, Peoples R China.
C3 China Medical University; China Medical University
RP Cheng, P; Wu, AH (corresponding author), China Med Univ, First Hosp, 155 Nanjingbei St, Shenyang 110001, Liaoning, Peoples R China.
EM chengpengcmu@sina.com; ahwu@cmu.edu.cn
RI Cheng, Peng/R-6211-2016
FU National Natural Science Foundation of China [81872057, 81872054];
   Natural Science Foundation of Liaoning Province [20180550063,
   20170541020, 2020BS117]
FX Funding This work was supported by the National Natural Science
   Foundation of China (no. 81872057 to P. Cheng; 81872054 to A. Wu) , and
   the Natural Science Foundation of Liaoning Province (no. 20180550063, to
   P. Cheng. no. 20170541020, no. 2020BS117, to Q. Guo.) .
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NR 103
TC 11
Z9 11
U1 1
U2 26
PU IVYSPRING INT PUBL
PI LAKE HAVEN
PA PO BOX 4546, LAKE HAVEN, NSW 2263, AUSTRALIA
SN 1837-9664
J9 J CANCER
JI J. Cancer
PY 2022
VL 13
IS 10
BP 3121
EP 3132
DI 10.7150/jca.75840
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 4U9ZP
UT WOS:000859144200003
PM 36046653
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU He, W
   Xu, JZ
   Mu, RY
   Li, Q
   Lv, DL
   Huang, Z
   Zhang, JF
   Wang, CM
   Dong, L
AF He, Wei
   Xu, Jinzhi
   Mu, Ruoyu
   Li, Qiu
   Lv, Da-lun
   Huang, Zhen
   Zhang, Junfeng
   Wang, Chunming
   Dong, Lei
TI High-salt diet inhibits tumour growth in mice via regulating
   myeloid-derived suppressor cell differentiation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID POPULATION-BASED COHORT; GASTRIC-CANCER; SODIUM; PROMOTES; MACROPHAGES;
   POLARIZATION; NEUTROPHILS; ACTIVATION; IMMUNITY; CONSUMPTION
AB High-salt intake can promote pro-inflammatory responses associated with pathological conditions. However, here, the authors show that high-salt diet may have an antitumor protective role by modulating the accumulation and phenotype of myeloid derived suppressor cells and enhancing immunosurveillance.
   High-salt diets are associated with an elevated risk of autoimmune diseases, and immune dysregulation plays a key role in cancer development. However, the correlation between high-salt diets (HSD) and cancer development remains unclear. Here, we report that HSD increases the local concentration of sodium chloride in tumour tissue, inducing high osmotic stress that decreases both the production of cytokines required for myeloid-derived suppressor cells (MDSCs) expansion and MDSCs accumulation in the blood, spleen, and tumour. Consequently, the two major types of MDSCs change their phenotypes: monocytic-MDSCs differentiate into antitumour macrophages, and granulocytic-MDSCs adopt pro-inflammatory functions, thereby reactivating the antitumour actions of T cells. In addition, the expression of p38 mitogen-activated protein kinase-dependent nuclear factor of activated T cells 5 is enhanced in HSD-induced M-MDSC differentiation. Collectively, our study indicates that high-salt intake inhibits tumour growth in mice by activating antitumour immune surveillance through modulating the activities of MDSCs.
C1 [He, Wei; Xu, Jinzhi; Mu, Ruoyu; Huang, Zhen; Zhang, Junfeng; Dong, Lei] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Sch Life Sci, 163 Xianlin Ave, Nanjing 210093, Peoples R China.
   [He, Wei; Xu, Jinzhi; Mu, Ruoyu; Huang, Zhen; Zhang, Junfeng; Dong, Lei] Nanjing Univ, Med Sch, 163 Xianlin Ave, Nanjing 210093, Peoples R China.
   [He, Wei; Mu, Ruoyu; Li, Qiu; Wang, Chunming] Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Taipa, Macao, Peoples R China.
   [He, Wei] Anhui Med Univ, Sch Basic Med Sci, Dept Immunol, Hefei 230032, Peoples R China.
   [Lv, Da-lun] Wannan Med Coll, Dept Burn & Plast Surg, Affiliated Hosp 1, Wuhu City 241000, Anhui, Peoples R China.
C3 Nanjing University; Nanjing University; University of Macau; Anhui
   Medical University; Wannan Medical College
RP Zhang, JF; Dong, L (corresponding author), Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Sch Life Sci, 163 Xianlin Ave, Nanjing 210093, Peoples R China.; Zhang, JF; Dong, L (corresponding author), Nanjing Univ, Med Sch, 163 Xianlin Ave, Nanjing 210093, Peoples R China.; Wang, CM (corresponding author), Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Taipa, Macao, Peoples R China.
EM jfzhang@nju.edu.cn; cmwang@umac.mo; leidong@nju.edu.cn
RI Wang, Chunming/I-3392-2013; Dong, Lei/J-3516-2013; zhang,
   junfeng/JHT-7871-2023
OI LI, QIU/0000-0002-0864-4885; Wang, Chunming/0000-0001-9185-9678; Dong,
   Lei/0000-0002-2013-4191; Xu, Jinzhi/0000-0002-1439-8924; Mu,
   Ruoyu/0000-0002-6093-0176
FU National Key Research and Development Programme of China
   [2017YFC0909702]; National Natural Science Foundation of China
   [81973273, 81673380, 31971309, 31671031]; Jiangsu Province Funds for
   Distinguished Young Scientists [BK20170015]; Fundamental Research Funds
   for the Central Universities [020814380115]; Science and Technology
   Development Fund, Macau SAR (FDCT) [080/2016/A2, 0018/2019/AFJ,
   0097/2019/A2]; University of Macau [MYRG2017-00028-ICMS]; Natural
   Science Foundation of China [31961160701]; Science and Technology
   Development Fund [31961160701]; Anhui provincial Natural Science
   Foundation [1908085QC131]; Grants for Scientific Research of BSKY from
   Anhui Medical University [XJ201726]
FX This study was funded by the National Key Research and Development
   Programme of China (2017YFC0909702), the National Natural Science
   Foundation of China (81973273, 81673380, 31971309 and 31671031), the
   Jiangsu Province Funds for Distinguished Young Scientists (BK20170015)
   and the Fundamental Research Funds for the Central Universities
   (020814380115). C.W. acknowledges the funding support from the Science
   and Technology Development Fund, Macau SAR (FDCT No. 080/2016/A2,
   0018/2019/AFJ, 0097/2019/A2) and the University of Macau
   (MYRG2017-00028-ICMS). L.D. acknowledges the UM Macau Distinguished
   Visiting Scholar (MDS) Programme. This study was also supported by the
   funds for the International Cooperation and Exchange of the Natural
   Science Foundation of China and the Science and Technology Development
   Fund (31961160701), Anhui provincial Natural Science Foundation
   (1908085QC131) and Grants for Scientific Research of BSKY (XJ201726)
   from Anhui Medical University.
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NR 69
TC 64
Z9 72
U1 4
U2 60
PU NATURE RESEARCH
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD APR 7
PY 2020
VL 11
IS 1
AR 1732
DI 10.1038/s41467-020-15524-1
PG 17
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA LE2DD
UT WOS:000526532500010
PM 32265505
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Wang, AT
   Huang, HY
   Shi, JH
   Yu, XY
   Ding, R
   Zhang, YR
   Han, QQ
   Ni, ZY
   Li, X
   Zhao, R
   Zou, Q
AF Wang, Aiting
   Huang, Haiyan
   Shi, Jian-Hong
   Yu, Xiaoyan
   Ding, Rui
   Zhang, Yuerong
   Han, Qiaoqiao
   Ni, Zhi-Yu
   Li, Xia
   Zhao, Ren
   Zou, Qiang
TI USP47 inhibits m6A-dependent c-Myc translation to maintain regulatory T
   cell metabolic and functional homeostasis
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID METHYLATION; EXPRESSION; GLUCOSE; FOXP3
AB The functional integrity of Tregs is interwoven with cellular metabolism; however, the mechanisms governing Treg metabolic programs remain elusive. Here, we identified that the deubiquitinase USP47 inhibited c-Myc translation mediated by the RNA N6-methyladenosine (m6A) reader YTHDF1 to maintain Treg metabolic and functional homeostasis. USP47 positively correlated with the tumor-infiltrating Treg signature in samples from patients with colorectal cancer and gastric cancer. USP47 ablation compromised Treg homeostasis and function in vivo, resulting in the development of inflammatory disorders, and boosted antitumor immune responses. USP47 deficiency in Tregs triggered the accumulation of the c-Myc protein and in turn exacerbated hyperglycolysis. Mechanistically, USP47 prevented YTHDF1 ubiquitination to attenuate the association of YTHDF1 with translation initiation machinery, thereby decreasing m6A-based c-Myc translation efficiency. Our findings reveal that USP47 directs m6A-dependent metabolic programs to orchestrate Treg homeostasis and suggest novel approaches for selective immune modulation in cancer and autoimmune diseases by targeting of USP47.
C1 [Wang, Aiting; Huang, Haiyan; Zhao, Ren] Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Gen Surg, Shanghai, Peoples R China.
   [Wang, Aiting; Yu, Xiaoyan; Ding, Rui; Zhang, Yuerong; Han, Qiaoqiao; Zou, Qiang] Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Dept Immunol & Microbiol, Sch Med,State Key Lab Syst Med Canc, Shanghai, Peoples R China.
   [Wang, Aiting] Huzhou Univ, Huzhou Cent Hosp, Clin Lab, Affiliated Cent Hosp, Huzhou, Zhejiang, Peoples R China.
   [Shi, Jian-Hong; Ni, Zhi-Yu] Hebei Univ, Affiliated Hosp, Hebei Collaborat Innovat Ctr Tumor Microecol Metab, Cent Lab, Baoding, Hebei, Peoples R China.
   [Li, Xia] Shandong Univ Tradit Chinese Med, Innovat Inst Chinese Med & Pharm, Jinan, Shandong, Peoples R China.
   [Zou, Qiang] Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Immunol, Dept Immunol & Microbiol, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.
   [Zhao, Ren] Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, 197 Ruijin Er Rd, Shanghai 200025, Peoples R China.
   [Li, Xia] Shandong Univ Tradit Chinese Med, Innovat Inst Chinese Med & Pharm, 4655 Daxue Rd, Jinan 250399, Peoples R China.
   [Ni, Zhi-Yu] Hebei Univ, Affiliated Hosp, Hebei Collaborat Innovat Ctr Tumor Microecol Metab, Cent Lab, 212 Yuhua East Rd, Baoding 071000, Hebei, Peoples R China.
C3 Shanghai Jiao Tong University; Shanghai Jiao Tong University; Chinese
   Academy of Sciences; Huzhou University; Hebei University; Shandong
   University of Traditional Chinese Medicine; Chinese Academy of Sciences;
   Shanghai Jiao Tong University; Shanghai Jiao Tong University; Shandong
   University of Traditional Chinese Medicine; Hebei University
RP Zou, Q (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Inst Immunol, Dept Immunol & Microbiol, 280 South Chongqing Rd, Shanghai 200025, Peoples R China.; Zhao, R (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Gen Surg, 197 Ruijin Er Rd, Shanghai 200025, Peoples R China.; Li, X (corresponding author), Shandong Univ Tradit Chinese Med, Innovat Inst Chinese Med & Pharm, 4655 Daxue Rd, Jinan 250399, Peoples R China.; Ni, ZY (corresponding author), Hebei Univ, Affiliated Hosp, Hebei Collaborat Innovat Ctr Tumor Microecol Metab, Cent Lab, 212 Yuhua East Rd, Baoding 071000, Hebei, Peoples R China.
EM nizhiyu@hbu.edu.cn; 60230033@sdutcm.edu.cn.Or; rjzhaoren@139.com;
   Qzou1984@sjtu.edu.cn
RI Li, Xia/GOK-1145-2022; Ding, Rui/AAL-7714-2021; Wang,
   Aiting/HNR-1997-2023; Shi, Jian-hong/AAF-6078-2019
OI Shi, Jian-hong/0000-0003-2232-1000; Wang, Aiting/0000-0003-3177-9961;
   Li, Xia/0000-0002-0194-0307
FU National Key Research and Development Program of China [2021YFA1301402,
   2020YFA0803603]; National Natural Science Foundation of China [81930040,
   82225020, 32200728, 82274575]; Guangdong Basic and Applied Basic
   Research Foundation [2021A1515110375]
FX Acknowledgments This study was supported by grants from the National Key
   Research and Development Program of China (2021YFA1301402,
   2020YFA0803603) , the National Natural Science Foundation of China
   (81930040, 82225020, 32200728, and 82274575) , and the Guangdong Basic
   and Applied Basic Research Foundation (2021A1515110375) .
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NR 48
TC 21
Z9 21
U1 2
U2 23
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 2015 MANCHESTER RD, ANN ARBOR, MI 48104 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC 1
PY 2023
VL 133
IS 23
AR e169365
DI 10.1172/JCI169365
PG 17
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CC9P1
UT WOS:001123171400003
PM 37788092
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Astl, J
   Sterzl, I
AF Astl, J.
   Sterzl, I.
TI Activation of Helicobacter Pylori Causes Either Autoimmune
   Thyroid Diseases or Carcinogenesis in the Digestive Tract
SO PHYSIOLOGICAL RESEARCH
LA English
DT Review
DE Helicobacter pylori; Autoimmune thyroiditis; MELISA; CagA gene;
   Tonsillar tissue; Oropharynx; Mutagen; Cancer
ID T-CELL PROLIFERATION; EXTRAGASTRIC MANIFESTATIONS; IMMUNE-RESPONSE;
   EXTRADIGESTIVE MANIFESTATIONS; LYMPHOCYTE-RESPONSES; CHRONIC
   TONSILLITIS; DUODENAL-ULCER; INFECTION; COLONIZATION; ERADICATION
AB Helicobacter pylori has been implicated in stimulation of immune system, development of autoimmune endocrinopathies as autoimmune thyroiditis (AT) and on other hand induction of immunosupresion activates gastric and extra-gastric diseases such as gastric ulcer or cancer. It causes persistent lifelong infection despite local and systemic immune response. Our results indicate that Helicobacter pylori might cause inhibition of the specific cellular immune response in Helicobacter pylori-infected patients with or without autoimmune diseases such as AT. We cannot also declare the carcinogenic effect in oropharynx. However the association of any infection agents and cancerogenesis exists. The adherence of Helicobacter pylori expression and enlargement of benign lymphatic tissue and the high incidence of the DNA of Helicobacter pylori in laryngopharyngeal and oropharyngeal cancer is reality. LTT appears to be a good tool for detection of immune memory cellular response in patients with Helicobacter pylori infection and AT. All these complications of Helicobacter pylori infection can be abrogated by successful eradication of Helicobacter pylori.
C1 [Astl, J.] Charles Univ Prague, Fac Med 3, Dept Otorhinolaryngol, Prague, Czech Republic.
   [Astl, J.] Mil Fac Hosp, Prague, Czech Republic.
   [Astl, J.] Charles Univ Prague, Univ Hosp Motol, Dept Otorhinolaryngol & Head & Neck Surg, Fac Med 1, Prague, Czech Republic.
   [Sterzl, I.] Inst Endocrinol, Dept Immunoendocrinol, Narodni 8, CZ-11694 Prague 1, Czech Republic.
C3 Charles University Prague; Motol University Hospital; Charles University
   Prague; Institute of Endocrinology - Prague
RP Sterzl, I (corresponding author), Inst Endocrinol, Dept Immunoendocrinol, Narodni 8, CZ-11694 Prague 1, Czech Republic.
EM isterzl@endo.cz
RI Astl, Jaromir/AAA-4810-2022
FU Ministry of Defense [MO 1012]; Internal Grant Agency of the Ministry of
   Health of the Czech Republic [NT11523]
FX This work was supported by project of Ministry of Defense MO 1012 and
   grant NT11523 of the Internal Grant Agency of the Ministry of Health of
   the Czech Republic.
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NR 89
TC 13
Z9 15
U1 1
U2 14
PU ACAD SCIENCES CZECH REPUBLIC, INST PHYSIOLOGY
PI PRAGUE 4
PA VIDENSKA 1083, PRAGUE 4 142 20, CZECH REPUBLIC
SN 0862-8408
EI 1802-9973
J9 PHYSIOL RES
JI Physiol. Res.
PY 2015
VL 64
SU 2
BP S291
EP S301
DI 10.33549/physiolres.933118
PG 11
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA CW5CA
UT WOS:000365011800025
PM 26680492
OA gold
DA 2025-06-01
ER

PT J
AU Egan, CA
   Lazarova, Z
   Darling, TN
   Yee, C
   Yancey, KB
AF Egan, CA
   Lazarova, Z
   Darling, TN
   Yee, C
   Yancey, KB
TI Anti-epiligrin cicatricial pemphigoid - Clinical findings,
   immunopothogenesis, and significant associations
SO MEDICINE
LA English
DT Article
ID SUBEPIDERMAL BULLOUS DISEASES; BASAL-CELL CARCINOMA; GASTRIC-CARCINOMA;
   IGG AUTOANTIBODIES; LAMININ-5 ALPHA-3-BETA-3-GAMMA-2; DIFFERENTIAL
   EXPRESSION; ALPHA-SUBUNIT; NEONATAL MICE; AUTOIMMUNE; CANCER
AB We report the clinical and immunopathologic findings in a cohort of 35 patients with anti-epiligrin cicatricial pemphigoid (AECP). These patients have a mucosal predominant subepithelial blistering disease that is clinically indistinguishable from other forms of cicatricial pemphigoid. The mucosal surfaces of the mouth and eye are most commonly involved. The skin is also involved in most patients, but usually this is less severe than mucosal involvement. AECP is characterized by the binding of circulating IgG autoantibodies to the dermal side of I M NaCl split human skin on indirect immunofluorescence microscopy. These IgG antibasement membrane autoantibodies target laminin 5, a heterotrimeric protein consisting of alpha3, beta3, and gamma2 subunits. IgG autoantibodies predominantly target the G domain within the a subunit. The presence of circulating IgG autoantibodies are specific for the diagnosis of AECP and are not seen in patients with other autoimmune blistering diseases or normal volunteers. Furthermore, we expand on data previously reported on the finding of an increased relative risk for solid cancer in patients with AECP, especially in the first year after blister onset. The majority of cancers documented in a cohort of 35 patients assembled over 12 years of study were adenocarcinomas that were at an advanced stage at their time of detection. This circumstance is thought to account for a high incidence of mortality among AECP patients who develop an associated cancer. AECP patients also demonstrate a significant risk for mortality as a consequence of treatment with systemic immunosuppressives. The current longitudinal study suggests that only a minority of AECP patients go into remission.
C1 NCI, Dermatol Branch, Div Clin Sci, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); Division of Clinical Sciences (DCS)
RP Egan, CA (corresponding author), Beaumont Hosp, Dept Dermatol, Beaumont Rd, Dublin 9, Ireland.
RI Yancey, Kim/AIC-0005-2022
OI Yancey, Kim/0000-0001-6101-4690; Darling, Thomas/0000-0002-5161-1974
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NR 59
TC 84
Z9 85
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7974
J9 MEDICINE
JI Medicine (Baltimore)
PD MAY
PY 2003
VL 82
IS 3
BP 177
EP 186
DI 10.1097/00005792-200305000-00004
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 679EC
UT WOS:000182907000004
PM 12792304
OA Bronze
DA 2025-06-01
ER

PT J
AU Omrane, I
   Baroudi, O
   Bougatef, K
   Mezlini, A
   Abidi, A
   Medimegh, I
   Stambouli, N
   Ayari, H
   Kourda, N
   Uhrhammer, N
   Bignon, YJ
   Elgaaied, AB
   Marrakchi, R
AF Omrane, Ines
   Baroudi, Olfa
   Bougatef, Karim
   Mezlini, Amel
   Abidi, Ahmed
   Medimegh, Imen
   Stambouli, Nejla
   Ayari, Hager
   Kourda, Nadia
   Uhrhammer, Nancy
   Bignon, Yves Jean
   Elgaaied, Amel Benammar
   Marrakchi, Raja
TI Significant association between IL23R and IL17F polymorphisms and
   clinical features of colorectal cancer
SO IMMUNOLOGY LETTERS
LA English
DT Article
DE IL17/IL23R; Th17 cells; Immunity; Polymorphism; Colorectal cancer;
   Clinical features
ID NF-KAPPA-B; INFLAMMATORY-BOWEL-DISEASE; SPORADIC COLON-CANCER; HUMAN
   GASTRIC-MUCOSA; CROHNS-DISEASE; IL-23 RECEPTOR; INTERLEUKIN-17A AND-17F;
   ULCERATIVE-COLITIS; GENE POLYMORPHISMS; T-CELLS
AB Th17 cells are involved in inflammatory and autoimmune diseases. These cells may be involved in pathological processes mainly producing pro-inflammatory cytokines. Recently, it was shown that the IL23/IL17 pathway plays an important role in the development of inflammatory bowel disease. In general, genes encoding cytokines are genetically polymorphic and polymorphisms in genes IL23R el IL17F were shown associated with susceptibility to Crohn's disease and ulcerative colitis which in their turn are considered as risk factors for developing colorectal cancer (CRC). Our approach is to study IL17F and IL23R polymorphisms as risk factor associated with CRC in the Tunisian population in patients and healthy controls. Interesting, we noted a significant association between IL17F and IL23R polymorphisms and tumor location (p = 0.0001 and p = 0.049, respectively), tumor histology (p = 0.007 and p = 0.049, respectively) and tumor architecture (p = 0.0000000001 and p = 0.07, respectively) in CRC patients. We also showed a significant association of IL17F variant with an increased risk of TNM stage III/IV (p = 0.007), showing an increased risk of advanced stage. Finally, we observed a positive link between IL17F polymorphism and CRC patients with lymph nodes (p = 0.0000000001) and metastasis (p = 0.00000009). However, we found no evidence to support a significant association between IL17F and IL23R polymorphisms and colorectal cancer susceptibility. Our findings suggest that IL17F and IL23R polymorphisms were significantly associated with clinical features variables. The IL17F cytokine appear to be involved in the control of tumor growth and invasion of gastrointestinal tumors. IL17 and IL23 polymorphisms or those of their receptors as important determinants of susceptibility to colorectal cancer are still subject to questioning. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Omrane, Ines; Baroudi, Olfa; Bougatef, Karim; Abidi, Ahmed; Medimegh, Imen; Stambouli, Nejla; Ayari, Hager; Elgaaied, Amel Benammar; Marrakchi, Raja] Univ Tunis, Fac Sci Tunis El Manar, Lab Human Genet Immunol & Pathol, Tunis, Tunisia.
   [Mezlini, Amel] Salah Azaiez Hosp Tunis, Gastroenterol Serv, Tunis, Tunisia.
   [Kourda, Nadia] Charles Nicolle Hosp Tunis, Lab Anat & Pathol, Tunis, Tunisia.
   [Uhrhammer, Nancy; Bignon, Yves Jean] Ctr Jean Perrin, Lab Diag & Mol Genet, Clermont Ferrand, France.
C3 Universite de Tunis-El-Manar; Faculte des Sciences de Tunis (FST);
   Universite de Tunis; Universite de Tunis-El-Manar; Hopital Charles
   Nicolle; UNICANCER; Centre Jean Perrin
RP Omrane, I (corresponding author), Fac Sci Tunis EL MANAR, Lab Genet Immunol & Pathol hUMAINE, Campus Univ, Tunis 2092, Tunisia.
EM inesomrane@hotmail.fr
RI BOUGATEF, karim/AAM-4385-2021; Stambouli, NEJLA/AAO-6434-2021; Elgaaied,
   Amel/AAL-1183-2020
OI Abidi, Ahmed/0000-0001-7868-5992; stambouli, NEJLA/0000-0001-7688-5210;
   raja, marrakchi/0000-0001-5183-3131
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NR 63
TC 34
Z9 34
U1 0
U2 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-2478
EI 1879-0542
J9 IMMUNOL LETT
JI Immunol. Lett.
PD MAR-APR
PY 2014
VL 158
IS 1-2
BP 189
EP 194
DI 10.1016/j.imlet.2014.01.002
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AE2GN
UT WOS:000333791400026
PM 24440568
DA 2025-06-01
ER

PT J
AU Sausen, DG
   Basith, A
   Muqeemuddin, S
AF Sausen, Daniel G.
   Basith, Ayeman
   Muqeemuddin, Syed
TI EBV and Lymphomagenesis
SO CANCERS
LA English
DT Review
DE EBV; latent proteins; cancer; lymphoma; treatment
ID EPSTEIN-BARR-VIRUS; REED-STERNBERG CELLS; HODGKIN LYMPHOMA;
   LYMPHOPROLIFERATIVE DISORDERS; B-CELLS; TUMOR-SUPPRESSOR;
   DOWN-REGULATION; GROWTH TRANSFORMATION; NUCLEAR ANTIGEN-1;
   BURKITT-LYMPHOMA
AB Epstein-Barr virus is a highly prevalent virus associated with a multitude of diseases, including autoimmune conditions such as multiple sclerosis and many types of cancer. As such, it is imperative to have a foundational understanding of this virus. This review discusses the contribution of the Epstein-Barr virus to key hematologic malignancies with a focus on the roles of latent proteins, including diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, NK/T-cell lymphoma, and primary CNS lymphoma. It then provides a brief overview of treatment for each of these diseases. The clinical significance of Epstein-Barr virus (EBV) cannot be understated. Not only does it infect approximately 90% of the world's population, but it is also associated with numerous pathologies. Diseases linked to this virus include hematologic malignancies such as diffuse large B-cell lymphoma, Hodgkin lymphoma, Burkitt lymphoma, primary CNS lymphoma, and NK/T-cell lymphoma, epithelial malignancies such as nasopharyngeal carcinoma and gastric cancer, autoimmune diseases such as multiple sclerosis, Graves' disease, and lupus. While treatment for these disease states is ever evolving, much work remains to more fully elucidate the relationship between EBV, its associated disease states, and their treatments. This paper begins with an overview of EBV latency and latency-associated proteins. It will then review EBV's contributions to select hematologic malignancies with a focus on the contribution of latent proteins as well as their associated management.
C1 [Sausen, Daniel G.] Eastern Virginia Med Sch, Sch Med, Norfolk, VA 23507 USA.
   [Basith, Ayeman] Eastern Virginia Med Sch, Dept Internal Med, Norfolk, VA 23507 USA.
C3 Eastern Virginia Medical School; Eastern Virginia Medical School
RP Sausen, DG (corresponding author), Eastern Virginia Med Sch, Sch Med, Norfolk, VA 23507 USA.
EM sausendg@evms.edu
RI Sausen, Daniel/JDC-6977-2023
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NR 208
TC 22
Z9 23
U1 4
U2 21
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2023
VL 15
IS 7
AR 2133
DI 10.3390/cancers15072133
PG 23
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA D6CU4
UT WOS:000969598900001
PM 37046794
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Yu, YF
   Tong, KK
   Shangguan, XL
   Yang, XY
   Wu, JY
   Hu, G
   Yu, R
   Tan, CC
AF Yu, Yun-Feng
   Tong, Ke-Ke
   Shangguan, Xue-Li
   Yang, Xin-Yu
   Wu, Jing-Yi
   Hu, Gang
   Yu, Rong
   Tan, Chuan-Chuan
TI Research status and hotspots of autoimmune gastritis: A bibliometric
   analysis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune gastritis; Autoimmune diseases; Bibliometric; CiteSpace;
   VOSviewer; Helicobacter pylori
ID HELICOBACTER-PYLORI; CLASSIFICATION; AUTOANTIBODIES; DIAGNOSIS; DISEASE
AB BACKGROUNDAs an emerging potential risk factor for gastric cancer, autoimmune gastritis (AIG) has garnered increasing attention from researchers.AIMTo analyze the research overview and popular topics in the field of AIG using bibliometrics.METHODSRelevant publications on AIG in the Web of Science Core Collection were collated, and data visualization and analysis of the number of publications, countries, institutions, journals, authors, keywords, and citations were performed using software such as VOSviewer, CiteSpace, and Scimago Graphic.RESULTSIn total, 316 relevant articles were included in the analysis. From 2015 to 2022, the number of publications increased annually. The countries, institutions, authors, and journals with the highest number of publications in this field were Italy, Monash University, Toh BH, and Internal Medicine. The main keywords used in this field of research were pathogenesis, Helicobacter pylori, autoantibody, parietal cell antibody, atrophic gastritis, classification, diagnosis, autoimmune disease, risk, cancer, gastric cancer, vitamin B12 deficiency, and pernicious anemia. The following directions may be popular for future research: (1) The role of Helicobacter pylori in the pathogenesis of AIG; (2) diagnostic criteria for AIG and reference values for serum antibodies; (3) comorbidity mechanisms between AIG and other autoimmune diseases; (4) specific risks of AIG complicating gastric and other cancers; and (5) the role of vitamin B12 supplementation in patients with early-stage AIG.CONCLUSIONThis bibliometric analysis reported on popular topics and emerging trends in AIG, with diagnosis and prognosis being research hotspots in this field.
C1 [Yu, Yun-Feng; Shangguan, Xue-Li; Hu, Gang; Yu, Rong; Tan, Chuan-Chuan] Hunan Univ Chinese Med, Hosp 1, 95 Shaoshan Middle Rd, Changsha 410007, Hunan Province, Peoples R China.
   [Tong, Ke-Ke] Hunan Univ Tradit Chinese Med, Hosp Hunan Univ Tradit Chinese Med, Changde 415213, Hunan Province, Peoples R China.
   [Yang, Xin-Yu] Hunan Univ Chinese Med, Coll Chinese Med, Changsha 410208, Hunan Province, Peoples R China.
   [Wu, Jing-Yi] Zhejiang Chinese Med Univ, Hosp 3, Hangzhou 310005, Zhejiang Provin, Peoples R China.
C3 Hunan University of Chinese Medicine; Hunan University of Chinese
   Medicine; Hunan University of Chinese Medicine; Zhejiang Chinese Medical
   University
RP Tan, CC (corresponding author), Hunan Univ Chinese Med, Hosp 1, 95 Shaoshan Middle Rd, Changsha 410007, Hunan Province, Peoples R China.
EM cchuan16@hotmail.com
RI Yu, Rong/A-3011-2008
FU National Natural Science Foundation of China [U21A20411]
FX Supported by National Natural Science Foundation of China, NO. U21A20411
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NR 60
TC 11
Z9 11
U1 6
U2 19
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD NOV 14
PY 2023
VL 29
IS 42
BP 5781
EP 5799
DI 10.3748/wjg.v29.i42.5781
PG 19
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AH9U9
UT WOS:001117700700006
PM 38075850
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Conti, L
   Annibale, B
   Lahner, E
AF Conti, Laura
   Annibale, Bruno
   Lahner, Edith
TI Autoimmune Gastritis and Gastric Microbiota
SO MICROORGANISMS
LA English
DT Review
DE autoimmune gastritis; atrophic gastritis; gastric microbiota
ID PARIETAL-CELL ANTIBODIES; ATROPHIC BODY GASTRITIS; HELICOBACTER-PYLORI;
   PERNICIOUS-ANEMIA; HYDROCHLORIC-ACID; IRON-DEFICIENCY; CANCER-RISK;
   CLASSIFICATION; BIOPSIES; STOMACH
AB Autoimmune atrophic gastritis is an organ-specific immune-mediated condition characterized by atrophy of the oxyntic mucosa. Autoimmune atrophic gastritis (AIG) is characterized by a progressive loss of acid-secreting parietal cells leading to hypo-achlorhydria. Due to this peculiar intra-gastric environment, gastric microbiota composition in individuals with autoimmune atrophic gastritis was first supposed and then recently reported to be different from subjects with a normal acidic healthy stomach. Recent data confirm the prominent role of Helicobacter pylori as the main bacterium responsible for gastric disease and long-term complications. However, other bacteria than Helicobacter pylori, for example, Streptococci, were found in subjects who developed gastric cancer and in subjects at risk of this fearful complication, as well as those with autoimmune gastritis. Gastric microbiota composition is challenging to study due to the acidic gastric environment, the difficulty of obtaining representative samples of the entire gastric microbiota, and the possible contamination by oral or throat microorganisms, which can potentially lead to the distortion of the original gastric microbial composition, but innovative molecular approaches based on the analysis of the hyper-variable region of the 16S rRNA gene have been developed, permitting us to obtain an overall microbial composition view of the RNA gene that is present only in prokaryotic cells.
C1 [Conti, Laura; Annibale, Bruno; Lahner, Edith] Sapienza Univ Rome, St Andrea Hosp, Med Surg Dept Clin Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea
RP Lahner, E (corresponding author), Sapienza Univ Rome, St Andrea Hosp, Med Surg Dept Clin Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM lau88.conti@gmail.com; bruno.annibale@uniroma1.it;
   edith.lahner@uniroma1.it
RI Annibale, Bruno/A-5372-2008; Lahner, Edith/AAM-1039-2021
OI LAHNER, EDITH/0000-0002-9503-8639; annibale, bruno/0000-0001-9120-5957
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NR 90
TC 28
Z9 28
U1 2
U2 27
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2076-2607
J9 MICROORGANISMS
JI Microorganisms
PD NOV
PY 2020
VL 8
IS 11
AR 1827
DI 10.3390/microorganisms8111827
PG 12
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA OX1LQ
UT WOS:000593335600001
PM 33228138
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Taietti, I
   Votto, M
   Castagnoli, R
   Bertozzi, M
   De Filippo, M
   Di Sabatino, A
   Luinetti, O
   Raffaele, A
   Vanoli, A
   Lenti, MV
   Marseglia, GL
   Licari, A
AF Taietti, Ivan
   Votto, Martina
   Castagnoli, Riccardo
   Bertozzi, Mirko
   De Filippo, Maria
   Di Sabatino, Antonio
   Luinetti, Ombretta
   Raffaele, Alessandro
   Vanoli, Alessandro
   Lenti, Marco Vincenzo
   Marseglia, Gian Luigi
   Licari, Amelia
TI Clinical Heterogeneity of Early-Onset Autoimmune Gastritis: From the
   Evidence to a Pediatric Tailored Algorithm
SO DISEASES
LA English
DT Article
DE autoimmune gastritis (AIG); anti-parietal cell antibodies (APCA);
   children
ID IRON-DEFICIENCY ANEMIA; ATROPHIC GASTRITIS; PERNICIOUS-ANEMIA;
   HELICOBACTER-PYLORI; PATHOLOGY; CHILDREN; ADOLESCENTS; MECHANISMS;
   MUCOSA
AB Autoimmune gastritis (AIG) is an uncommon and often underestimated condition in children, characterized by chronic stomach inflammation leading to the destruction of oxyntic glands with subsequent atrophic and metaplastic changes. This condition is associated with hypo-/achlorhydria, impairing iron and vitamin B12 absorption. The pathogenesis involves the activation of helper type 1 CD4+/CD25-T-cells against parietal cells. Clinical manifestations in children are not specific and include abdominal pain, bloating, nausea, vomiting, and iron deficiency anemia (IDA). The disease is also linked to an increased risk of pernicious anemia, intestinal-type gastric cancer, and type I neuroendocrine tumors. AIG is often diagnosed through the presence of autoantibodies in the serum, such as parietal cell (APCA) and intrinsic factor (IF) antibodies. However, therapeutic recommendations for pediatric AIG are currently lacking. We aim to present two clinical cases of pediatric-onset AIG, highlighting the heterogeneous clinical manifestations and the challenges in diagnosis with the support of an updated literature review. A 9-year-old girl presented with refractory IDA, initial hypogammaglobulinemia, and a 12-year-old boy was initially diagnosed with eosinophilic esophagitis. Both cases underline the importance of considering AIG in children with chronic gastrointestinal symptoms and gastric atrophy. Diagnostic workup, including endoscopy and serological tests, is crucial for accurate identification. A better understanding of this condition is imperative for timely intervention and regular monitoring, given the potential long-term complications, including the risk of malignancy. These cases contribute to expanding the clinical spectrum of pediatric AIG and highlight the necessity for comprehensive evaluation and management in affected children.
C1 [Taietti, Ivan; Votto, Martina; Castagnoli, Riccardo; Bertozzi, Mirko; De Filippo, Maria; Marseglia, Gian Luigi; Licari, Amelia] Univ Pavia, Dept Clin Surg Diagnost & Pediat Sci, I-27100 Pavia, Italy.
   [Taietti, Ivan; Votto, Martina; Castagnoli, Riccardo; De Filippo, Maria; Marseglia, Gian Luigi; Licari, Amelia] Fdn IRCCS Policlin San Matteo, Pediat Clin, I-27100 Pavia, Italy.
   [Bertozzi, Mirko; Raffaele, Alessandro] Fdn IRCCS Policlin San Matteo, Pediat Surg Unit, I-27100 Pavia, Italy.
   [Di Sabatino, Antonio; Lenti, Marco Vincenzo] Univ Pavia, Dept Internal Med & Med Therapeut, I-27100 Pavia, Italy.
   [Di Sabatino, Antonio; Lenti, Marco Vincenzo] Fdn IRCCS Policlin San Matteo, Dept Internal Med 1, I-27100 Pavia, Italy.
   [Luinetti, Ombretta; Vanoli, Alessandro] Fdn IRCCS Policlin San Matteo, Unit Anat Pathol, I-27100 Pavia, Italy.
   [Vanoli, Alessandro] Univ Pavia, Dept Mol Med, Unit Anat Pathol, I-27100 Pavia, Italy.
C3 University of Pavia; IRCCS Fondazione San Matteo; IRCCS Fondazione San
   Matteo; University of Pavia; IRCCS Fondazione San Matteo; IRCCS
   Fondazione San Matteo; University of Pavia
RP Votto, M (corresponding author), Univ Pavia, Dept Clin Surg Diagnost & Pediat Sci, I-27100 Pavia, Italy.; Votto, M (corresponding author), Fdn IRCCS Policlin San Matteo, Pediat Clin, I-27100 Pavia, Italy.
EM ivan.taietti@gmail.com; martina.votto@unipv.it;
   riccardo.castagnoli@unipv.it; mirko.bertozzi@unipv.it;
   maria.defilippo01@universitadipavia.it; antonio.disabatino@unipv.it;
   o.luinetti@smatteo.pv.it; a.raffaele@smatteo.pv.it;
   alessandro.vanoli@unipv.it; marco.lenti@unipv.it;
   gianluigi.marseglia@unipv.it; amelia.licari@unipv.it
RI Castagnoli, Riccardo/AAF-8555-2019
OI Castagnoli, Riccardo/0000-0003-0029-9383
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NR 37
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2079-9721
J9 DISEASES-BASEL
JI Diseases
PD APR 25
PY 2025
VL 13
IS 5
AR 133
DI 10.3390/diseases13050133
PG 15
WC Medicine, Research & Experimental
WE Emerging Sources Citation Index (ESCI)
SC Research & Experimental Medicine
GA 3BE7F
UT WOS:001496172700001
PM 40422565
OA gold
DA 2025-06-01
ER

PT J
AU Reddy, RA
   Varshini, MS
   Kumar, RS
AF Reddy, Ramakkamma Aishwarya
   Varshini, Magham Sai
   Kumar, Raman Suresh
TI Matrix Metalloproteinase-2 (MMP-2): As an Essential Factor in Cancer
   Progression
SO RECENT PATENTS ON ANTI-CANCER DRUG DISCOVERY
LA English
DT Review
DE Cancer; matrix metalloproteinase; extracellular matrix; metastasis;
   cancer progression; endopeptidases
ID SQUAMOUS-CELL CARCINOMA; LYMPH-NODE METASTASIS; UP-REGULATING MMP-2;
   NF-KAPPA-B; BREAST-CANCER; IN-VITRO; LUNG-CANCER; BLADDER-CANCER; MOUSE
   MODELS; GASTRIC-CANCER
AB The development of cancer has been a multistep process involving mutation, proliferation, survival, invasion, and metastasis. Of all the characteristics of cancer, metastasis is believed to be the hallmark as it is responsible for the highest number of cancer-related deaths. In connection with this, Matrix metalloproteinases (MMPs), that has a role in metastasis, are one of the novel therapeutic targets. MMPs belong to the family of zinc-dependent endopeptidases and are capable of degrading the components of the extracellular matrix (ECM). The role of MMPs in ECM remodeling includes tissue morphogenesis, uterine cycling, growth, tissue repair, and angiogenesis. During pathological conditions, MMPs play a critical role in the excessive degradation of ECM which includes arthritis, tumour invasion, tumour metastasis, and several other autoimmune disorders. Moreover, they are believed to be involved in many physiological aspects of the cell, such as proliferation, migration, differentiation, angiogenesis, and apoptosis. It is reported that dysregulation of MMP in a variety of cancer subtypes have a dual role in tumour growth and metastasis processes. Further, multiple studies suggest the therapeutic potential of targeting MMP in invading cancer. The expression of MMP-2 correlates with the clinical characteristics of cancer patients, and its expression profile is a new diagnostic and prognostic biomarker for a variety of human diseases. Hence, manipulating the expression or function of MMP-2 may be a potential treatment strategy for different diseases, including cancers. Hence, the present review discusses the therapeutic potential of targeting MMP in various types of cancers and their recent patents.
C1 [Reddy, Ramakkamma Aishwarya; Kumar, Raman Suresh] JSS Coll Pharm, Dept Pharmaceut, Ooty, India.
   [Varshini, Magham Sai] JSS Coll Pharm, Dept Pharmacol, Ooty, India.
C3 JSS Academy of Higher Education & Research; JSS College of Pharmacy,
   Ooty; JSS Academy of Higher Education & Research; JSS College of
   Pharmacy, Ooty
RP Kumar, RS (corresponding author), JSS Coll Pharm, Dept Pharmaceut, Ooty, India.
EM sureshcoonoor@jssuni.edu.in
RI Magham, Sai Varshini/JQJ-1520-2023; Sureshkumar/AAG-1269-2021
OI Magham, Dr Sai Varshini/0009-0001-0046-7079
FU JSS College of Pharmacy, JSS Academy of Higher Education and Research,
   Ooty, Nilgiris, Tamilnadu, India; DST FIST
FX Author R. Aishwarya Reddy expresses her gratitude to JSS College of
   Pharmacy, JSS Academy of Higher Education and Research, Ooty, Nilgiris,
   Tamilnadu, India. And also we acknowledge gratitude to DST PURSE and DST
   FIST.
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NR 167
TC 6
Z9 6
U1 8
U2 12
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8928
EI 2212-3970
J9 RECENT PAT ANTI-CANC
JI Recent Patents Anti-Canc. Drug Discov.
PY 2025
VL 20
IS 1
BP 26
EP 44
DI 10.2174/0115748928251754230922095544
PG 19
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA Q6S9O
UT WOS:001385962700005
PM 37861020
DA 2025-06-01
ER

PT J
AU Chiba, T
   Seno, H
   Marusava, H
   Wakatsuki, Y
   Okazaki, K
AF Chiba, T
   Seno, H
   Marusava, H
   Wakatsuki, Y
   Okazaki, K
TI Host factors are important in determining clinical outcomes of
   Helicobacter pylori infection
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE H. pylori; gastritis; peptic ulcer; gastric cancer; MALT lymphoma
ID DUODENAL-ULCER DISEASE; SECONDARY LYMPHOID FOLLICLES; GASTRIC-ACID
   SECRETION; BALB/C MICE; AUTOIMMUNE GASTRITIS; PERNICIOUS-ANEMIA; NODULAR
   GASTRITIS; INCREASED RISK; TYROSINE PHOSPHATASE; FOLLICULAR GASTRITIS
C1 Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kyoto 6068507, Japan.
   Kyoto Univ, Grad Sch Med, Dept Geriatr Med, Kyoto, Japan.
   Kansai Med Univ, Dept Gastroenterol, Osaka, Japan.
C3 Kyoto University; Kyoto University; Kansai Medical University
RP Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Sakyo Ku, Kawaharacho 54, Kyoto 6068507, Japan.
OI Marusawa, Hiroyuki/0000-0002-4286-2712; Seno,
   Hiroshi/0000-0002-8509-8128
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NR 70
TC 38
Z9 40
U1 0
U2 4
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JAN
PY 2006
VL 41
IS 1
BP 1
EP 9
DI 10.1007/s00535-005-1743-4
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 016GE
UT WOS:000235607900001
PM 16501851
DA 2025-06-01
ER

PT J
AU Chaves, C
   da Silva, TN
   Pereira, BD
   Anselmo, J
   Claro, I
   Cavaco, BM
   Saramago, A
   Leite, V
AF Chaves, Carolina
   da Silva, Tiago Nunes
   Pereira, Bernardo Dias
   Anselmo, Joao
   Claro, Isabel
   Cavaco, Branca M.
   Saramago, Ana
   Leite, Valeriano
TI A case report of multiple endocrine neoplasia type 1 and autoimmune
   disease Coincidence or correlation?
SO MEDICINE
LA English
DT Article
DE autoimmunity; genetics; multiple endocrine neoplasia; mutations
ID MEN1; LYMPHOMA
AB Rationale: Multiple Endocrine Neoplasia type 1 (MEN1) is a familial syndrome that results from the disruption of a tumor suppressor protein called MENIN. Its management is challenging, as MEN1 affects different endocrine tissues and predisposes to both benign and malignant tumors. MENIN-deficient cells have recently been recognized to play a role in triggering autoimmunity. Herein, we present a case of MEN1 with multiple endocrine and autoimmune disorders. Patient concerns: A 50 years old female with a 25 years history of complicated nephrolithiasis presented with primary hyperparathyroidism. Diagnoses: Over several decades, she was diagnosed with recurrent primary hyperparathyroidism, autoimmune thyroiditis, multinodular goiter, pernicious anemia, metastatic gastric type 1 neuroendocrine tumor, macroprolactinemia, gonadotropin deficiency, mucosa-associated lymphoid tissue lymphoma of the thyroid gland, positive anti-calcium sensor receptor antibodies, and BRCA 1/2-negative invasive breast cancer. The autoimmune regulator gene was sequenced, but no pathogenic variants were found. Next-generation sequencing revealed both a pathogenic MEN1 mutation and a benign CDC73 gene variant. Familial genetic screening revealed a large kindred with multiple carriers of one or both genetic variants (MEN1 = 19; CDC73 = 7). Interventions: The patient underwent surgical excision of three parathyroid glands, total thyroidectomy and breast tumorectomy plus tamoxifen, and monthly injections of octreotide. The patient and family members with the MEN1 mutation are under a life-long surveillance program for MEN1 prototypic tumors. Outcomes: The patient was stable and alive during a 24-years follow-up period. Lessons: With the present case, the authors highlight a new interplay between MENIN and the immune system, which may have implications for future targeted life-long surveillance and treatment of MEN1 patients.
C1 [Chaves, Carolina; Pereira, Bernardo Dias; Anselmo, Joao] Hosp Divino Espirito Santo Ponta Delgada, Serv Endocrinol & Nutr, Ponta Delgada, Azores Isl, Portugal.
   [da Silva, Tiago Nunes; Leite, Valeriano] Inst Portugues Oncol Francisco Gentil, Serv Endocrinol, Lisbon, Portugal.
   [da Silva, Tiago Nunes; Cavaco, Branca M.; Saramago, Ana; Leite, Valeriano] Inst Portugues Oncol Lisboa Francisco Gentil Lisb, Unidade Invast Patobiol Mol UIPM, Lisbon, Portugal.
   [Claro, Isabel] Inst Portugues Oncol Francisco Gentil, Serv Gastroenterol, Lisbon, Portugal.
   [Leite, Valeriano] Nova Med Sch, Lisbon, Portugal.
C3 Portuguese Institute of Oncology; Portuguese Institute of Oncology
RP Chaves, C (corresponding author), Hosp Divino Espirito Santo Ponta Delgada, Serv Endocrinol & Nutr, Ponta Delgada, Azores Isl, Portugal.
EM carolina.m.chs@gmail.com
RI Cavaco, Branca/A-4848-2013; Chaves, Carolina/AAA-2253-2022
OI Leite, Valeriano/0000-0001-5479-7332
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NR 19
TC 4
Z9 5
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD DEC 10
PY 2021
VL 100
IS 49
AR e28145
DI 10.1097/MD.0000000000028145
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA XM4WJ
UT WOS:000728829100048
PM 34889280
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Kishimoto, M
   Komine, M
   Sashikawa-Kimura, M
   Ansary, TM
   Kamiya, K
   Sugai, J
   Mieno, M
   Kawata, H
   Sekimoto, R
   Fukushima, N
   Ohtsuki, M
AF Kishimoto, Megumi
   Komine, Mayumi
   Sashikawa-Kimura, Miho
   Ansary, Tuba Musarrat
   Kamiya, Koji
   Sugai, Junichi
   Mieno, Makiko
   Kawata, Hirotoshi
   Sekimoto, Ryutaro
   Fukushima, Noriyoshi
   Ohtsuki, Mamitaro
TI STAT3 Activation in Psoriasis and Cancers
SO DIAGNOSTICS
LA English
DT Article
DE psoriasis; STAT3; cancer; immunohistochemistry
ID EXPRESSION; KERATINOCYTES; SKIN; TARGET; MOUSE; PHOSPHORYLATION;
   TRANSCRIPTION; AUTOIMMUNE; HEAD
AB Activation of signal transducer and activator of transcription (STAT)3 has been reported in many cancers. It is also well known that STAT3 is activated in skin lesions of psoriasis, a chronic skin disease. In this study, to ascertain whether patients with psoriasis have a predisposition to STAT3 activation, we examined phosphorylated STAT3 in cancer cells of psoriasis patients via immunohistochemistry. We selected patients with psoriasis who visited the Department of Dermatology, Jichi Medical University Hospital, from January 2000 to May 2015, and had a history of cancer. We performed immunostaining for phosphorylated STAT3 in tumor cells of five, four, and six cases of gastric, lung, and head and neck cancer, respectively. The results showed that there was no significant difference in STAT3 activation in any of the three cancer types between the psoriasis and control groups. Although this study presents limitations in its sample size and inconsistency in the histology and differentiation of the cancers, results suggest that psoriasis patients do not have a predisposition to STAT3 activation. Instead, STAT3 activation is intricately regulated by each disorder or cellular microenvironment in both cancer and psoriasis.</p>
C1 [Kishimoto, Megumi; Komine, Mayumi; Sashikawa-Kimura, Miho; Ansary, Tuba Musarrat; Kamiya, Koji; Sugai, Junichi; Ohtsuki, Mamitaro] Jichi Med Univ, Dept Dermatol, Shimotsuke, Tochigi 3290498, Japan.
   [Mieno, Makiko] Jichi Med Univ, Ctr Informat, Dept Med Informat, Shimotsuke, Tochigi 3290498, Japan.
   [Kawata, Hirotoshi; Fukushima, Noriyoshi] Jichi Med Univ, Dept Diagnost Pathol, Shimotsuke, Tochigi 3290498, Japan.
   [Sekimoto, Ryutaro] Komagome Hosp, Tokyo Metropolitan Canc & Infect Dis Ctr, Dept Pathol, Bunkyo Ku, Tokyo 1138677, Japan.
C3 Jichi Medical University; Jichi Medical University; Jichi Medical
   University; Tokyo Metropolitan Cancer & Infectious Diseases Center
   Komagome Hospital
RP Komine, M (corresponding author), Jichi Med Univ, Dept Dermatol, Shimotsuke, Tochigi 3290498, Japan.
EM megumihkishimoto@gmail.com; mkomine12@jichi.ac.jp;
   sashikawa@jichi.ac.jp; tuba2020@jichi.ac.jp; m01023kk@jichi.ac.jp;
   junsugar1112@gmail.com; mnaka@jichi.ac.jp; kawata@jichi.ac.jp;
   rsekimoto@gmail.com; nfukushima@jichi.ac.jp; mamitaro@jichi.ac.jp
RI Sekimoto, Ryutaro/AAN-1099-2021
OI Komine, Mayumi/0000-0002-1086-1803; Kishimoto,
   Megumi/0000-0002-5136-1282; Sekimoto, Ryutaro/0009-0000-2711-2553
FU Ministry of Education, Culture, Sports, Science and Technology (MEXT)
   [20K08661]; Grants-in-Aid for Scientific Research [20K08661] Funding
   Source: KAKEN
FX This study is supported by The Ministry of Education, Culture, Sports,
   Science and Technology (MEXT) Grant-in-Aid for Scientific Research (C)
   20K08661.
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NR 42
TC 20
Z9 20
U1 1
U2 13
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD OCT
PY 2021
VL 11
IS 10
AR 1903
DI 10.3390/diagnostics11101903
PG 9
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA WR6GX
UT WOS:000714597100001
PM 34679602
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Monti, M
   Marconi, G
   Ambrosini-Spaltro, A
   Gallio, C
   Ghini, V
   Esposito, L
   Antonini, S
   Montanari, D
   Frassineti, GL
AF Monti, Manlio
   Marconi, Giovanni
   Ambrosini-Spaltro, Andrea
   Gallio, Chiara
   Ghini, Virginia
   Esposito, Luca
   Antonini, Stefano
   Montanari, Daniela
   Frassineti, Giovanni Luca
TI Hemophagocytic lymphohistiocytosis in gastric cancer: A rare syndrome
   for the oncologist. Case report and brief review
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE hemophagocytic lymphohistiocytosis; gastric cancer; secondary
   hemophagocytic lymphohistiocytosis; disseminated intravascular
   coagulation; case report
ID MACROPHAGE ACTIVATION SYNDROME; ADULTS; DIAGNOSIS; FEATURES
AB Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening condition characterized by uncontrolled activation of the immune system. HLH is a reactive mononuclear phagocytic response that occurs in association with a constellation of conditions such as malignancies and infections. The clinical diagnosis of HLH remains challenging because HLH can present with symptoms that significantly overlap with other causes of cytopenia, such as sepsis, autoimmune diseases, hematological cancers, and multiorgan failure. A 50-year-old man went to the emergency room (ER) for hyperchromic urine, melena, gingivorrhagia, and spontaneous abdominal wall hematomas. The first blood tests showed severe thrombocytopenia, alteration of the INR, and consumption of fibrinogen, and therefore, a diagnosis of disseminated intravascular coagulation (DIC) was made. A bone marrow aspirate showed numerous images of hemophagocytosis. With the suspicion of immune-mediated cytopenia, oral etoposide, intravenous immunoglobulin, and intravenous methylprednisolone were administered. Then, a diagnosis of gastric carcinoma was performed with a lymph node biopsy and gastroscopy. On the 30th day, the patient was transferred to the oncology ward of another hospital. On admission, he had serious piastrinopenia, anemia, hypertriglyceridemia, and hyperferritinemia. He was supported with a platelet transfusion and underwent a bone biopsy that showed a picture compatible with myelophthisis from diffuse medullary localization of a carcinoma of gastric origin. A diagnosis of HLH secondary to solid neoplasm was formulated. The patient started chemotherapy with oxaliplatin, calcium levofolinate, 5-fluorouracil bolus, 5-fluorouracil for 48 h (mFOLFOX6), and methylprednisolone. Six days after the third cycle of mFOLFOX6, the patient was discharged with the stabilization of his piastrinopenia condition. The patient continued chemotherapy with an improvement in his clinical conditions and normalization of hematological values. After 12 cycles of mFOLFOX, it was decided to start maintenance chemotherapy with capecitabine but, unfortunately, after only one cycle, HLH reappeared. The oncologist has to keep in mind the existence of HLH when there is an unusual clinical presentation of cancer, such as cytopenia affecting >= 2 lineages and alterations of ferritin and triglycerides other than fibrinogen and coagulation. Increased attention and additional research as well as a close collaboration with hematologists are needed to benefit patients with solid tumors complicated by HLH.
C1 [Monti, Manlio; Gallio, Chiara; Ghini, Virginia; Esposito, Luca; Antonini, Stefano; Montanari, Daniela; Frassineti, Giovanni Luca] IRCCS, Dept Med Oncol, Ist Romagnolo Studio Tumori IRST Dino Amadori, Meldola, Italy.
   [Marconi, Giovanni] IRCCS, Haematol Unit, Ist Romagnolo Studio Tumori IRST Dino Amadori, Meldola, Italy.
   [Ambrosini-Spaltro, Andrea] AUSL Romagna, Morgagni Pierantoni Hosp, Pathol Unit, Forli, Italy.
C3 AUSL della Romagna
RP Monti, M (corresponding author), IRCCS, Dept Med Oncol, Ist Romagnolo Studio Tumori IRST Dino Amadori, Meldola, Italy.
EM manlio.monti@irst.emr.it
RI ; Ambrosini-Spaltro, Andrea/ABD-7068-2020; Marconi,
   Giovanni/AAX-7449-2020
OI Gallio, Chiara/0009-0003-7380-1255; Ambrosini-Spaltro,
   Andrea/0000-0001-7800-4229; Marconi, Giovanni/0000-0001-6309-0515
FU Italian Ministry of Health
FX This work was partially funded by the Italian Ministry of Health.
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NR 29
TC 1
Z9 1
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD FEB 8
PY 2023
VL 13
AR 1010561
DI 10.3389/fonc.2023.1010561
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 9D2IV
UT WOS:000935927100001
PM 36845741
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Audia, S
   Brescia, C
   Dattilo, V
   Torchia, N
   Trapasso, F
   Amato, R
AF Audia, Salvatore
   Brescia, Carolina
   Dattilo, Vincenzo
   Torchia, Naomi
   Trapasso, Francesco
   Amato, Rosario
TI The IL-23R and Its Genetic Variants: A Hitherto Unforeseen Bridge
   Between the Immune System and Cancer Development
SO CANCERS
LA English
DT Review
DE IL-23R; immune cells; genetic variants; Th17; tumor microenvironment
ID INTERLEUKIN 23 RECEPTOR; INNATE LYMPHOID-CELLS; T-CELLS; IL-17
   PRODUCTION; ULCERATIVE-COLITIS; IL-23/IL-17 AXIS; CYTOKINE IL-23;
   BLADDER-CANCER; GASTRIC-CANCER; ADULT PATIENTS
AB IL-23R (interleukin-23 receptor), found on the surface of several immune cells, plays a key role in the immune system. Indeed, this process is not limited to the inflammatory response but also plays a role in the adaptive immune response. The binding between IL-23R and its specific ligand, the interleukin 23, initiates a number of specific signals by modulating both properties and behavior of immune cells. In particular, it is critical for the regulation of T helper 17 cells (Th17). Th17s are a subset of T cells involved in autoimmune and inflammatory diseases, as well as in cancer. The clinical relevance of IL-23R is underscored by its association with an elevated susceptibility or diminished vulnerability to a spectrum of diseases, including psoriasis, ankylosing spondylitis, and inflammatory bowel disease (IBD). Evidence has emerged that suggests it may also serve to predict both tumor progression and therapeutic responsiveness. It is noteworthy that the IL-23/IL-23R pathway is emerging as a promising therapeutic target. A number of biologic drugs, such as monoclonal antibodies, are currently developing with the aim of blocking this interaction, thus reducing inflammation. This represents a significant advancement in the field of medicine, offering new hope for pursuing more effective and personalized treatments. Recent studies have also investigated the role of such a pathway in autoimmune diseases, and its potential impact on infections as well as in carcinogenesis. The aim of this review is to focus on the role of IL-23R in immune genetics and its potential for modulating the natural history of neoplastic disease.
C1 [Audia, Salvatore; Brescia, Carolina; Torchia, Naomi; Amato, Rosario] Magna Graecia Univ Catanzaro, Med Sch, Dept Hlth Sci, Immunogenet Lab, I-88100 Catanzaro, Italy.
   [Dattilo, Vincenzo; Trapasso, Francesco] Magna Graecia Univ Catanzaro, Med Sch, Dept Expt & Clin Med, I-88100 Catanzaro, Italy.
C3 Magna Graecia University of Catanzaro; Magna Graecia University of
   Catanzaro
RP Amato, R (corresponding author), Magna Graecia Univ Catanzaro, Med Sch, Dept Hlth Sci, Immunogenet Lab, I-88100 Catanzaro, Italy.; Trapasso, F (corresponding author), Magna Graecia Univ Catanzaro, Med Sch, Dept Expt & Clin Med, I-88100 Catanzaro, Italy.
EM salvatore.audia001@studenti.unicz.it; brescia@unicz.it;
   dattilo@unicz.it; naomi.torchia@studenti.unicz.it; trapasso@unicz.it;
   rosario.amato@unicz.it
RI Dattilo, Vincenzo/AAB-3167-2020
OI Dattilo, Vincenzo/0000-0001-8493-6188; Audia,
   Salvatore/0009-0000-8145-8686; Amato, Rosario/0000-0001-7162-1099
FU Stillitani Family
FX This work was supported by a generous donation from the Stillitani
   Family, in memory of Carmelo.
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NR 159
TC 2
Z9 2
U1 2
U2 2
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2025
VL 17
IS 1
AR 55
DI 10.3390/cancers17010055
PG 29
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA R7S6E
UT WOS:001393403600001
PM 39796684
OA gold
DA 2025-06-01
ER

PT J
AU Tsuboi, M
   Niikura, R
   Hayakawa, Y
   Hirata, Y
   Ushiku, T
   Koike, K
AF Tsuboi, Mayo
   Niikura, Ryota
   Hayakawa, Yoku
   Hirata, Yoshihiro
   Ushiku, Tetsuo
   Koike, Kazuhiko
TI Distinct Features of Autoimmune Gastritis in Patients with Open-Type
   Chronic Gastritis in Japan
SO BIOMEDICINES
LA English
DT Article
DE gastritis; atrophy; microbiota; helicobacter infections; autoimmune
   diseases
ID INTESTINAL METAPLASIA; CANCER
AB In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according to anti-parietal cell antibody positivity. Laboratory, histological findings, and gastric cancer incidence were compared between AIG and non-AIG patients. The AIG group had more females and a higher rate of thyroid disease. Serum levels of gastrin were significantly higher in AIG patients (mean 1412 and 353 pg/mL, p < 0.001). The endoscopic findings included a significantly higher percentage of corpus-dominant atrophy in AIG (31.67%) than in non-AIG (7.04%) patients (p < 0.001). Clusters of ECL cells were observed in 28% of AIG patients and 7% of non-AIG patients (p = 0.032). The cumulative incidence of gastric cancer at 5 and 10 years was 0% and 0.03% in the AIG group and 0.03% and 0.05% in the non-AIG group, and no significant difference in gastric cancer incidence was observed. Despite significant differences in gastrin levels between AIG and non-AIG patients, there was no evidence of an impact of AIG on the incidence of gastric cancer.
C1 [Tsuboi, Mayo; Niikura, Ryota; Hayakawa, Yoku; Koike, Kazuhiko] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138655, Japan.
   [Hirata, Yoshihiro] Univ Tokyo, Inst Med Sci, Div Adv Genome Med, Tokyo 108863, Japan.
   [Ushiku, Tetsuo] Univ Tokyo, Grad Sch Med, Dept Pathol, Tokyo 1138655, Japan.
C3 University of Tokyo; University of Tokyo; University of Tokyo
RP Niikura, R (corresponding author), Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138655, Japan.
EM tsuboim-int@h.u-tokyo.ac.jp; niikura-dky@umin.ac.jp;
   yhayakawa-tky@umin.ac.jp; hiratay-int@h.u-tokyo.ac.jp;
   ushikut-tky@umin.ac.jp; kkoike-tky@umin.ac.jp
RI Hayakawa, Yoku/AAI-8581-2020
OI Niikura, Ryota/0000-0001-5047-6195; Hayakawa, Yoku/0000-0002-3988-2499
FU KAKENHI [20K08375, 20H03656, 20K08377]; Grants-in-Aid for Scientific
   Research [20K08375, 20K08377, 20H03656] Funding Source: KAKEN
FX This study was supported by KAKENHI Grants-in-Aid for Scientific
   Research (grant numbers 20K08375 (R.N.), 20H03656 (Y.H. (Yoku
   Hayakawa)), and 20K08377 Y.H. (Yoshihiro Hirata)).
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NR 13
TC 11
Z9 12
U1 0
U2 4
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD OCT
PY 2020
VL 8
IS 10
AR 419
DI 10.3390/biomedicines8100419
PG 11
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA OJ8HZ
UT WOS:000584196400001
PM 33066474
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Inoue, K
   Okubo, T
   Kato, T
   Shimamura, K
   Sugita, T
   Kubota, M
   Kanaya, K
   Yamachika, D
   Sato, M
   Inoue, D
   Harada, K
   Kawano, M
AF Inoue, Koichi
   Okubo, Takehiko
   Kato, Takashi
   Shimamura, Kazuo
   Sugita, Teruji
   Kubota, Mitsuhiro
   Kanaya, Kohji
   Yamachika, Daisuke
   Sato, Makoto
   Inoue, Dai
   Harada, Kenichi
   Kawano, Mitsuhiro
TI IgG4-related stomach muscle lesion with a renal pseudotumor and multiple
   renal rim-like lesions: A rare manifestation of IgG4-related disease
SO MODERN RHEUMATOLOGY
LA English
DT Article
DE Gastric cancer; IgG4-related disease; IgG4-related kidney disease;
   muscularis propria
ID AUTOIMMUNE PANCREATITIS; INFLAMMATORY PSEUDOTUMOR; SCLEROSING
   CHOLANGITIS; MALIGNANCIES; INVOLVEMENT; KIDNEY; RISK
AB We describe a 74-year-old man with immunoglobulin G4-related disease (IgG4-RD) presenting with gastric cancer, stomach and kidney lesions. For 15 years, the patient had been treated under a diagnosis of sclerosing cholangitis, which was revealed to be IgG4-RD only when the cancer was found. Histology revealed the gastric cancer and IgG4-related lesion in the muscularis propria to be separate. This case suggests that the stomach muscle can also be a site of involvement of IgG4-RD.
C1 [Inoue, Koichi; Sugita, Teruji; Kubota, Mitsuhiro; Kanaya, Kohji; Yamachika, Daisuke; Sato, Makoto] Yamachika Mem Hosp, Div Surg, Odawara, Kanagawa, Japan.
   [Okubo, Takehiko] Yamachika Mem Hosp, Div Internal Med, Odawara, Kanagawa, Japan.
   [Kato, Takashi] Yamachika Mem Hosp, Div Rheumatol, Odawara, Kanagawa, Japan.
   [Shimamura, Kazuo] Yamachika Mem Hosp, Div Pathol, Odawara, Kanagawa, Japan.
   [Inoue, Dai] Kanazawa Univ, Grad Sch Med, Dept Radiol, Kanazawa, Ishikawa, Japan.
   [Harada, Kenichi] Kanazawa Univ, Grad Sch Med, Dept Human Pathol, Kanazawa, Ishikawa, Japan.
   [Kawano, Mitsuhiro] Kanazawa Univ, Grad Sch Med, Dept Internal Med, Div Rheumatol, Kanazawa, Ishikawa, Japan.
C3 Kanazawa University; Kanazawa University; Kanazawa University
RP Kawano, M (corresponding author), Kanazawa Univ Hosp, Dept Internal Med, Div Rheumatol, Takara Machi 13-1, Kanazawa, Ishikawa 9208641, Japan.
EM sk33166@gmail.com
FU Health and Labour Sciences Research Grants for the Study of Intractable
   Diseases from the Ministry of Health, Labor and Welfare, Japan
FX This work was supported by Health and Labour Sciences Research Grants
   for the Study of Intractable Diseases from the Ministry of Health, Labor
   and Welfare, Japan.
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NR 20
TC 12
Z9 13
U1 0
U2 4
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1439-7595
EI 1439-7609
J9 MOD RHEUMATOL
JI Mod. Rheumatol.
PY 2018
VL 28
IS 1
BP 188
EP 192
DI 10.3109/14397595.2015.1081743
PG 5
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA GA2DB
UT WOS:000428125900028
PM 26381653
OA hybrid
DA 2025-06-01
ER

PT J
AU Zhang, XF
   Liu, JH
   Liang, X
   Chen, J
   Hong, JJ
   Li, LB
   He, Q
   Cai, XJ
AF Zhang, Xiaofeng
   Liu, Jinghua
   Liang, Xiao
   Chen, Jiang
   Hong, Junjie
   Li, Libo
   He, Qiang
   Cai, Xiujun
TI History and progression of Fat cadherins in health and disease
SO ONCOTARGETS AND THERAPY
LA English
DT Review
DE Fat cadherins; FAT1; FAT2; FAT3; FAT4; CpG island; Hippo pathway; WNT
   signaling
ID REVEALS RECURRENT MUTATIONS; HIPPO SIGNALING PATHWAY; EGF-LIKE MOTIFS;
   GASTRIC-CANCER; ACTIN DYNAMICS; BREAST CANCERS; CELL-ADHESION; GENES;
   IDENTIFICATION; EXPRESSION
AB Intercellular adhesions are vital hubs for signaling pathways during multicellular development and animal morphogenesis. In eukaryotes, under aberrant intracellular conditions, cadherins are abnormally regulated, which can result in cellular pathologies such as carcinoma, kidney disease, and autoimmune diseases. As a member of the Ca2+-dependent adhesion superfamily, Fat proteins were first described in the 1920s as an inheritable lethal mutant phenotype in Drosophila, consisting of four member proteins, FAT1, FAT2, FAT3, and FAT4, all of which are highly conserved in structure. Functionally, FAT1 was found to regulate cell migration and growth control through specific protein-protein interactions of its cytoplasmic tail. FAT2 and FAT3 are relatively less studied and are thought to participate in the development of human cancer through a pathway similar to that of the Ena/VASP proteins. In contrast, FAT4 has been widely studied in the context of biological functions and tumor mechanisms and has been shown to regulate the planar cell polarity pathway, the Hippo signaling pathway, the canonical Wnt signaling cascade, and the expression of YAP1. Overall, Fat cadherins may be useful as emerging disease biomarkers and as novel therapeutic targets.
C1 [Zhang, Xiaofeng; Liang, Xiao; Chen, Jiang; Hong, Junjie; Li, Libo; Cai, Xiujun] Zhejiang Univ, Dept Gen Surg, Hangzhou, Zhejiang, Peoples R China.
   [Zhang, Xiaofeng; Liang, Xiao; Chen, Jiang; Hong, Junjie; Cai, Xiujun] Zhejiang Univ, Sir Run Run Shaw Hosp, Key Lab Surg Zhejiang Prov, Hangzhou, Zhejiang, Peoples R China.
   [Liu, Jinghua; He, Qiang] Linyi Peoples Hosp, Dept Hepatobiliary Surg, 27 East Jiefang Rd, Linyi 276000, Shandong, Peoples R China.
C3 Zhejiang University; Zhejiang University
RP He, Q (corresponding author), Linyi Peoples Hosp, Dept Hepatobiliary Surg, 27 East Jiefang Rd, Linyi 276000, Shandong, Peoples R China.; Cai, XJ (corresponding author), Zhejiang Univ, Sir Run Run Shaw Hosp, Dept Gen Surg, Hangzhou 310016, Zhejiang, Peoples R China.
EM heq_lyrmyy@163.com; cxjzu@zju.edu.cn
RI li, libo/C-8296-2014; Chen, Jiang/AAO-6940-2021; Cai, Jun/GLS-4538-2022
OI Hong, Junjie/0000-0003-1179-1832
FU International Scientific and Technological Cooperation Projects
   [2012DFA30410]; Science-technology Projects of Zhejiang Province
   [LY15H160043]; National Science-technology Support Plan Projects
   [2012BAI14B06]
FX This study was supported by the International Scientific and
   Technological Cooperation Projects (2012DFA30410), the
   Science-technology Projects of Zhejiang Province (LY15H160043), and the
   National Science-technology Support Plan Projects (2012BAI14B06). We
   thank Wenbin Jiang, Jiacheng Tang, and Xu Feng for revising the figures
   and writing and advising, in the manuscript.
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NR 49
TC 38
Z9 44
U1 1
U2 11
PU DOVE MEDICAL PRESS LTD
PI ALBANY
PA PO BOX 300-008, ALBANY, AUCKLAND 0752, NEW ZEALAND
SN 1178-6930
J9 ONCOTARGETS THER
JI OncoTargets Ther.
PY 2016
VL 9
BP 7337
EP 7343
DI 10.2147/OTT.S111176
PG 7
WC Biotechnology & Applied Microbiology; Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Oncology
GA ED6PF
UT WOS:000388977000001
PM 27942226
OA gold, Green Submitted, Green Published
DA 2025-06-01
ER

PT J
AU Wei, Q
   Wang, ZY
   Liu, XY
   Liang, HB
   Chen, L
AF Wei, Qi
   Wang, Ziyu
   Liu, Xuanyu
   Liang, Haibin
   Chen, Lei
TI Association between Gastric Cancer and 12 Autoimmune Diseases: A
   Mendelian Randomization Study
SO GENES
LA English
DT Article
DE Mendelian randomization; gastric cancer; autoimmune disease;
   inflammatory bowel disease; causal relationship
ID CELIAC-DISEASE; RISK; METAANALYSIS; VARIANTS; HISTORY; COHORT; ASTHMA
AB Background: Whether the positive associations of gastric cancer (GC) with autoimmune diseases are causal has always been controversial. This study aims to estimate the causal relationship between GC and 12 autoimmune diseases by means of Mendelian randomization (MR) analysis. Methods: After rigorous evaluation, potential candidate single nucleotide polymorphisms (SNPs) for GC and 12 autoimmune diseases were extracted from genome-wide association study (GWAS) datasets. We performed the MR analyses using the inverse variance weighted (IVW) method as the primary approach to the analysis. Three sensitivity analysis methods were added to assess the robustness of the results. In addition, heterogeneity was measured using Cochran's Q-value, and horizontal pleiotropy was assessed using MR-Egger regression and leave-one-out analysis. Results: The IVW result, which is the main method of analysis, shows no evidence of a causal association between GC and any autoimmune disease. The results of IVW analysis show the relationship between rheumatoid arthritis (p = 0.1389), systemic lupus erythematosus (p = 0.1122), Crohn's disease (p = 0.1509), multiple sclerosis (p = 0.3944), primary sclerosing cholangitis (p = 0.9022), primary biliary cirrhosis (p = 0.7776), type 1 diabetes (p = 0.9595), ulcerative colitis (p = 0.5470), eczema (p = 0.3378), asthma (p = 0.7436), celiac disease (p = 0.4032), and psoriasis (p = 0.7622) and GC susceptibility. The same result was obtained with the weighted median and the MR-egger (p > 0.05). Conclusion: Our study did not find a genetic causal relationship between susceptibility to these autoimmune diseases and GC, which suggests that unmeasured confounders (e.g., inflammatory processes) or shared genetic architecture may be responsible for the reported epidemiologic associations. Further studies of ancestral diversity are warranted to validate such causal associations.
C1 [Wei, Qi; Liu, Xuanyu; Liang, Haibin; Chen, Lei] Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Gen Surg, Sch Med, Shanghai 200092, Peoples R China.
   [Wei, Qi] Fudan Univ, Huashan Hosp, Dept Gen Surg, Jingan Branch, Shanghai 200060, Peoples R China.
   [Wang, Ziyu] Shanghai Jiao Tong Univ, Shanghai Tong Ren Hosp, Sch Med, Dept Clin Lab, Shanghai 200050, Peoples R China.
C3 Shanghai Jiao Tong University; Fudan University; Shanghai Jiao Tong
   University
RP Chen, L (corresponding author), Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Gen Surg, Sch Med, Shanghai 200092, Peoples R China.
EM 18895363028@163.com; chenlei@xinhuamed.com.cn
RI Chen, Lei/AAG-6304-2020; liu, xuanyu/GLS-4123-2022
OI Wei, Qi/0000-0002-3730-9998
FU We would like to thank all of the GWASs for making their summary data
   available to the public, and all of the investigators and participants
   who contributed to these studies. In addition, we want to acknowledge
   the participants and investigators of the Fin
FX We would like to thank all of the GWASs for making their summary data
   available to the public, and all of the investigators and participants
   who contributed to these studies. In addition, we want to acknowledge
   the participants and investigators of the FinnGen study.
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NR 58
TC 4
Z9 4
U1 2
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2073-4425
J9 GENES-BASEL
JI Genes
PD OCT
PY 2023
VL 14
IS 10
AR 1844
DI 10.3390/genes14101844
PG 12
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA X4EW5
UT WOS:001098011000001
PM 37895193
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Dho, SH
   Lim, JC
   Kim, LK
AF Dho, So Hee
   Lim, Jae Cheong
   Kim, Lark Kyun
TI Beyond the Role of CD55 as a Complement Component
SO IMMUNE NETWORK
LA English
DT Review
DE CD55; Complement; Cancer; Malaria; Immunotherapy
ID DECAY-ACCELERATING FACTOR; MEMBRANE COFACTOR PROTEIN; SENSITIZES
   TUMOR-CELLS; REGULATORY PROTEINS; FACTOR DAF; PROGNOSTIC-SIGNIFICANCE;
   INHIBITORY PROTEINS; ANTITUMOR-ACTIVITY; GENE-EXPRESSION; GASTRIC-CANCER
AB The complement is a part of the immune system that plays several roles in removing pathogens. Despite the importance of the complement system, the exact role of each component has been overlooked because the complement system was thought to be a nonspecific humoral immune mechanism that worked against pathogens. Decay-accelerating factor (DAF or CD55) is a known inhibitor of the complement system and has recently attracted substantial attention due to its role in various diseases, such as cancer, protein-losing enteropathy, and malaria. Some protein-losing enteropathy cases are caused by CD55 deficiency, which leads to complement hyperactivation, malabsorption, and angiopathic thrombosis. In addition, CD55 has been reported to be an essential host receptor for infection by the malaria parasite. Moreover, CD55 is a ligand of the seven-span transmembrane receptor CD97. Since CD55 is present in various cells, the functional role of CD55 has been expanded by showing that CD55 is associated with a variety of diseases, including cancer, malaria, protein-losing enteropathy, paroxysmal nocturnal hemoglobinuria, and autoimmune diseases. This review summarizes the current understanding of CD55 and the role of CD55 in these diseases. It also provides insight into the development of novel drugs for the diagnosis and treatment of diseases associated with CD55.
C1 [Dho, So Hee; Lim, Jae Cheong] Korea Atom Energy Res Inst, Radioisotope Res Div, Dept Res Reactor Utilizat, Daejeon 34057, South Korea.
   [Kim, Lark Kyun] Yonsei Univ, Coll Med, Gangnam Severance Hosp, Severance Biomed Sci Inst, Seoul 06230, South Korea.
   [Kim, Lark Kyun] Yonsei Univ, Coll Med, Gangnam Severance Hosp, PLUS Project Med Sci BK21, Seoul 06230, South Korea.
C3 Korea Atomic Energy Research Institute (KAERI); Yonsei University;
   Yonsei University Health System; Yonsei University; Yonsei University
   Health System
RP Kim, LK (corresponding author), Yonsei Univ, Coll Med, Gangnam Severance Hosp, Severance Biomed Sci Inst, 20 Eonju Ro 63 Gil, Seoul 06229, South Korea.; Kim, LK (corresponding author), Yonsei Univ, Coll Med, Gangnam Severance Hosp, PLUS Project Med Sci BK21, 20 Eonju Ro 63 Gil, Seoul 06230, South Korea.
EM lkkim@yuhs.ac
RI Kim, Byung/L-6884-2019
OI Kim, Lark Kyun/0000-0001-5983-4470; Dho, So Hee/0000-0001-7343-713X
FU Korea Atomic Energy Research Institute major project Development of
   Radioisotope Production and Application Technology [525330-18]; National
   Research Foundation of Korea (NRF) - Ministry of Science, ICT and Future
   Planning [NRF-2017M2A2A6A01071321]; Basic Science Research Program
   through the National Research Foundation of Korea (NRF) - Ministry of
   Education [NRF-2016R1D1A1B01015292]
FX This work was supported by the Korea Atomic Energy Research Institute
   major project Development of Radioisotope Production and Application
   Technology (525330-18 to J.C.L.), by the National Research Foundation of
   Korea (NRF), which is funded by the Ministry of Science, ICT and Future
   Planning (NRF-2017M2A2A6A01071321 to J.C.L.), and by the Basic Science
   Research Program through the National Research Foundation of Korea
   (NRF), which is funded by the Ministry of Education
   (NRF-2016R1D1A1B01015292 to L.K.K.).
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NR 90
TC 71
Z9 80
U1 3
U2 27
PU KOREA ASSOC IMMUNOLOGISTS
PI SEOUL
PA KOREA SCIENCE & TECHNOLOGY CENTER, RM 701, 7 GIL 22, TEHERAN-RO, (635-4
   YEOKSAM-DONG) GANGMAN-GU, SEOUL, 06130, SOUTH KOREA
SN 1598-2629
EI 2092-6685
J9 IMMUNE NETW
PD FEB
PY 2018
VL 18
IS 1
AR e11
DI 10.4110/in.2018.18.e11
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GE2WI
UT WOS:000431075000006
PM 29503741
OA Green Submitted, Green Published
DA 2025-06-01
ER

PT J
AU Roseland, ME
   Francis, IR
   Shampain, KL
   Stein, EB
   Wasnik, AP
   Millet, JD
AF Roseland, Molly E.
   Francis, Isaac R.
   Shampain, Kimberly L.
   Stein, Erica B.
   Wasnik, Ashish P.
   Millet, John D.
TI Gastric neuroendocrine neoplasms: a primer for radiologists
SO ABDOMINAL RADIOLOGY
LA English
DT Article
DE Gastric neuroendocrine neoplasm; Gastric carcinoid; Autoimmune atrophic
   gastritis; Zollinger-Ellison syndrome; Computed tomography (CT);
   Magnetic resonance imaging (MRI); Somatostatin receptor imaging
ID ENETS CONSENSUS GUIDELINES; CARCINOID-TUMORS; IMAGING FEATURES;
   FOLLOW-UP; DIAGNOSIS; MANAGEMENT; STOMACH; EXPERIENCE; SURVIVAL; UPDATE
AB Gastric neuroendocrine neoplasms are uncommon tumors with variable differentiation and malignant potential. Three main subtypes are recognized: type 1, related to autoimmune atrophic gastritis; type 2, associated with Zollinger-Ellison and MEN1 syndrome; and type 3, sporadic. Although endoscopy alone is often sufficient for diagnosis and management of small, indolent, multifocal type 1 tumors, imaging is essential for evaluation of larger, high-grade, and type 2 and 3 neoplasms. Hypervascular intraluminal gastric masses are typically seen on CT/MRI, with associated perigastric lymphadenopathy and liver metastases in advanced cases. Somatostatin receptor nuclear imaging (such as Ga-68-DOTATATE PET/CT) may also be used for staging and assessing candidacy for peptide receptor radionuclide therapy. Radiotracer uptake is more likely in well-differentiated, lower-grade tumors, and less likely in poorly differentiated tumors, for which F-18-FDG-PET/CT may have additional value. Understanding disease pathophysiology and evolving histologic classifications is particularly useful for radiologists, as these influence tumor behavior, preferred imaging, therapy options, and patient prognosis.
   [GRAPHICS]
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C1 [Roseland, Molly E.; Francis, Isaac R.; Shampain, Kimberly L.; Stein, Erica B.; Wasnik, Ashish P.; Millet, John D.] Univ Michigan, Dept Radiol, Michigan Med, 1500 East Med Ctr Dr,B1D502, Ann Arbor, MI 48109 USA.
C3 University of Michigan System; University of Michigan
RP Roseland, ME (corresponding author), Univ Michigan, Dept Radiol, Michigan Med, 1500 East Med Ctr Dr,B1D502, Ann Arbor, MI 48109 USA.
EM mollyroselandmd@gmail.com
OI Francis, Isaac/0000-0003-1953-7740; Shampain,
   Kimberly/0000-0002-6094-1676; Stein, Erica/0000-0002-7339-8107; Wasnik,
   Ashish P./0000-0002-4823-8929; Roseland, Molly/0000-0002-5885-1487
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NR 69
TC 5
Z9 5
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2366-004X
EI 2366-0058
J9 ABDOM RADIOL
JI Abdom. Radiol.
PD DEC
PY 2022
VL 47
IS 12
SI SI
BP 3993
EP 4004
DI 10.1007/s00261-022-03509-1
EA APR 2022
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Radiology, Nuclear Medicine & Medical Imaging
GA 5W2HC
UT WOS:000780971700001
PM 35411433
DA 2025-06-01
ER

PT J
AU Suzuki, A
   Hayashi, K
   Hayashi, M
   Nakaya, Y
   Sato, M
AF Suzuki, Asuka
   Hayashi, Koji
   Hayashi, Maho
   Nakaya, Yuka
   Sato, Mamiko
TI A Case of Autoimmune Polyendocrine Syndrome Type 3B and Peripheral
   Neuropathy Due to Thiamine Deficiency
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE thyroid gland; vitamin b12; polyneuropathy; thiamine; autoimmune
   polyendocrine syndromes
AB Autoimmune polyendocrine syndrome (APS) type 3B is characterized by presence of autoimmune thyroid disease, chronic atrophic gastritis and pernicious anemia. In this report, we present a rare case of APS type 3B with neuropathy by thiamine deficiency. A 65-year-old man had a history with hypothyroidism, gastritis, gastrectomy for gastric cancer and subacute combined degeneration of the spinal cord. Patient developed polyneuropathy with not mecobalamin but thiamine deficiency. Serum anti-thyroglobin (TG), anti-thyroid peroxidase (TPO), and anti-gastric parietal cell antibodies were positive. He was treated with thiamine supplementation and improved muscle weakness, sensory impairment and gait disturbance. Classically, it is reported gastric cancer related to hypothyroidism. Additionally, thiamine deficiency can be caused by gastrectomy. Here, his thiamine deficiency was related to APS type 3B, leading to polyneuropathy.
C1 [Suzuki, Asuka; Hayashi, Koji; Nakaya, Yuka; Sato, Mamiko] Fukui Gen Hosp, Dept Rehabil Med, Fukui, Japan.
   [Hayashi, Maho] Fukui Gen Hosp, Dept Internal Med, Fukui, Japan.
RP Hayashi, K (corresponding author), Fukui Gen Hosp, Dept Rehabil Med, Fukui, Japan.
EM kjhayashi@f-gh.jp
RI Hayashi, K/C-4685-2015
OI Hayashi, Koji/0000-0003-3446-0913
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NR 11
TC 0
Z9 0
U1 0
U2 1
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JAN 11
PY 2024
VL 16
IS 1
AR e52123
DI 10.7759/cureus.52123
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA GQ0V1
UT WOS:001154025100025
PM 38344613
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Karavanaki, K
   Karayianni, C
   Vassiliou, I
   Tzanela, M
   Sdogou, T
   Kakleas, K
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   Vakaki, M
   Soldatou, A
   Kallinikou, D
   Kostaki, M
   Tsitsopoulos, S
   Papathanasiou, A
AF Karavanaki, Kyriaki
   Karayianni, Christina
   Vassiliou, Ioannis
   Tzanela, Marinella
   Sdogou, Triantafyllia
   Kakleas, Kostas
   Tsentidis, Charalambos
   Vakaki, Marina
   Soldatou, Alexandra
   Kallinikou, Dimitra
   Kostaki, Maria
   Tsitsopoulos, Stathis
   Papathanasiou, Asteroula
TI Multiple autoimmunity, type 1 diabetes (T1DM), autoimmune thyroiditis
   and thyroid cancer: is there an association? A case report and
   literature review
SO JOURNAL OF PEDIATRIC ENDOCRINOLOGY & METABOLISM
LA English
DT Article
DE childhood; multiple autoimmunity; thyroid cancer; T1DM
ID HASHIMOTOS-THYROIDITIS; CLINICAL-SIGNIFICANCE; GASTRIC AUTOIMMUNITY;
   ISLET-CELL; CHILDREN; ADOLESCENTS; AUTOANTIBODIES; PREVALENCE;
   ANTIBODIES; MELLITUS
AB Type 1 diabetes mellitus (T1DM) is characterized by selective autoimmune destruction of pancreatic b-cells, resulting in insulin deficiency. Associated autoimmune disorders, such as celiac disease, autoimmune thyroiditis, and gastritis, can coexist in patients with T1DM. These disorders are characterized by the presence of antibodies against tissue transglutaminase (anti-tTG-IgA), thyroglobulin, and thyroid peroxidase (anti-TG, anti-TPO), as well as antibodies against gastric parietal cells. Children with T1DM may also develop organ-specific multiple autoimmunity, with the coexistence of one or more autoimmune disorders. Furthermore, there is a lot of controversy regarding the role of thyroid autoimmunity in the pathogenesis of thyroid cancer. We present a child with T1DM and multiple autoimmunity including autoimmune Hashimoto's thyroiditis (HT), who developed thyroid cancer. The literature on the prevalence of associated autoimmunity in children with T1DM and the prevalence, pathogenesis, and timely diagnosis of thyroid cancer among patients with HT is also reviewed.
C1 [Karavanaki, Kyriaki] Second Univ, P&A Kyriakou Childrens Hosp, Dept Pediat, Athens, Greece.
   [Karavanaki, Kyriaki; Karayianni, Christina; Sdogou, Triantafyllia; Kakleas, Kostas; Tsentidis, Charalambos; Soldatou, Alexandra; Kallinikou, Dimitra] Univ Athens, P&A Kyriakou Childrens Hosp, Dept Pediat 2, Diabet Clin, Athens, Greece.
   [Vassiliou, Ioannis] Univ Athens, Aretaieion Hosp, Dept Surg 2, Athens, Greece.
   [Tzanela, Marinella] Evangelismos Med Ctr, Dept Endocrinol, Athens, Greece.
   [Vakaki, Marina] PA Kyriakou Childrens Hosp, Dept Radiol, Athens, Greece.
   [Kostaki, Maria] Univ Athens, P&A Kyriakou Childrens Hosp, Dept Pediat 2, Gastroenterol Clin, Athens, Greece.
   [Tsitsopoulos, Stathis] Biomed Mol Genet Lab, Athens, Greece.
   [Papathanasiou, Asteroula] PA Kyriakou Childrens Hosp, Endocrine Dept, Athens, Greece.
C3 National & Kapodistrian University of Athens; National & Kapodistrian
   University of Athens; Evangelismos Hospital; National & Kapodistrian
   University of Athens
RP Karavanaki, K (corresponding author), Second Univ, P&A Kyriakou Childrens Hosp, Dept Pediat, Athens, Greece.
EM kkarav@yahoo.gr
RI Vakaki, Marina/AFH-8509-2022; Kakleas, Konstantinos/F-4988-2010
OI Kakleas, Konstantinos/0000-0002-7993-8418; Vakaki,
   Marina/0000-0002-7242-0122
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NR 48
TC 11
Z9 12
U1 0
U2 17
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 0334-018X
EI 2191-0251
J9 J PEDIATR ENDOCR MET
JI J. Pediatr. Endocrinol. Metab.
PD SEP
PY 2014
VL 27
IS 9-10
BP 1011
EP 1016
DI 10.1515/jpem-2013-0370
PG 6
WC Endocrinology & Metabolism; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Pediatrics
GA AO6AG
UT WOS:000341429100035
PM 24854531
DA 2025-06-01
ER

PT J
AU Hu, XP
   Wang, XS
   Xue, XK
AF Hu, Xiaopeng
   Wang, Xisheng
   Xue, Xingkui
TI Therapeutic Perspectives of CD26 Inhibitors in Imune-Mediated Diseases
SO MOLECULES
LA English
DT Review
DE CD26; DPP4 inhibitor; immune-mediated diseases; diabetic cardiovascular
   disease; autoimmune diabetes; inflammatory bowel disease (IBD);
   graft-versus-host disease (GVHD); coronavirus-related immunological
   response; multiple sclerosis (MS); anti-tumor immune response
ID DIPEPTIDYL PEPTIDASE-4 INHIBITOR; VERSUS-HOST-DISEASE; BETA-CELL MASS;
   IV DP-IV; MOLECULAR-MECHANISMS; SITAGLIPTIN; LINAGLIPTIN; EXPRESSION;
   MODEL
AB The enzymatic activity of CD26/DPP4 (dipeptidyl peptidase 4/DPP4) is highlighted in multiple studies to play a vital role in glucose metabolism by cleaving and inactivating the incretins glucagon-like peptide-1 (GLP) and gastric inhibitory protein (GIP). A large number of studies demonstrate that CD26 also plays an integral role in the immune system, particularly in T cell activation. CD26 is extensively expressed in immune cells, such as T cells, B cells, NK cells, dendritic cells, and macrophages. The enzymatic activity of CD26 cleaves and regulates numerous chomokines and cytokines. CD26 inhibitors have been widely used for the treatment of diabetes mellitus, while it is still under investigation as a therapy for immune-mediated diseases. In addition, CD26's involvement in cancer immunology was also described. The review aims to summarize the therapeutic effects of CD26 inhibitors on immune-mediated diseases, as well as the mechanisms that underpin them.
C1 [Hu, Xiaopeng; Wang, Xisheng; Xue, Xingkui] Peoples Hosp Longhua, Med Res Ctr, Shenzhen 518109, Peoples R China.
C3 The People's Hospital of Longhua, Shenzhen
RP Wang, XS; Xue, XK (corresponding author), Peoples Hosp Longhua, Med Res Ctr, Shenzhen 518109, Peoples R China.
EM xiaopenghu661@outlook.com; xishengwangdoctor@outlook.com;
   xuexk@outlook.com
RI Hu, Xueyan/JMB-3961-2023
OI Hu, Xiaopeng/0000-0002-6533-8024
FU Shenzhen Fundamental Research Program [JCYJ20190808095607768];
   Innovation and Technology Bureau of Longhua, Shenzhen (Public platform
   of Technique service of molecular Immunology and Molecular Diagnostics)
FX This research was funded by Shenzhen Fundamental Research Program, grant
   number JCYJ20190808095607768 and Innovation and Technology Bureau of
   Longhua, Shenzhen (Public platform of Technique service of molecular
   Immunology and Molecular Diagnostics).
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NR 75
TC 15
Z9 15
U1 0
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD JUL
PY 2022
VL 27
IS 14
AR 4498
DI 10.3390/molecules27144498
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA 3H3PF
UT WOS:000831950100001
PM 35889373
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Tasci, YY
   Nalcacoglu, P
   Gumusyayla, S
   Vural, G
   Toklu, Y
   Yesilirmak, N
AF Tasci, Yelda Yildiz
   Nalcacoglu, Pinar
   Gumusyayla, Sadiye
   Vural, Gonul
   Toklu, Yasin
   Yesilirmak, Niluefer
TI Aquaporin-4 protein antibody-associated optic neuritis related to
   neuroendocrine tumor after receiving an inactive COVID-19 vaccine
SO INDIAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
DE Aquaporin-4 protein antibody; gastric neuroendocrine tumor; inactive
   COVID-19 vaccine; optic neuritis
AB Neuromyelitis optica (NMO), also known as Devic's disease, is a rare, autoimmune, and recurrent demyelinating disorder that primarily affects the spinal cord and optic nerve. We report a case with recurrent optic neuritis caused by the paraneoplastic NMO spectrum disorder in the setting of a gastric neuroendocrine tumor 2 weeks after receiving an inactive COVID-19 vaccine.
C1 [Tasci, Yelda Yildiz; Nalcacoglu, Pinar; Toklu, Yasin; Yesilirmak, Niluefer] Yildirim Beyazit Univ, Bilkent City Hosp, Dept Ophthalmol, Ankara, Turkiye.
   [Gumusyayla, Sadiye; Vural, Gonul] Bilkent City Hosp, Dept Neurol, Ankara, Turkiye.
C3 Ankara Yildirim Beyazit University
RP Tasci, YY (corresponding author), Ankara City Hosp, Univ Mah, Ankara, Turkiye.
EM yeldayldz83@gmail.com
RI Vural, Gönül/KPA-1782-2024; Yesilirmak, Nilufer/AAD-7299-2020
OI Gumusyayla, Sadiye/0000-0002-2279-2016; Vural, Gonul/0000-0002-1245-7273
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NR 10
TC 0
Z9 0
U1 0
U2 0
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, Maharashtra, INDIA
SN 0301-4738
EI 1998-3689
J9 INDIAN J OPHTHALMOL
JI Indian J. Ophthalmol.
PD MAY
PY 2022
VL 70
IS 5
BP 1828
EP 1831
DI 10.4103/ijo.IJO_2494_21
PG 4
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA 2C1CH
UT WOS:000810614200084
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Kumar, MA
   Baba, SK
   Sadida, HQ
   Marzooqi, SA
   Jerobin, J
   Altemani, FH
   Algehainy, N
   Alanazi, MA
   Abou-Samra, AB
   Kumar, R
   Akil, ASAS
   Macha, MA
   Mir, R
   Bhat, AA
AF Kumar, Mudasir A.
   Baba, Sadaf K.
   Sadida, Hana Q.
   Marzooqi, Sara Al.
   Jerobin, Jayakumar
   Altemani, Faisal H.
   Algehainy, Naseh
   Alanazi, Mohammad A.
   Abou-Samra, Abdul-Badi
   Kumar, Rakesh
   Al-Shabeeb Akil, Ammira S.
   Macha, Muzafar A.
   Mir, Rashid
   Bhat, Ajaz A.
TI Extracellular vesicles as tools and targets in therapy for diseases
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID MESENCHYMAL STEM-CELLS; PLATELET-DERIVED MICROPARTICLES; PRE-METASTATIC
   NICHE; HUMAN ATHEROSCLEROTIC PLAQUES; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
   IMPAIR ENDOTHELIAL FUNCTION; PROMOTE TUMOR PROGRESSION; FIELD-FLOW
   FRACTIONATION; BREAST-CANCER CELLS; MEMBRANE-VESICLES
AB Extracellular vesicles (EVs) are nano-sized, membranous structures secreted into the extracellular space. They exhibit diverse sizes, contents, and surface markers and are ubiquitously released from cells under normal and pathological conditions. Human serum is a rich source of these EVs, though their isolation from serum proteins and non-EV lipid particles poses challenges. These vesicles transport various cellular components such as proteins, mRNAs, miRNAs, DNA, and lipids across distances, influencing numerous physiological and pathological events, including those within the tumor microenvironment (TME). Their pivotal roles in cellular communication make EVs promising candidates for therapeutic agents, drug delivery systems, and disease biomarkers. Especially in cancer diagnostics, EV detection can pave the way for early identification and offers potential as diagnostic biomarkers. Moreover, various EV subtypes are emerging as targeted drug delivery tools, highlighting their potential clinical significance. The need for non-invasive biomarkers to monitor biological processes for diagnostic and therapeutic purposes remains unfulfilled. Tapping into the unique composition of EVs could unlock advanced diagnostic and therapeutic avenues in the future. In this review, we discuss in detail the roles of EVs across various conditions, including cancers (encompassing head and neck, lung, gastric, breast, and hepatocellular carcinoma), neurodegenerative disorders, diabetes, viral infections, autoimmune and renal diseases, emphasizing the potential advancements in molecular diagnostics and drug delivery.
C1 [Kumar, Mudasir A.; Baba, Sadaf K.; Macha, Muzafar A.] Islamic Univ Sci & Technol, Watson Crick Ctr Mol Med, Awantipora 192122, Kashmir, India.
   [Sadida, Hana Q.; Marzooqi, Sara Al.; Al-Shabeeb Akil, Ammira S.; Bhat, Ajaz A.] Sidra Med, Dept Human Genet Precis Med Diabet, Obes & Canc Program, Doha, Qatar.
   [Jerobin, Jayakumar; Abou-Samra, Abdul-Badi] Hamad Med Corp, Qatar Metab Inst, Acad Hlth Syst, Doha, Qatar.
   [Altemani, Faisal H.; Algehainy, Naseh; Alanazi, Mohammad A.; Mir, Rashid] Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk, Saudi Arabia.
   [Kumar, Rakesh] Shri Mata Vaishno Devi Univ, Sch Biotechnol, Katra, India.
C3 Sidra Medical & Research Center; Hamad Medical Corporation; University
   of Tabuk; Shri Mata Vaishno Devi University
RP Bhat, AA (corresponding author), Sidra Med, Dept Human Genet Precis Med Diabet, Obes & Canc Program, Doha, Qatar.; Mir, R (corresponding author), Univ Tabuk, Fac Appl Med Sci, Prince Fahad Bin Sultan Chair Biomed Res, Dept Med Lab Technol, Tabuk, Saudi Arabia.
EM rashidmirtabuk@gmail.com; abhat@sidra.org
RI MIR, RASHID/AAH-1895-2019; Altemani, Faisal/GQQ-3323-2022; Algehainy,
   Naseh A./JNR-2432-2023; Bhat, Ajaz/V-3642-2019; MACHA,
   MUZAFAR/AAN-5735-2020; Mir, Rashid/GOV-3522-2022; Abou-Samra,
   Abdul/ABE-8723-2020; Alanazi, Mohammad/HTP-5235-2023
OI Alanazi, Mohammad/0000-0001-6766-3237; Algehainy,
   Naseh/0000-0001-8557-0499; Altemani, Faisal H./0000-0003-1746-1631;
   Jerobin, Jayakumar/0000-0001-6421-3601; Sadida, Hana/0009-0003-2932-0323
FU Sidra Medicine Research Fund to Ajaz A. Bhat [SDR400105]; Sidra Medicine
   Precision Program
FX The authors thank the Sidra Medicine Precision Program for providing the
   funding necessary to carry out this study. Figures were created using
   BioRender.
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NR 688
TC 290
Z9 296
U1 141
U2 268
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD FEB 5
PY 2024
VL 9
IS 1
AR 27
DI 10.1038/s41392-024-01735-1
PG 41
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA GY6V0
UT WOS:001156284100001
PM 38311623
OA Green Published, gold
HC Y
HP Y
DA 2025-06-01
ER

PT J
AU Toh, BH
AF Toh, Ban-Hock
TI Diagnosis and classification of autoimmune gastritis
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
ID PARIETAL-CELL ANTIBODIES; HELICOBACTER-PYLORI INFECTION; ATROPHIC BODY
   GASTRITIS; INTRINSIC-FACTOR ANTIBODIES; PERNICIOUS-ANEMIA; FOLLOW-UP;
   DIABETES-MELLITUS; CORPUS GASTRITIS; THYROID-DISEASE; PEPSINOGEN-I
AB Autoimmune gastritis is a silent and highly prevalent disease that only becomes clinically manifested with progression to corpus atrophy and development of iron deficient or B12-deficient (pernicious) anaemia. Autoimmune gastritis is associated with autoimmune thyroiditis and type 1 diabetes mellitus. Corpus atrophy may be complicated by gastric carcinoids and gastric cancer. Laboratory diagnosis of autoimmune gastritis rests on serum biomarkers of antibody to parietal cell H/K ATPase and intrinsic factor and corpus atrophy on serum biomarkers of gastrin and pepsinogen levels. Subjects with asymptomatic parietal cell antibody should be regularly assessed for serum biomarkers for progression to corpus atrophy, development of iron and B12 deficiency anaemia and for associated autoimmune thyroiditis and type 1 diabetes mellitus. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Toh, Ban-Hock] Monash Univ, Dept Med, Southern Clin Sch,Australia Healthscope Pathol, Fac Med Nursing & Hlth Sci,Ctr Inflammatory Dis, Clayton, Vic 3168, Australia.
C3 Monash University
RP Toh, BH (corresponding author), Monash Inst Med Res, 27-31 Wright St, Clayton, Vic 3168, Australia.
EM ban-hock.tob@monash.edu
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NR 56
TC 101
Z9 112
U1 1
U2 28
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD APR-MAY
PY 2014
VL 13
IS 4-5
SI SI
BP 459
EP 462
DI 10.1016/j.autrev.2014.01.048
PG 4
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AE2AM
UT WOS:000333775700026
PM 24424193
DA 2025-06-01
ER

PT J
AU Salagacka, A
   Zebrowska, M
   Jelen, A
   Mirowski, M
   Balcerczak, E
AF Salagacka, Aleksandra
   Zebrowska, Marta
   Jelen, Agnieszka
   Mirowski, Marek
   Balcerczak, Ewa
TI Haplotype Analysis of TNFA Gene in Peptic Ulcer Patients
SO INTERNATIONAL JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE TNFA; Polymorphism; Haplotype; Helicobacter pylori; Peptic Ulcer
ID TUMOR-NECROSIS-FACTOR; HELICOBACTER-PYLORI INFECTION; FACTOR-ALPHA;
   DUODENAL-ULCER; GASTRIC-CANCER; PROMOTER REGION; POLYMORPHISMS; RISK;
   ASSOCIATION; POPULATION
AB The TNFA gene product TNF-alpha is a cytokine promoting an immune response after,bacterial infections. An excessive production of the cytokine is thought to be connected with Helicobacter pylon-induced disorders like gastritis, peptic ulcer disease (PUD), intestinal metaplasia, or even gastric cancer. The synthesis of TNF-a is controlled at transcriptional level and dependent on single nucleotide polymorphisms (SNPs) of TNFA promoter region. SNPs assembled in haplotype have been implicated as potential risk factors for various autoimmune and infectious diseases. The aim of this study was to determine the frequencies of TNFA haplotypes composed of the four common single-nucleotide polymorphisms of the gene (-1031C>T: rs1799964, -863C>A: rs1800630, -857C>T: rs1799724, -308G>A: rs1800629) in peptic ulcer patients and to assess the significance of the haplotypes as the risk factors of H. pylon infection development. 203 peptic ulcer patients were genotyped using polymerase chain reaction-restriction fragment length polymorphism method. Haplotypes and degree of linkage disequilibrium (LD) were inferred with PHASE 2.1 and EMLD software. There was no statistically significant difference in haplotype frequencies between the H. pylon-infected and -uninfected peptic ulcer cases (p=0.62). Analogous association was also absent in the subgroups: peptic ulcer woman (p=0.69), peptic ulcer men (p=0.17). The locus pairs -308_-857, -863_-1031, and -857_-1031 was found to be in very strong LD, -308_-1031 and -857 and -863 in strong LD, and -308_-863 - in modest LD. TNFA haplotype structure is not connected with individual differences in susceptibility to development of H. pylon infection in peptic ulcer patients.
C1 [Salagacka, Aleksandra; Zebrowska, Marta; Jelen, Agnieszka; Mirowski, Marek; Balcerczak, Ewa] Med Univ Lodz, Dept Pharmaceut Biochem, Lab Mol Diag & Pharmacogen, PL-91151 Lodz, Poland.
C3 Medical University Lodz
RP Salagacka, A (corresponding author), Med Univ Lodz, Musuynskiego 1, PL-90151 Lodz, Poland.
EM aleksandra.salagacka@umed.lodz.pl
RI Salagacka-Kubiak, Aleksandra/V-9782-2019; Zebrowska-Nawrocka,
   Marta/S-9933-2016; Jelen, Agnieszka/S-9588-2016; Balcerczak,
   Ewa/S-9838-2016
OI Zebrowska-Nawrocka, Marta/0000-0001-7478-7860; Jelen,
   Agnieszka/0000-0002-3565-7075; Balcerczak, Ewa/0000-0001-5257-2914;
   Salagacka-Kubiak, Aleksandra/0000-0002-6360-1538
FU Ministry of Science and Higher Education, Warsaw, Poland
   [507-13-0511613/B/P01/2010/39]; Statutory Funds of Department of
   Pharmaceutical Biochemistry, Medical University of Lodz
   [503/3-015-02/503-01]; Funds of Faculty of Pharmacy, Medical University
   of Lodz [2012502-03/3-015-02/502-34-021]
FX The presented research was supported by grant
   507-13-0511613/B/P01/2010/39 from the Ministry of Science and Higher
   Education, Warsaw, Poland; Statutory Funds of Department of
   Pharmaceutical Biochemistry, Medical University of Lodz
   503/3-015-02/503-01; and Funds of Faculty of Pharmacy, Medical
   University of Lodz 2012502-03/3-015-02/502-34-021.
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NR 33
TC 3
Z9 3
U1 0
U2 3
PU KAMLA-RAJ ENTERPRISES
PI GURGAON
PA B2-GROUND FLR, SOUTH CITY II, GURGAON, HARYANA 122 018, INDIA
SN 0972-3757
J9 INT J HUM GENET
JI Int. J. Hum. Genet.
PD MAR
PY 2014
VL 14
IS 1
BP 9
EP 15
DI 10.1080/09723757.2014.11886221
PG 7
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA AM7VZ
UT WOS:000340078100002
DA 2025-06-01
ER

PT J
AU Zhang, ZP
   Zhu, TT
   Zhang, L
   Xing, YC
   Yan, ZQ
   Li, QS
AF Zhang, Zepeng
   Zhu, Tongtong
   Zhang, Lei
   Xing, Yanchao
   Yan, Zhiqiang
   Li, Qingsong
TI Critical influence of cytokines and immune cells in autoimmune gastritis
SO AUTOIMMUNITY
LA English
DT Review
DE Gastric cancer; autoimmune gastritis; immune cells; cytokines;
   Helicobacter pylori
ID REGULATORY T-CELLS; HELICOBACTER-PYLORI; TGF-BETA; INTERFERON-GAMMA;
   IFN-GAMMA; H+,K+-ADENOSINE TRIPHOSPHATASE; INTERLEUKIN-17 FAMILY; FOXP3
   EXPRESSION; DENDRITIC CELLS; DISEASE
AB Gastric cancer (GC) is a type of the most common cancers. Autoimmune gastritis (AIG) and infection with Helicobacter pylori (HP) are the risk factors of triggering GC. With the emphasis on the treatment of HP, the incidence and prevalence of HP infection in population is decreasing. However, AIG lacks accurate diagnosis and treatment methods, which occupies high cancer risk factors. AIG is controlled by the immune environment of the stomach, including immune cells, inflammatory cells, and infiltrating intercellular material. Various immune cells or cytokines play a central role in the process of regulating gastric parietal cells. Abnormal expression levels of cytokines involved in immunity are bound to face the risk of tumorigenesis. Therefore, it is particularly important for preventing or treating AIG and avoiding the risk of gastric cancer to clarify the confirmed action mode of immune cells and cytokines in the gastric system. Herein, we briefly reviewed the role of the immune environment under AIG, focussing on describing these double-edged effects between immune cells and cytokines, and pointing out potential research challenges.
C1 [Zhang, Zepeng; Zhang, Lei; Yan, Zhiqiang; Li, Qingsong] Kunshan Hosp Chinese Med, Suzhou, Jiangsu, Peoples R China.
   [Zhu, Tongtong] Kunshan Hosp Tradit Chinese & Western Med, Suzhou, Jiangsu, Peoples R China.
   [Xing, Yanchao] Wenzhou Med Univ, Sch Pharmaceut Sci, Wenzhou, Zhejiang, Peoples R China.
C3 Wenzhou Medical University
RP Zhang, L (corresponding author), Kunshan Hosp Chinese Med, Suzhou, Jiangsu, Peoples R China.; Xing, YC (corresponding author), Wenzhou Med Univ, Sch Pharmaceut Sci, Wenzhou, Zhejiang, Peoples R China.
EM zhl0320@163.com; xingyanchao@wmu.edu.cn
RI Yan, Zhiqiang/P-9909-2017; LI, QS/IED-7767-2023; Zhu,
   Tongtong/J-2081-2016
OI Zhu, Tongtong/0000-0002-5481-6836
FU Kunshan Municipal Science and Technology Project, China [KS2222]
FX This review was financially supported by Kunshan Municipal Science and
   Technology Project, China [Grant number KS2222].
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NR 122
TC 11
Z9 11
U1 1
U2 26
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0891-6934
EI 1607-842X
J9 AUTOIMMUNITY
JI Autoimmunity
PD DEC 31
PY 2023
VL 56
IS 1
AR 2174531
DI 10.1080/08916934.2023.2174531
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 8X3OG
UT WOS:000931924400001
PM 36762543
OA gold
DA 2025-06-01
ER

PT J
AU Sennikov, SV
   Alshevskaya, AA
   Zhukova, J
   Belomestnova, I
   Karaulov, AV
   Lopatnikova, JA
AF Sennikov, Sergey Vitalievich
   Alshevskaya, Alina A.
   Zhukova, Julia
   Belomestnova, Irina
   Karaulov, Alexander V.
   Lopatnikova, Julia A.
TI Expression Density of Receptors as a Potent Regulator of Cell Function
   and Property in Health and Pathology
SO INTERNATIONAL ARCHIVES OF ALLERGY AND IMMUNOLOGY
LA English
DT Review
DE Cellular immunology; Cytokine expression; Cytokines; Immune regulation;
   Cytokine receptors
ID EPIDERMAL-GROWTH-FACTOR; LYMPH-NODE METASTASIS; PROGNOSTIC IMPLICATIONS;
   RHEUMATOID-ARTHRITIS; LARYNGEAL-CANCER; GASTRIC-CANCER; FAS-LIGAND;
   T-CELLS; CCR5; OVEREXPRESSION
AB The expression of cytokine receptors has a crucial role in many cellular processes. Recent studies reported that changes of receptor expression could control the action of mediators on target cells. The initiation of different signaling pathways and, therefore, specific effects on cells, depends on certain components forming the cytokine-receptor complex. These mechanisms control the immune response and affect both the course of diseases (oncological, autoimmune, inflammatory) and the effectiveness of therapy. This review describes the potential of immune mediator receptors to regulate the efficiency of cytokine activity during pathologic processes and ensure the variability of their biological effects. Our aim was to investigate the spectrum of potential roles of changes in mediator receptor expression for main classes of pathologies. For all major types of immune media-tors (cytokines, interleukins, chemokines, growth factors, and tumor necrosis factors), it has been shown that changes in their receptor expression are associated with impaired functioning of the organism in chronic diseases. (C) 2018 S. Karger AG, Basel
C1 [Sennikov, Sergey Vitalievich; Alshevskaya, Alina A.; Zhukova, Julia; Belomestnova, Irina; Lopatnikova, Julia A.] RIFCI, Fed State Budgetary Sci Inst, Novosibirsk, Russia.
   [Sennikov, Sergey Vitalievich] Novosibirsk State Univ, Novosibirsk, Russia.
   [Karaulov, Alexander V.] IM Sechenov First Moscow State Med Univ, Minist Hlth Russian Federat, Fed State Autonomous Educ Inst Higher Educ, Moscow, Russia.
C3 Novosibirsk State University; Ministry of Health of the Russian
   Federation; Sechenov First Moscow State Medical University
RP Sennikov, SV (corresponding author), RIFCI, Lab Mol Immunol, Yadrintsevskaya St 14, RU-630099 Novosibirsk, Russia.
EM sennikovsv@gmail.com
RI Alshevskaya, Alina/JCE-5434-2023; SENNIKOV, SERGEY/GPS-7277-2022;
   Zhukova, Julia/AAR-2876-2021; Lopatnikova, Julia/O-2157-2013; Karaulov,
   Alexander/C-2482-2016; Alshevskaya, Alina/O-2444-2013
OI Lopatnikova, Julia/0000-0003-0089-5054; Karaulov,
   Alexander/0000-0002-1930-5424; Sennikov, Sergey/0000-0002-7366-7768;
   Zhukova, Julia/0000-0002-2287-0918; Alshevskaya,
   Alina/0000-0002-7307-4524
FU Russian Academic Excellence Project [5-100]
FX The study was supported by the Russian Academic Excellence Project
   "5-100."
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NR 81
TC 11
Z9 13
U1 0
U2 4
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 1018-2438
EI 1423-0097
J9 INT ARCH ALLERGY IMM
JI Int. Arch. Allergy Immunol.
PY 2019
VL 178
IS 2
BP 182
EP 191
DI 10.1159/000494387
PG 10
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA HM5JO
UT WOS:000459512200010
PM 30544119
OA Bronze
DA 2025-06-01
ER

PT J
AU Oksanen, AM
   Haimila, KE
   Rautelin, HIK
   Partanen, JA
AF Oksanen, Aino Mirjam
   Haimila, Katri Eerika
   Rautelin, Hilpi Iris Kaarina
   Partanen, Jukka Antero
TI Immunogenetic characteristics of patients with autoimmune gastritis
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Atrophic gastritis; Autoimmune diseases; Cytokines; Genetic
   polymorphisms; Human leukocyte antigens; Killer cell immunoglobulin-like
   receptor
ID CYTOKINE GENE POLYMORPHISMS; HELICOBACTER-PYLORI; ATROPHIC GASTRITIS;
   PERNICIOUS-ANEMIA; INCREASED RISK; HLA ANTIGENS; DISEASE; DIVERSITY;
   PATTERNS; CANCER
AB AIM: To explore whether predisposition to autoimmune gastritis (AIG) is found in human leukocyte antigen (HLA), cytokine or killer cell immunoglobulin-like receptor (KIR) gene variations.
   METHODS: Twelve Finnish patients with autoimmune-type severe atrophy of the gastric corpus were included. The patients' serum was analyzed for pepsinogen I and Helicobacter pylori (H. pylori) antibodies. DNA was separated and the patients were genotyped for HLA-A, B, Cw, DRB1 and DQB1 antigens, and studied for single nucleotide polymorphisms for the following cytokines: interleukin (IL)-1 gene cluster, IL-2, IL-4, IL 6, IL-10, IL-12, interferon gamma, transforming growth factor beta, and tumor necrosis factor alpha. Variation in KIR genes was also explored. The results were compared with prevalence of the polymorphisms in Finnish or European populations.
   RESULTS: All patients had pepsinogen I levels below normal (mean: 11 mu g/L, range: < 5 to 25 mu g/L). Three patients had elevated H. pylori IgG antibodies, while H. pylori serology was negative in the rest of the patients. AIG patients carried significantly more often HLA-DRB1*04 (58%) and DQB1*03 (83%) than the general Finnish population did (28% and 51%, respectively; P = 0.045 and 0.034 by the Fisher's exact test). No patient was positive for HLA-B8-DRB1*03, a well-established autoimmune marker. Neither cytokine polymorphisms nor KIR gene variation showed association with AIG.
   CONCLUSION: As explored with modern DNA-based methods, HLA-DRB1*04 and DQB1*03 alleles, but not HLA-B8-DRB1*03, may predispose to AIG. (C) 2010 Baishideng. All rights reserved.
C1 [Oksanen, Aino Mirjam] Herttoniemi Hosp, Ctr Hlth, Helsinki 00099, Finland.
   [Haimila, Katri Eerika] Finnish Red Cross Blood Serv, Clin Lab, Helsinki 00310, Finland.
   [Rautelin, Hilpi Iris Kaarina] Univ Helsinki, Dept Bacteriol & Immunol, Haartman Inst, FIN-00014 Helsinki, Finland.
   [Rautelin, Hilpi Iris Kaarina] Univ Helsinki, Cent Hosp, HUSLAB, Helsinki 00029, Finland.
   [Rautelin, Hilpi Iris Kaarina] Univ & Univ Hosp Uppsala, Dept Med Sci, S-75185 Uppsala, Sweden.
   [Partanen, Jukka Antero] Finnish Red Cross Blood Serv, Res & Dev, Helsinki 00310, Finland.
C3 University of Helsinki; University of Helsinki; Helsinki University
   Central Hospital; Uppsala University; Uppsala University Hospital
RP Oksanen, AM (corresponding author), Herttoniemi Hosp, Ctr Hlth, POB 6300, Helsinki 00099, Finland.
EM aino.oksanen@hel.fi
RI Partanen, Jukka/B-7207-2014
OI Partanen, Jukka/0000-0001-6681-4734; Haimila, Katri/0000-0001-8904-666X
FU Research Unit of the Health Centre, City of Helsinki
FX Supported by A grant from the Research Unit of the Health Centre, City
   of Helsinki
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NR 33
TC 21
Z9 23
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 21
PY 2010
VL 16
IS 3
BP 354
EP 358
DI 10.3748/wjg.v16.i3.354
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 547JZ
UT WOS:000273884700012
PM 20082482
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Wojciechowicz, K
   Spodzieja, M
   Wardowska, A
AF Wojciechowicz, Karolina
   Spodzieja, Marta
   Wardowska, Anna
TI The BTLA-HVEM complex - The future of cancer immunotherapy
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Review
DE BTLA-HVEM; Immune checkpoint; Cancer; Immunotherapies; Oncology;
   Immunotherapy; Inhibitor
ID HERPESVIRUS ENTRY MEDIATOR; T-LYMPHOCYTE ATTENUATOR; VIRUS
   GLYCOPROTEIN-D; B-CELL LYMPHOMA; INHIBITORY RECEPTOR; HIGH EXPRESSION;
   POOR-PROGNOSIS; GASTRIC-CANCER; BINDING; ANTIBODY
AB The BTLA-HVEM complex plays a pivotal role in cancer and cancer immunotherapy by regulating immune responses. Dysregulation of BTLA and HVEM expression contributes to immunosuppression and tumor progression across various cancer types. Targeting the interaction between BTLA and HVEM holds promise for enhancing anti-tumor immune responses. Disruption of this complex presents a valuable avenue for advancing cancer immunotherapy strategies. Aberrant expression of BTLA and HVEM adversely affects immune cell function, particularly T cells, exacerbating tumor evasion mechanisms. Understanding and modulating the BTLA-HVEM axis represents a crucial aspect of designing effective immunotherapeutic interventions against cancer. Here, we summarize the current knowledge regarding the structure and function of BTLA and HVEM, along with their interaction with each other and various immune partners. Moreover, the expression of soluble and transmembrane forms of BTLA and HVEM in different types of cancer and their impact on the prognosis of patients is also discussed. Additionally, inhibitors of the proteins binding that might be used to block BTLA-HVEM interaction are reviewed. All the presented data highlight the plausible clinical application of BTLA-HVEM targeted therapies in cancer and autoimmune disease management. However, further studies are required to confirm the practical use of this concept. Despite the increasing number of reports on the BTLA-HVEM complex, many aspects of its biology and function still need to be elucidated. This review can be regarded as an encouragement and a guide to follow the path of BTLA-HVEM research.
C1 [Wojciechowicz, Karolina; Wardowska, Anna] Med Univ Gdansk, Fac Med, Dept Physiopathol, Debinki 7, PL-80210 Gdansk, Poland.
   [Spodzieja, Marta] Univ Gdansk, Fac Chem, Dept Biomed Chem, Gdansk, Poland.
   [Wojciechowicz, Karolina; Wardowska, Anna] Med Univ Gdansk, Fac Med, Dept Physiopathol, Debinki 7, PL-80210 Gdansk, Poland.
C3 Fahrenheit Universities; Medical University Gdansk; Fahrenheit
   Universities; University of Gdansk; Fahrenheit Universities; Medical
   University Gdansk
RP Wojciechowicz, K; Wardowska, A (corresponding author), Med Univ Gdansk, Fac Med, Dept Physiopathol, Debinki 7, PL-80210 Gdansk, Poland.; Wojciechowicz, K; Wardowska, A (corresponding author), Med Univ Gdansk, Fac Med, Dept Physiopathol, Debinki 7, PL-80210 Gdansk, Poland.
EM k.wojciechowicz@gumed.edu.pl; anna.wardowska@gumed.edu.pl
RI Wardowska, Anna/R-3384-2018; Spodzieja, Marta/HSB-7719-2023
OI Wojciechowicz, Karolina/0000-0001-5458-4273
FU SONATA 13 grant [UMO-2017/26/D/ST5/00919]; National Science Center
   (Poland)
FX This work was supported by a SONATA 13 grant (No.
   UMO-2017/26/D/ST5/00919) "Inhibitors of BTLA-HVEM complex formation as
   potential targets for cancer immunotherapy", financed by the National
   Science Center (Poland).
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NR 129
TC 12
Z9 13
U1 2
U2 9
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI ISSY-LES-MOULINEAUX
PA 65 RUE CAMILLE DESMOULINS, CS50083, 92442 ISSY-LES-MOULINEAUX, FRANCE
SN 0223-5234
EI 1768-3254
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD MAR 15
PY 2024
VL 268
AR 116231
DI 10.1016/j.ejmech.2024.116231
EA FEB 2024
PG 15
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA NS5U7
UT WOS:001202464600001
PM 38387336
OA hybrid
DA 2025-06-01
ER

PT J
AU Smyk, DS
   Koutsoumpas, AL
   Mytilinaiou, MG
   Rigopoulou, EI
   Sakkas, LI
   Bogdanos, DP
AF Smyk, Daniel S.
   Koutsoumpas, Andreas L.
   Mytilinaiou, Maria G.
   Rigopoulou, Eirini I.
   Sakkas, Lazaros I.
   Bogdanos, Dimitrios P.
TI Helicobacter pylori and autoimmune disease: Cause or bystander
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmunity; Helicobacter pylori; Infection; Gastritis; Mimicry;
   Rheumatology
ID PRIMARY BILIARY-CIRRHOSIS; IDIOPATHIC THROMBOCYTOPENIC PURPURA;
   NEUTROPHIL-ACTIVATING PROTEIN; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
   LYMPHOID-TISSUE LYMPHOMA; MULTIPLE-SCLEROSIS; MOLECULAR MIMICRY;
   RHEUMATOID-ARTHRITIS; CHRONIC URTICARIA; WEGENERS-GRANULOMATOSIS
AB Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjorens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Smyk, Daniel S.; Koutsoumpas, Andreas L.; Mytilinaiou, Maria G.; Sakkas, Lazaros I.; Bogdanos, Dimitrios P.] Kings Coll Hosp London, Kings Coll London, Sch Med, Inst Liver Studies,Div Transplantat Immunol & Muc, London SE5 9RS, England.
   [Koutsoumpas, Andreas L.; Rigopoulou, Eirini I.; Bogdanos, Dimitrios P.] Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Med, Larisa 41110, Greece.
   [Sakkas, Lazaros I.] Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Rheumatol, Larisa 41110, Greece.
   [Bogdanos, Dimitrios P.] Inst REs & Technol THessaly I RE TE TH, Ctr Res & TEchnol Hellas CE R T H, Cellular Immunotherapy & Mol Immunodiagnost Biome, Thessaloniki, Greece.
C3 University of London; King's College London; King's College Hospital NHS
   Foundation Trust; King's College Hospital; University of Thessaly;
   University of Thessaly; Centre for Research & Technology Hellas
RP Bogdanos, DP (corresponding author), Univ Thessaly, Fac Med, Sch Hlth Sci, Dept Med, Mezourlo Campus, Larisa 41110, Greece.
EM dimitrios.bogdanos@kcl.ac.uk
RI Bogdanos, Dimitrios/AAF-8620-2020; Mytilinaiou, Maria/HPE-8131-2023
OI Bogdanos, Dimitrios/0000-0002-9697-7902
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NR 159
TC 110
Z9 118
U1 0
U2 32
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JAN 21
PY 2014
VL 20
IS 3
BP 613
EP 629
DI 10.3748/wjg.v20.i3.613
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AA1KZ
UT WOS:000330856400001
PM 24574735
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Repetto, O
   De Re, V
   Giuffrida, P
   Lenti, MV
   Magris, R
   Venerito, M
   Steffan, A
   Di Sabatino, A
   Cannizzaro, R
AF Repetto, Ombretta
   De Re, Valli
   Giuffrida, Paolo
   Lenti, Marco Vincenzo
   Magris, Raffaella
   Venerito, Marino
   Steffan, Agostino
   Di Sabatino, Antonio
   Cannizzaro, Renato
TI Proteomics signature of autoimmune atrophic gastritis: towards a link
   with gastric cancer
SO GASTRIC CANCER
LA English
DT Article
DE Autoimmune disease; Biological markers; Gastric cancer; Gastritis;
   Proteomics
AB Background Autoimmune atrophic gastritis (AAG) is a chronic disease that can progress to gastric cancer (GC). To better understand AAG pathology, this proteomics study investigated gastric proteins whose expression levels are altered in this disease and also in GC. Methods Using two-dimensional difference gel electrophoresis (2D-DIGE), we compared protein maps of gastric corpus biopsies from AAG patients and controls. Differentially abundant spots (|fold change|>= 1.5, P < 0.01) were selected and identified by LC-MS/MS. The spots were further assessed in gastric antrum biopsies from AAG patients (without and with Helicobacter pylori infection) and from GC patients and unaffected first-degree relatives of GC patients. Results 2D-DIGE identified 67 differentially abundant spots, with 28 more and 39 less abundant in AAG-corpus than controls. LC-MS/MS identified these as 53 distinct proteins. The most significant (adjusted P < 0.01) biological process associated with the less abundant proteins was "tricarboxylic acid cycle". Of the 67 spots, 57 were similarly differentially abundant in AAG-antrum biopsies irrespective of H. pylori infection status. The differential abundance was also observed in GC biopsies for 14 of 28 more abundant and 35 of 39 less abundant spots, and in normal gastric biopsies of relatives of GC patients for 6 and 25 spots, respectively. Immunoblotting confirmed the different expression levels of two more abundant proteins (PDIA3, GSTP gene products) and four less abundant proteins (ATP5F1A, PGA3, SDHB, PGC). Conclusion This study identified a proteomics signature of AAG. Many differential proteins were shared by GC and may be involved in the progression of AAG to GC.
C1 [Repetto, Ombretta; De Re, Valli] Ctr Riferimento Oncol Aviano CRO IRCCS, Facil Bioprote Immunopathol & Canc Biomarkers, Aviano, PN, Italy.
   [Giuffrida, Paolo; Lenti, Marco Vincenzo; Di Sabatino, Antonio] Univ Pavia, San Matteo Hosp Fdn, Dept Internal Med, Pavia, Italy.
   [Magris, Raffaella; Cannizzaro, Renato] Ctr Riferimento Oncol Aviano CRO IRCCS, Gastroenterol, Aviano, PN, Italy.
   [Venerito, Marino] Otto von Guericke Univ Hosp, Dept Gastroenterol Hepatol & Infect Dis, Magdeburg, Germany.
   [Steffan, Agostino] Ctr Riferimento Oncol Aviano CRO IRCCS, Immunopathol & Canc Biomarkers, Aviano, PN, Italy.
C3 University of Pavia; University Hospital Magdeburg; Otto von Guericke
   University
RP Repetto, O; De Re, V (corresponding author), Ctr Riferimento Oncol Aviano CRO IRCCS, Facil Bioprote Immunopathol & Canc Biomarkers, Aviano, PN, Italy.
EM orepetto@cro.it; vdere@cro.it; paolo.giuffrida01@universitadipavia.it;
   marco.lenti@unipv.it; raffaella.magris@cro.it; m.venerito@med.ovgu.de;
   asteffan@cro.it; a.disabatino@smatteo.pv.it; rcannizzaro@cro.it
RI Magris, Raffaella/ABD-7791-2020; Venerito, Marino/AAF-4493-2020; De Re,
   Valli/K-4121-2016; Steffan, Agostino/ABE-5972-2020; Lenti,
   Marco/F-9044-2018; Di Sabatino, Antonio/K-8015-2016; Repetto,
   Ombretta/V-6342-2019; Cannizzaro, Renato/V-3804-2018
OI Repetto, Ombretta/0000-0002-0785-5066; Cannizzaro,
   Renato/0000-0002-2020-222X
FU Italian Ministry of Health [RF-2016-02361525]; Ministero della
   Salute-Ricerca Corrente
FX The authors thank the patients for donating tissue samples, Valerie
   Matarese for scientific editing on versions of the manuscript, and Dr.
   Simona Celentano from CEINGE-Biotecnologie Avanzate (Naples, Italy) for
   doing the LC-MS/MS analyses. Research reported in this publication was
   supported by the Italian Ministry of Health (Grant number
   RF-2016-02361525 to R. Cannizzaro) and Ministero della Salute-Ricerca
   Corrente. Manuscript editing was paid for by Centro di Riferimento
   Oncologico di Aviano (CRO), IRCCS.
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NR 52
TC 11
Z9 13
U1 0
U2 19
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1436-3291
EI 1436-3305
J9 GASTRIC CANCER
JI Gastric Cancer
PD MAY
PY 2021
VL 24
IS 3
BP 666
EP 679
DI 10.1007/s10120-020-01148-3
EA FEB 2021
PG 14
WC Oncology; Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Gastroenterology & Hepatology
GA RR2FB
UT WOS:000620855300001
PM 33620602
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Zan, Y
   Wei, YD
   Zhang, WX
   Gao, XL
   Si, JG
AF Zan, Ying
   Wei, Yedong
   Zhang, Wenxue
   Gao, Xiaolu
   Si, Jigang
TI Sintilimab-induced diabetes mellitus and thyroid dysfunction in patient
   with gastric adenocarcinoma: A case report and literature review
SO MEDICINE
LA English
DT Article
DE DIRE; ICI-induced diabetes mellitus; ICI-induced thyroid dysfunction;
   irAEs; sintilimab
ID IMMUNE CHECKPOINT INHIBITOR; AUTOIMMUNE; ANTIBODIES; NIVOLUMAB; PD-1;
   KETOACIDOSIS
AB Rationale: Immune checkpoint inhibitors bring hope to cancer patients but may also lead to severe immune-related adverse events (irAEs). Although irAEs during treatment are well-characterized, delayed immune-related events (DIRE) remain underreported. Here, we report a case of sintilimab-induced delayed immune-related diabetes mellitus, accompanied by ICI-related thyroid disease (ICI-TD). Cases involving both ICI-TD and ICI-related diabetes mellitus (ICI-DM) are also relatively rare. This study systematically aggregates dual endocrine irAEs to provide valuable insights for clinical practice. Patient concerns: A 60-year-old Chinese male diagnosed with gastric adenocarcinoma received a multimodal treatment regimen consisting of sintilimab, chemotherapy, and apatinib. He completed 3 cycles of chemotherapy and 4 cycles of sintilimab. Due to disease progression, sintilimab was discontinued, but apatinib was continued for an additional 1 month. No further antitumor therapy was administered afterward. Four months later, he was admitted to the emergency department due to persistent nausea, vomiting, and abdominal pain. Diagnoses: Thyroid dysfunction induced by sintilimab was identified during treatment. His laboratory tests contributed to the diagnosis of diabetes ketoacidosis. Fulminant type 1 diabetes mellitus attributed to sintilimab met diagnostic criteria: plasma glucose 42.01 mmol/L, glycated hemoglobin 7.5%, C-peptide <0.02 <mu>g/L, and negative islet autoantibodies. Interventions: Levothyroxine replacement therapy was initiated for hypothyroidism, whereas diabetes ketoacidosis during hospitalization required intensive insulin therapy combined with fluid resuscitation. Outcomes: The patient exhibited persistent blood glucose fluctuations during hospitalization, including 2 hypoglycemic episodes. Post-treatment stabilization required basal-bolus insulin at discharge, with continued levothyroxine for hypothyroidism. Lessons: We report a rare case of concurrent ICI-TD and ICI-DM following sintilimab therapy. This case underscores the potential for DIRE, with onset occurring months posttreatment. Combined with a systematic review of existing cases, this study provides critical insights into surveillance strategies and pathogenesis of irAEs.
C1 [Zan, Ying; Wei, Yedong; Si, Jigang] Zibo Cent Hosp, Dept Pharm, Zibo, Peoples R China.
   [Zhang, Wenxue] Zhangdian Tradit Chinese Med Hosp, Dept Pharm, Zibo, Peoples R China.
   [Gao, Xiaolu] Jinshan Town Hlth Ctr, Dept Pharm, Zibo, Peoples R China.
RP Zan, Y (corresponding author), Zibo Cent Hosp, Dept Pharm, Zibo, Peoples R China.
EM hpyyq1211@163.com; 809406211@qq.com; 381814528@qq.com;
   1625307632@qq.com; sjg1019@163.com
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NR 60
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD MAY 16
PY 2025
VL 104
IS 20
AR e42490
DI 10.1097/MD.0000000000042490
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 2SZ5V
UT WOS:001490592300031
PM 40388765
DA 2025-06-01
ER

PT J
AU Ahmed, AR
   Kalesinskas, M
   Kooper-Johnson, S
AF Ahmed, A. Razzaque
   Kalesinskas, Mikole
   Kooper-Johnson, Sarah
TI Paraneoplastic autoimmune Laminin-332 syndrome (PALS): Anti-Laminin-332
   mucous membrane pemphigoid as a prototype
SO AUTOIMMUNITY REVIEWS
LA English
DT Article
DE Anti-laminin-332 mucous membrane; pemphigoid; Laminin-332; Autoimmune
   diseases; Malignancy; Cancer biomarkers; Autoantibodies
ID EPIDERMOLYSIS-BULLOSA-ACQUISITA; SQUAMOUS-CELL CARCINOMA;
   CLINICAL-SIGNIFICANCE; BIOLOGICAL-ACTIVITY; GASTRIC-CARCINOMA; LATE
   RECURRENCE; BETA-3 SUBUNIT; GAMMA-2 CHAIN; CANCER-RISK; SHORT ARM
AB Importance: Laminin-332 is an important component of the basement membrane. Recently, autoantibodies to Laminin-332 have been described in several autoimmune diseases. Many of these autoimmune diseases have a high incidence of malignancy. The importance of Laminin-332 autoantibodies and its relationship to malignancy is highlighted by using Laminin-332 Pemphigoid (LM-332Pg) as a prototype.Objective: To identify several autoimmune diseases that have autoantibodies to Laminin-332 present, and to determine the prevalence of malignancy in them. Using Laminin-332 Pemphigoid (LM-332Pg) as a prototype, to compare clinical profiles of LM-332Pg patients with and without cancer. By identifying the temporal detection of cancer, can the influence of autoantibodies to Laminin-332 on prognosis be determined.Evidence review: A literature search was conducted to identify autoimmune and inflammatory diseases in which autoantibodies to Laminin-332 were present. Subsequently, the rate of malignancy in these autoimmune diseases was determined. A search for publications on LM-332Pg patients to determine cancer rates and clinical outcomes to examine if a relationship can be proposed, was performed.Findings: Autoantibodies to Laminin-332 were detected in recent studies of systemic lupus erythematosus (SLE), psoriasis, bronchiolitis obliterans (BO), graft-vs-host disease (GVH), bullous pemphigoid (BP), lichen planus (LP), epidermolysis bullosa acquisita (EBA), and membranous glomerulonephropathy (MGN). A high incidence of cancer rate was reported in these autoimmune diseases including primary Sjo center dot gren's syndrome (pSS), systemic sclerosis (SS), dermatomyositis (DM), multiple sclerosis (MS), immune thrombocytopenia purpura (ITP), and rheumatoid arthritis (RA). Data analysis demonstrated that LM-332Pg patients had a higher risk of developing ovarian, uterine, lung, gastric cancers and leukemia. The incidence for breast cancer was lower, when compared with global cancer rates. Patients diagnosed with cancer after the presence of LM-332Pg had higher rates of mortality and lower rates of remission, compared to those diagnosed with cancer prior to the discovery/diagnosis of LM-332Pg. When studied, levels of Laminin-332 autoantibodies correlated with the presence or absence of malignancy.Conclusions and relevance: Preliminary analysis suggests that autoantibodies to Laminin-332 are present in multiple autoimmune diseases, which also have a high incidence of malignancy. Detailed analysis of available data highlights that patients who developed LM-332Pg after cancer was diagnosed, had a more favorable prognosis, compared to patients who developed cancer when LM-332Pg was previously present. Preliminary data would suggest that autoantibodies to Laminin-332 could serve as an important biomarker in certain patients, for correlation with possible incidence of malignancy.
C1 [Ahmed, A. Razzaque] Tufts Univ, Sch Med, Dept Dermatol, Boston, MA 02111 USA.
   [Ahmed, A. Razzaque; Kalesinskas, Mikole; Kooper-Johnson, Sarah] Ctr Blistering Dis, Boston, MA 02135 USA.
   [Ahmed, A. Razzaque] Tufts Univ, Sch Med, Ctr Blistering Dis, 697 Cambridge St,Suite 302, Boston, MA 02135 USA.
C3 Tufts University; Tufts University
RP Ahmed, AR (corresponding author), Tufts Univ, Sch Med, Ctr Blistering Dis, 697 Cambridge St,Suite 302, Boston, MA 02135 USA.
EM arahmedmd@msn.com
FU Dysimmune Disease Foundation (DDF)
FX This review was supported, in part, by an unrestricted educational grant
   from the Dysimmune Disease Foundation (DDF) . The DDF was not involved
   in the conduct of the research or preparation of the manuscript. DDF had
   no role in study design, data collection, datal analysis or
   interpretation, or in the decision to submit the article for
   publication.
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NR 148
TC 3
Z9 3
U1 0
U2 2
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD OCT
PY 2023
VL 22
IS 10
AR 103444
DI 10.1016/j.autrev.2023.103444
EA SEP 2023
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA U2NV7
UT WOS:001083231700001
PM 37673192
OA hybrid
DA 2025-06-01
ER

PT J
AU Zádori, N
   Németh, D
   Szakó, L
   Váncsa, S
   Vörhendi, N
   Szakács, Z
   Frim, L
   Hegyi, P
   Czimmer, J
AF Zadori, Noemi
   Nemeth, David
   Szako, Lajos
   Vancsa, Szilard
   Vorhendi, Nora
   Szakacs, Zsolt
   Frim, Levente
   Hegyi, Peter
   Czimmer, Jozsef
TI Prevalence of Autoimmune-phenomena behind Chronic Gastritis of Unknown
   Origin, and their Role in the Poor Histological Outcome of the Stomach:
   A Single-centre, Retrospective Cross-sectional Study
SO JOURNAL OF GASTROINTESTINAL AND LIVER DISEASES
LA English
DT Article
DE chronic gastritis; autoimmunity; autoantibodies; intestinal metaplasia;
   gastric atrophy; gastric cancer
ID HELICOBACTER-PYLORI INFECTION; CHRONIC ATROPHIC GASTRITIS; EPIDEMIOLOGY;
   ANTIBODIES; CANCER; CLASSIFICATION; GUIDELINES; CARCINOMA; COHORT
AB Background & Aims: The underlying aetiology of chronic gastritis (CG) often remains unknown due to its underrated significance in clinical practice. However, the role of chronic inflammation of the stomach in the development of atrophy, intestinal metaplasia (IM) and eventually of gastric cancer is well documented. We aimed to explore the possible aetiological factors of CG, determine the prevalence of systemic autoimmune disorders in patients with CG of unknown aetiology, and clarify the role of autoantibodies in the development of precancerous lesions in the stomach.
   Methods: This is a retrospective, cross-sectional study, conducted from January 2016 to January 2020, including data from 175 patients with CG. Exclusion criteria were: (1) acute gastritis; (2) reactive gastropathy; (3) gastric cancer; (4) subjects without any serology testing results; and (5) Helicobacter pylori positivity. The primary endpoint was a composite endpoint involving gastric atrophy and IM.
   Results: Fifty-five per cent of patients with CG had autoantibodies. Systemic lupus erythematosus (SLE)-related antibodies were positive in most of the cases, including antinuclear antibody (ANA) positivity, which was found in 19.13% of the patients. Autoimmune positivity was shown to be associated with precancerous lesions in the stomach (p<0.001): IM, atrophy and IM with atrophy. Anti-parietal cell antibody positivity seems to be a significant risk factor for IM and IM with atrophy. Autoimmune thyroiditis-related antibodies and ANA positivity by itself were only associated with atrophy; SLE-related antibodies and inflammatory bowel diseases related antibodies (ASCA and ANCA) correlated either with IM or with atrophy. No significant relationship was found between any other investigated autoimmune disease-related antibodies and precancerous lesions.
   Conclusions: Autoimmune positivity often underlies gastritis of unknown aetiology and predisposes to precancerous lesions in the stomach. These antibodies can serve as non-invasive markers for the of optimal timing of an endoscopic follow-up strategy. Furthermore, CG can be an early symptom of a systemic autoimmune disorder.
C1 [Zadori, Noemi; Nemeth, David; Szako, Lajos; Vancsa, Szilard; Vorhendi, Nora; Szakacs, Zsolt; Frim, Levente; Hegyi, Peter; Czimmer, Jozsef] Univ Pecs, Med Sch, Inst Translat Med, Pecs, Hungary.
   [Zadori, Noemi; Szako, Lajos; Vancsa, Szilard; Vorhendi, Nora; Hegyi, Peter] Univ Pecs, Janos Szentagothai Res Ctr, Pecs, Hungary.
   [Szakacs, Zsolt] Univ Pecs, Med Sch, Dept Internal Med 1, Ifjusag St 13, H-7624 Pecs, Hungary.
   [Hegyi, Peter] Semmelweis Univ, Ctr Translat Med, Budapest, Hungary.
   [Hegyi, Peter] Semmelweis Univ, Heart & Vasc Ctr, Div Pancreat Dis, Budapest, Hungary.
   [Czimmer, Jozsef] Univ Pecs, Med Sch, Dept Internal Med 1, Div Gastroenterol, Pecs, Hungary.
C3 University of Pecs; University of Pecs; University of Pecs; Semmelweis
   University; Semmelweis University; University of Pecs
RP Czimmer, J (corresponding author), Univ Pecs, Med Sch, Dept Internal Med 1, Ifjusag St 13, H-7624 Pecs, Hungary.
EM czimmer.jozsef@pte.hu
RI Hegyi, Péter/B-3163-2016
OI Frim, Levente/0000-0003-0097-6663
FU STAY ALIVE project [GINOP-2.3.2-15-2016-00048]; European Union (European
   Regional Development Fund); Human Resources Development Operational
   Programme Grant [EFOP-3.6.2-16-2017-00006]
FX This study was funded by the GINOP-2.3.2-15-2016-00048 -STAY ALIVE
   project, co-financed by the European Union (European Regional
   Development Fund) within the Szechenyi 2020 Programme, and by a Human
   Resources Development Operational Programme Grant, Grant Number:
   EFOP-3.6.2-16-2017-00006 -LIVE LONGER, co-financed by the European Union
   (European Regional Development Fund) within the Szechenyi 2020
   Programme. The funders had no role in the study design, data collection
   and analysis, or the decision to publish or the preparation of the
   manuscript.
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NR 34
TC 5
Z9 5
U1 0
U2 3
PU MEDICAL UNIV PRESS
PI CLUJ-NAPOCA
PA 3RD MEDICAL CLINIC, STR CROITORILOR NO 19-21, CLUJ-NAPOCA, 400162,
   ROMANIA
SN 1841-8724
EI 1842-1121
J9 J GASTROINTEST LIVER
JI J. Gastrointest. Liver Dis.
PD JUN
PY 2022
VL 31
IS 2
BP 168
EP 175
DI 10.15403/jgld-4218
EA MAY 2022
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 2D2FD
UT WOS:000805990400001
PM 35574624
OA gold
DA 2025-06-01
ER

PT J
AU Marshall, ACJ
   Alderuccio, F
   Murphy, K
   Toh, BH
AF Marshall, ACJ
   Alderuccio, F
   Murphy, K
   Toh, BH
TI Mechanisms of gastric mucosal cell loss in autoimmune gastritis
SO INTERNATIONAL REVIEWS OF IMMUNOLOGY
LA English
DT Review
DE Fas; Fas ligand; apoptosis
ID TUMOR-NECROSIS-FACTOR; GROWTH-FACTOR-ALPHA; TRANSGENIC MICE; TNF
   RECEPTOR; PARIETAL-CELLS; DEFICIENT MICE; T-CELLS; FAS; DIFFERENTIATION;
   PATHOGENESIS
AB The causes of target cell death in organ-specific autoimmune diseases are not precisely known. In the case of EAG, parietal cell death depends on Th1. CD4 T cells and Fas/Fas-ligand, either through interaction between infiltrating CD4 T cells with gastric parietal cells that have upregulated Fas expression or through homotypic interactions between the parietal cells. TNF-alpha does not appear to have a role in this process. The accompanying loss of zymogenic cells is likely a consequence of the interruption of the normal developmental pathway in the gastric mucosa that follows the destruction of parietal cells in the gastric mucosa.
C1 Monash Univ, Sch Med, Dept Pathol & Immunol, Prahran, Vic 3181, Australia.
C3 Monash University
RP Monash Univ, Sch Med, Dept Pathol & Immunol, Commercial Rd, Prahran, Vic 3181, Australia.
EM ban-hock.toh@med.monash.edu.au
RI Murphy, Kim/JLL-0314-2023; Alderuccio, Frank/D-5808-2011
OI Alderuccio, Frank/0000-0003-4853-3394
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NR 29
TC 4
Z9 6
U1 0
U2 0
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0883-0185
EI 1563-5244
J9 INT REV IMMUNOL
JI Int. Rev. Immunol.
PD JAN-APR
PY 2005
VL 24
IS 1-2
BP 123
EP 134
DI 10.1080/08830180590884567
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 888QN
UT WOS:000226389400007
PM 15763993
DA 2025-06-01
ER

PT J
AU Gravina, AG
   Priadko, K
   Ciamarra, P
   Granata, L
   Facchiano, A
   Miranda, A
   Dallio, M
   Federico, A
   Romano, M
AF Gravina, Antonietta G.
   Priadko, Kateryna
   Ciamarra, Paola
   Granata, Lucia
   Facchiano, Angela
   Miranda, Agnese
   Dallio, Marcello
   Federico, Alessandro
   Romano, Marco
TI Extra-Gastric Manifestations of Helicobacter pylori Infection
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE extra-gastric manifestations; H; pylori; vitamin B12 deficiency anemia;
   iron deficiency anemia; ophthalmic manifestations; dermatologic
   manifestations; IBD; eosinophilic esophagitis; Parkinson&#8217; s
   disease; diabetes mellitus; allergy
ID CENTRAL SEROUS CHORIORETINOPATHY; INTESTINAL BACTERIAL OVERGROWTH;
   AUTOIMMUNE BULLOUS DISEASES; INFLAMMATORY-BOWEL-DISEASE; FORMYL PEPTIDE
   RECEPTORS; IRON-DEFICIENCY; CEREBROSPINAL-FLUID; ULCERATIVE-COLITIS;
   EPITHELIAL-CELLS; INCREASED RISK
AB Helicobacter Pylori (H. pylori) is a Gram-negative flagellated microorganism that has been extensively studied since its first isolation due to its widespread diffusion and association with numerous diseases. While the bacterium is proved to be a causative factor for a number of gastric diseases such as gastritis, gastric adenocarcinoma, and MALT-lymphoma, its role at other gastrointestinal levels and in other systems is being thoroughly studied. In this article, we reviewed the latest published clinical and laboratory studies that investigated associations of H. pylori with hematologic diseases such as Vitamin B12- and iron-deficiency anemia, primary immune thrombocytopenia, and with a number of dermatologic and ophthalmic diseases. In addition, the putative role of the bacterium in inflammatory bowel diseases, esophageal disorders, metabolic, diseases, neurologic diseases and allergy were outlined.
C1 [Gravina, Antonietta G.; Priadko, Kateryna; Ciamarra, Paola; Granata, Lucia; Facchiano, Angela; Miranda, Agnese; Dallio, Marcello; Federico, Alessandro; Romano, Marco] Univ Campania Luigi Vanvitelli, Dept Precis Med, Hepatogastroenterol Div, Via Pansini 5, I-80131 Naples, Italy.
C3 Universita della Campania Vanvitelli
RP Gravina, AG; Romano, M (corresponding author), Univ Campania Luigi Vanvitelli, Dept Precis Med, Hepatogastroenterol Div, Via Pansini 5, I-80131 Naples, Italy.
EM antoniettagerarda.gravina@unicampania.it;
   kateryna.priadko@unicampania.it; pciamarra@hotmail.com;
   luciagranata91@gmail.com; angela.facchiano@gmail.com;
   mirandaagnese@gmail.com; marcello.dallio@gmail.com;
   alessandro.federico@unicampania.it; marco.romano@unicampania.it
RI Federico, Alessandro/AAB-3893-2019; Dallio, Marcello/ABG-7693-2020;
   Romano, Marco/G-9300-2016; Gravina, Antonietta Gerarda/AAC-1528-2019
OI Priadko, Kateryna/0000-0003-3551-1006; Gravina, Antonietta
   Gerarda/0000-0001-8049-0115; Granata, Lucia/0000-0002-1370-0394;
   Federico, Alessandro/0000-0002-0885-0793; DALLIO,
   MARCELLO/0000-0003-4153-815X
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NR 100
TC 64
Z9 65
U1 0
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD DEC
PY 2020
VL 9
IS 12
AR 3887
DI 10.3390/jcm9123887
PG 17
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA PJ9VI
UT WOS:000602105000001
PM 33265933
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Appelmelk, BJ
   SimoonsSmit, I
   Negrini, R
   Moran, AP
   Aspinall, GO
   Forte, JG
   DeVries, T
   Quan, H
   Verboom, T
   Maaskant, JJ
   Ghiara, P
   Kuipers, EJ
   Bloemena, E
   Tadema, TM
   Townsend, RR
   Tyagarajan, K
   Crothers, JM
   Monteiro, MA
   Savio, A
   DeGraaff, J
AF Appelmelk, BJ
   SimoonsSmit, I
   Negrini, R
   Moran, AP
   Aspinall, GO
   Forte, JG
   DeVries, T
   Quan, H
   Verboom, T
   Maaskant, JJ
   Ghiara, P
   Kuipers, EJ
   Bloemena, E
   Tadema, TM
   Townsend, RR
   Tyagarajan, K
   Crothers, JM
   Monteiro, MA
   Savio, A
   DeGraaff, J
TI Potential role of molecular mimicry between Helicobacter pylori
   lipopolysaccharide and host Lewis blood group antigens in autoimmunity
SO INFECTION AND IMMUNITY
LA English
DT Article
ID PERNICIOUS-ANEMIA; H+,K+-ADENOSINE TRIPHOSPHATASE; BETA-SUBUNIT;
   H+/K+-ATPASE; PROTON PUMP; GASTRITIS; ANTIBODIES; PURIFICATION;
   PROTEINS; STOMACH
AB Helicobacter pylori is involved in gastritis, gastric and duodenal ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Earlier studies already suggested a role for autoimmune phenomena in H. pylori-linked disease. We now report that lipopolysaccharides (LPS) of H. pylori express Lewis y, Lewis x, and H type I blood group structures similar to those commonly occurring in gastric mucosa. Immunization of mice and rabbits with H. pylori cells or purified LPS induced an anti-Lewis x or y or anti-a type I response, yielding antibodies that bound human and murine gastric glandular tissue, granulocytes, adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma cells. Experimental oral infections in mice or natural infection in humans yielded anti-Lewis antibodies also. The beta chain of gastric H+,K+-ATPase, the parietal cell proton pump involved in acid secretion, contained Lewis y epitopes; gastric mucin contained Lewis x and y antigenic determinants. Growth in mice of a hybridoma that secretes H. pylori-induced anti-Lewis y monoclonal antibodies resulted in histopathological evidence of gastritis, which indicates a direct pathogenic role for anti-Lewis antibodies. In conclusion, our observations demonstrate that molecular mimicry between H. pylori LPS and the host, based on Lewis antigens, and provide understanding of an autoimmune mechanism for H. pylori-associated type B gastritis.
C1 VRIJE UNIV AMSTERDAM,SCH MED,DEPT MED CHEM,1081 BT AMSTERDAM,NETHERLANDS.
   VRIJE UNIV AMSTERDAM,SCH MED,DEPT GASTROENTEROL,1081 BT AMSTERDAM,NETHERLANDS.
   VRIJE UNIV AMSTERDAM,SCH MED,DEPT PATHOL,1081 BT AMSTERDAM,NETHERLANDS.
   ACAD HOSP,1081 BT AMSTERDAM,NETHERLANDS.
   SPEDALI CIVIL BRESCIA,BIOTECHNOL LAB,BRESCIA,ITALY.
   S ORSOLA FATEBENEFRATELLI HOSP,BRESCIA,ITALY.
   IMMUNOBIOL RES INST,SIENA,ITALY.
   UNIV COLL,DEPT MICROBIOL,GALWAY,IRELAND.
   YORK UNIV,DEPT CHEM,N YORK,ON M3J 1P3,CANADA.
   UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720.
   UNIV CALIF SAN FRANCISCO,DEPT PHARMACEUT CHEM,SAN FRANCISCO,CA 94143.
C3 Vrije Universiteit Amsterdam; Vrije Universiteit Amsterdam; Vrije
   Universiteit Amsterdam; Hospital Spedali Civili Brescia; Ollscoil na
   Gaillimhe-University of Galway; York University - Canada; University of
   California System; University of California Berkeley; University of
   California System; University of California San Francisco
RP Appelmelk, BJ (corresponding author), VRIJE UNIV AMSTERDAM,SCH MED,DEPT MED MICROBIOL,VAN BOECHORSTRAAT 7,1081 BT AMSTERDAM,NETHERLANDS.
RI Kuipers, Ernst/H-3293-2019; Bloemena, Elisabeth/V-1095-2018
OI Bloemena, Elisabeth/0000-0002-0221-9538; Kuipers, Ernst
   J./0000-0002-0633-3098
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NR 44
TC 366
Z9 395
U1 0
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD JUN
PY 1996
VL 64
IS 6
BP 2031
EP 2040
DI 10.1128/IAI.64.6.2031-2040.1996
PG 10
WC Immunology; Infectious Diseases
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Infectious Diseases
GA UN189
UT WOS:A1996UN18900022
PM 8675304
OA Green Published, Bronze
DA 2025-06-01
ER

PT J
AU Filippou, PS
   Ren, AH
   Korbakis, D
   Dimitrakopoulos, L
   Soosaipillai, A
   Barak, V
   Frenkel, S
   Pe'er, J
   Lotem, M
   Merims, S
   Molina, R
   Blasutig, I
   Bogdanos, DP
   Diamandis, EP
AF Filippou, Panagiota S.
   Ren, Annie H.
   Korbakis, Dimitrios
   Dimitrakopoulos, Lampros
   Soosaipillai, Antoninus
   Barak, Vivian
   Frenkel, Shahar
   Pe'er, Jacob
   Lotem, Michal
   Merims, Sharon
   Molina, Rafael
   Blasutig, Ivan
   Bogdanos, Dimitrios P.
   Diamandis, Eleftherios P.
TI Exploring the potential of mucin 13 (MUC13) as a biomarker for
   carcinomas and other diseases
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE autoimmune diseases; cancer cell lines; immunoassays; malignancies;
   MUC13; renal failure
ID CELL-SURFACE MUCIN; OVARIAN-CANCER; MONOCLONAL-ANTIBODY; GASTRIC-CANCER;
   EXPRESSION; OVEREXPRESSION; INFLAMMATION; ONCOPROTEIN; PROGRESSION;
   PROGNOSIS
AB Background: Mucin 13 (MUC13) is a cell surface glycoprotein aberrantly expressed in a variety of epithelial carcinomas. Thus far, the role of MUC13 in various diseases remains elusive. To the best of our knowledge, this is the first study to examine the potential of MUC13 as a serum biomarker in a variety of carcinomas and other conditions.
   Methods: We developed a recombinant MUC13 protein, mouse monoclonal antibodies and enzyme immunoassay (ELISA) for MUC13. We used this assay to measure MUC13 levels in the supernatants of cancer cell lines and a large cohort of serum samples from healthy and diseased individuals.
   Results: MUC13 is secreted from cancer cell lines, with highest levels found in ovarian cancer cell lines. MUC13 levels in human sera were significantly increased in patients with renal failure and 20%-30% of patients with ovarian, liver, lung and other cancers. MUC13 was also elevated in 70% of patients with active cutaneous melanoma, but not uveal melanoma. Furthermore, we identified significant MUC13 elevations in the serum of patients with vasculitis (ANCA-positive) autoantibodies, but not in those with inflammatory bowel disease.
   Conclusions: Serum MUC13 is frequently elevated not only in a variety of malignant cases but also in some benign pathologies, thus appearing to be a non-specific disease biomarker. Nonetheless, serum MUC13 is clearly highly elevated in some carcinoma patients, and its relationship with tumor progression in this context warrant further research. Future studies that examine the correlation between serum MUC13 levels to stage of cancer could elucidate prognostic potential.
C1 [Diamandis, Eleftherios P.] Mt Sinai Hosp, Joseph & Wolf Lebov Ctr, 60 Murray St Box 32,Flr 6 Rm L6-201, Toronto, ON M5T 3L9, Canada.
   [Filippou, Panagiota S.; Ren, Annie H.; Korbakis, Dimitrios; Dimitrakopoulos, Lampros; Diamandis, Eleftherios P.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
   [Filippou, Panagiota S.; Blasutig, Ivan; Diamandis, Eleftherios P.] Univ Hlth Network, Dept Clin Biochem, Toronto, ON, Canada.
   [Ren, Annie H.; Dimitrakopoulos, Lampros; Soosaipillai, Antoninus; Diamandis, Eleftherios P.] Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON, Canada.
   [Korbakis, Dimitrios; Diamandis, Eleftherios P.] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada.
   [Barak, Vivian] Hadassah Hebrew Univ, Dept Oncol, Med Ctr, Jerusalem, Israel.
   [Frenkel, Shahar; Pe'er, Jacob] Hadassah Hebrew Univ, Dept Ophthalmol, Med Ctr, Jerusalem, Israel.
   [Lotem, Michal; Merims, Sharon] Hadassah Hebrew Univ Hosp, Sharett Inst Oncol, Jerusalem, Israel.
   [Molina, Rafael] Univ Barcelona, Hosp Clin, Barcelona, Spain.
   [Bogdanos, Dimitrios P.] Univ Thessaly, Dept Rheumatol & Clin Immunol, Larisa, Greece.
C3 University of Toronto; Sinai Health System Toronto; University of
   Toronto; University of Toronto; University Health Network Toronto;
   University of Toronto; Sinai Health System Toronto; Lunenfeld Tanenbaum
   Research Institute; University of Toronto; Sinai Health System Toronto;
   Lunenfeld Tanenbaum Research Institute; Hebrew University of Jerusalem;
   Hadassah University Medical Center; Hebrew University of Jerusalem;
   Hadassah University Medical Center; Hebrew University of Jerusalem;
   Hadassah University Hospital; Hadassah University Medical Center;
   University of Barcelona; Hospital Clinic de Barcelona; University of
   Thessaly
RP Diamandis, EP (corresponding author), Mt Sinai Hosp, Joseph & Wolf Lebov Ctr, 60 Murray St Box 32,Flr 6 Rm L6-201, Toronto, ON M5T 3L9, Canada.; Diamandis, EP (corresponding author), Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Univ Hlth Network, Dept Clin Biochem, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Mt Sinai Hosp, Dept Pathol & Lab Med, Toronto, ON, Canada.; Diamandis, EP (corresponding author), Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada.
EM Eleftherios.Diamandis@sinaihealthsystem.ca
RI Peer, Jacob/HSE-3187-2023; Filippou, Panagiota/ABF-1969-2021; Bogdanos,
   Dimitrios/AAF-8620-2020
OI Filippou, Panagiota/0000-0003-3974-988X; Diamandis,
   Eleftherios/0000-0002-1589-820X; Bogdanos, Dimitrios/0000-0002-9697-7902
FU Mount Sinai Hospital
FX This study was funded by the principal investigator's research fund from
   Mount Sinai Hospital.
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NR 37
TC 14
Z9 18
U1 2
U2 16
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD NOV
PY 2018
VL 56
IS 11
BP 1945
EP 1953
DI 10.1515/cclm-2018-0139
PG 9
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA GV8UV
UT WOS:000446425900026
PM 29768245
DA 2025-06-01
ER

PT J
AU Alexandraki, KI
   Nikolaou, A
   Thomas, D
   Syriou, V
   Korkolopoulou, P
   Sougioultzis, S
   Kaltsas, G
AF Alexandraki, Krystallenia I.
   Nikolaou, Argiro
   Thomas, Dimitrios
   Syriou, Vassiliki
   Korkolopoulou, Penelope
   Sougioultzis, Stavros
   Kaltsas, Gregory
TI Are patients with autoimmune thyroid disease and autoimmune gastritis at
   risk of gastric neuroendocrine neoplasms type 1?
SO CLINICAL ENDOCRINOLOGY
LA English
DT Article
ID ATROPHIC BODY GASTRITIS; PARIETAL-CELL ANTIBODIES; FOLLOW-UP;
   CLASSIFICATION; AUTOANTIBODIES; CARCINOIDS; PREVALENCE; LESIONS; ANEMIA;
   TUMORS
AB ObjectiveThe aim of this study was to investigate the prevalence of autoimmune gastritis, enterochromaffin-like cell (ECL-cell) hyperplasia and gastric neuroendocrine neoplasms type 1 (GNEN1) in patients with autoimmune thyroid disease.
   DesignProspective observational study in a single institutional study.
   Patients and MeasurementsOne hundred and twenty patients with autoimmune thyroid disease were consecutively recruited from the Endocrine Unit. Upper gastrointestinal tract endoscopy (UGE) and biochemical parameters for autoimmune thyroid disease and autoimmune gastritis were assessed at recruitment and annually thereafter in patients with a mean follow-up of 375144months. Autoimmune gastritis was defined by the presence of antiparietal cell antibodies (APCA) and histological confirmation after UGE. Serum gastrin and chromogranin were also measured.
   ResultsOne hundred and eleven patients had Hashimoto's thyroiditis and nine Graves' disease. Autoimmune gastritis was identified in 40 (38 with Hashimoto's thyroiditis and two with Graves' disease) patients all of whom had increased levels of gastrin and chromogranin ; Helicobacter pylori infection was histologically identified in 15 of 40 (375%) patients. Six patients had isolated nodular ECL-cell hyperplasia and one mixed nodular and linear ECL-cell hyperplasia [7 of 40 (175%)]. Only increased gastrin (P=003) levels predicted the presence ECL-cell hyperplasia. A GNEN1 developed in one patient with nodular ECL-cell hyperplasia after 39months of follow-up.
   ConclusionsConcomitant autoimmune gastritis was found in 333% of patients with autoimmune thyroid disease, 175% of whom had ECL-cell hyperplasia that evolved to GNEN1 in one (25%). Larger studies with longer follow-up are needed to define the incidence of GNEN1 in patients with autoimmune thyroid disease and ECL-cell hyperplasia and potential implications.
C1 [Alexandraki, Krystallenia I.; Nikolaou, Argiro; Thomas, Dimitrios; Syriou, Vassiliki; Kaltsas, Gregory] Univ Athens, Dept Pathophysiol, Endocrine Unit, Athens 11528, Greece.
   [Korkolopoulou, Penelope] Univ Athens, Dept Pathol 1, Athens 11528, Greece.
   [Sougioultzis, Stavros] Univ Athens, Dept Pathophysiol, Gastroenterol Unit, Athens 11528, Greece.
C3 National & Kapodistrian University of Athens; National & Kapodistrian
   University of Athens; National & Kapodistrian University of Athens
RP Alexandraki, KI (corresponding author), Laiko Univ Hosp, Athens Med Sch, Endocrine Unit, Dept Pathophysiol, Mikras Asias 75, Athens 11527, Greece.
EM alexandrakik@gmail.com
RI Kaltsas, Gregory/AAD-7193-2019; Alexandraki, Krystallenia/S-4058-2019;
   Syriou, Vassiliki/HSD-9211-2023; Nikolaou, Argyro/GRO-2701-2022
OI Nikolaou, Argyro/0000-0002-1604-6113; Alexandraki,
   Krystallenia/0000-0003-2398-6768; Kaltsas, Gregory/0000-0002-5876-7883
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NR 20
TC 24
Z9 24
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD MAY
PY 2014
VL 80
IS 5
BP 685
EP 690
DI 10.1111/cen.12346
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA AE3XP
UT WOS:000333912100011
PM 24118101
OA Bronze
DA 2025-06-01
ER

PT J
AU Horita, S
   Fujii, H
   Mizushima, I
   Fujisawa, Y
   Hara, S
   Yamada, K
   Inoue, D
   Nakajima, K
   Harada, K
   Kawano, M
AF Horita, Shigeto
   Fujii, Hiroshi
   Mizushima, Ichiro
   Fujisawa, Yuhei
   Hara, Satoshi
   Yamada, Kazunori
   Inoue, Dai
   Nakajima, Kenichi
   Harada, Kenichi
   Kawano, Mitsuhiro
TI A case of IgG4-related tubulointerstitial nephritis and membranous
   glomerulonephritis during the clinical course of gastric cancer: Imaging
   features of IgG4-related kidney disease
SO MODERN RHEUMATOLOGY
LA English
DT Article
DE Fluorodeoxyglucose positron emission tomography; IgG4; Malignancy;
   Membranous glomerulonephritis; Tubulointerstitial nephritis
ID AUTOIMMUNE PANCREATITIS; RISK; MALIGNANCIES; DIAGNOSIS
AB We describe an 81-year-old man with immunoglobulin G4-related disease (IgG4-RD) presenting with submandibular gland, lymph node, lung, kidney, aortic wall, and prostate lesions with concomitant gastric cancer. After curative surgical treatment of the gastric cancer, corticosteroid therapy for progressively decreasing renal function was started. Before starting steroid therapy, fluorodeoxyglucose positron emission tomography-computed tomography revealed multiple lesions of IgG4-RD but no metastasis of the cancer. However, the patient died 3 months after initiation of corticosteroid therapy because of recurrence of the gastric cancer. In this case, the imaging features of IgG4-tubulointerstitial nephritis dramatically changed during the clinical course of co-existing gastric cancer. The imaging features of the present case may provide clues to the pattern of spread of IgG4 lesions in the kidney.
C1 [Horita, Shigeto; Fujii, Hiroshi; Mizushima, Ichiro; Fujisawa, Yuhei; Hara, Satoshi; Yamada, Kazunori; Kawano, Mitsuhiro] Kanazawa Univ, Grad Sch Med, Div Rheumatol, Kanazawa, Ishikawa, Japan.
   [Inoue, Dai] Kanazawa Univ, Grad Sch Med Sci, Dept Radiol, Kanazawa, Ishikawa, Japan.
   [Nakajima, Kenichi] Kanazawa Univ, Dept Nucl Med, Kanazawa, Ishikawa, Japan.
   [Harada, Kenichi] Kanazawa Univ, Grad Sch Med, Dept Human Pathol, Kanazawa, Ishikawa, Japan.
C3 Kanazawa University; Kanazawa University; Kanazawa University; Kanazawa
   University
RP Kawano, M (corresponding author), Kanazawa Univ Hosp, Div Rheumatol, 13-1 Takaramachi, Kanazawa, Ishikawa 9208641, Japan.
EM sk33166@gmail.com
RI Hara, Satoshi/AAA-3930-2020
OI Hara, Satoshi/0000-0002-3640-4133; Fujisawa, Yuhei/0000-0002-1718-0752
FU Health and Labour Sciences Research Grants for the Study of Intractable
   Disease from Ministry of Health, Labor and Welfare, Japan
FX This work was supported in part by grants from Health and Labour
   Sciences Research Grants for the Study of Intractable Disease from
   Ministry of Health, Labor and Welfare, Japan.
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NR 18
TC 5
Z9 6
U1 0
U2 6
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1439-7595
EI 1439-7609
J9 MOD RHEUMATOL
JI Mod. Rheumatol.
PD MAY 4
PY 2019
VL 29
IS 3
BP 542
EP 546
DI 10.1080/14397595.2016.1245238
PG 5
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA HV7PC
UT WOS:000466172000022
PM 27785920
DA 2025-06-01
ER

PT J
AU Panarese, A
AF Panarese, Alba
TI Endoscopic resection for early gastric cancer: Towards a global
   understanding
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Early gastric cancer; Artificial intelligence; Malignancy; Helicobacter
   pylori; Autoimmune gastritis; Dysplasia
AB Gastric cancer is widespread globally, and disease diagnosis is accompanied by high mortality and morbidity rates. However, prognoses and survivability have improved following implementation of surveillance and screening programs, which have led to earlier diagnoses. Indeed, early diagnosis itself supports increased surgical curability, which is the main treatment goal and guides therapeutic choice. The most recent Japanese guidelines for endoscopic submucosal dissection and endoscopic mucosal resection for early gastric cancer consider the degree of endoscopic curability in relation to the characteristics of the gastric lesions. In clinical practice, the management approach for both prevention and treatment should be similar to that of colon lesions; however, unlike the established practices for colorectal cancer, the diagnostic and therapeutic pathways are not shared nor widespread for gastric cancer. Ultimately, this negatively impacts the opportunity to perform an endoscopic resection with curative intent.
C1 [Panarese, Alba] Cent Hosp, Dept Gastroenterol & Digest Endoscopy, I-74123 Taranto, Italy.
   [Panarese, Alba] Cent Hosp, Dept Gastroenterol & Digest Endoscopy, 1 Francesco Bruno St, I-74123 Taranto, Italy.
RP Panarese, A (corresponding author), Cent Hosp, Dept Gastroenterol & Digest Endoscopy, 1 Francesco Bruno St, I-74123 Taranto, Italy.
EM albapanarese@libero.it
RI panarese, alba/AGJ-3243-2022
OI Panarese, Alba/0000-0002-6931-2171
CR Arnold M, 2020, GUT, V69, P823, DOI 10.1136/gutjnl-2019-320234
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   International Agency for ResearchonCancer, GLOB 2020 STOM CANC
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NR 11
TC 3
Z9 3
U1 0
U2 13
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD APR 7
PY 2022
VL 28
IS 13
BP 1377
EP 1379
DI 10.3748/wjg.v28.i13.1377
PG 3
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 1I6KR
UT WOS:000797337500008
PM 35645546
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Jebreel, A
   England, J
   Bedford, K
   Murphy, J
   Karsai, L
   Atkin, S
AF Jebreel, Ala'eddin
   England, James
   Bedford, Karen
   Murphy, Justin
   Karsai, Laszlo
   Atkin, Stephen
TI Vascular endothelial growth factor (VEGF), VEGF receptors expression and
   microvascular density in benign and malignant thyroid diseases
SO INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE MVD; thyroid; VEGF; VEGF receptors
ID SQUAMOUS-CELL CARCINOMA; INDEPENDENT PROGNOSTIC INDICATOR; TUMOR
   ANGIOGENESIS; BREAST-CANCER; GASTRIC-CARCINOMA; BLADDER-CANCER;
   GRAVES-DISEASE; PROLIFERATION; ASSOCIATION; METASTASIS
AB Angiogenesis is critical for the growth and metastatic spread of tumours. Vascular endothelial growth factor (VEGF) is the most potent inducer of neovasculature, and its increased expression has been related to a worse clinical outcome in many diseases. The purpose of this study was to evaluate the relation between VEGF, its receptors (VEGFR-1 and VEGFR-2) and microvessel density (MVD) in thyroid diseases. Immunostaining for VEGF and VEGF receptors was performed in 66 specimens of thyroid tissue, comprising 17 multinodular goitre (MNG), 14 Graves' disease, 10 follicular adenoma, 8 Hashimoto's thyroiditis, 7 papillary carcinoma and 10 normal thyroid specimens. Thyrocyte positivity for VEGF and VEGF receptors was scored 0-3. Immunohistochemistry for CD31, and CD34 on the same sections was performed to evaluate MVD. Immunohistochemical staining of VEGF in thyrocytes was positive in 92% of all the thyroid tissues studied. Using an immunostaining intensity cut off of 2, increased thyrocyte staining was seen in follicular adenoma specimens, MNG and normal thyroids compared with Hashimoto's thyroiditis and Graves' disease (P < 0.05). Similarly, VEGF thyrocyte expression in Graves' disease was less than other pathologies (P < 0.05). VEGFR-1 expression and the average MVD score did not differ between the different thyroid pathologies. VEGF expression was lower in autoimmune pathologies compared to autonomous growth processes. Conversely, both VEGFR-1 and VEGFR-2 were widely expressed in benign and neoplastic thyroid disease, suggesting that the up-regulation of VEGF and not its receptors occurs as tissue becomes autonomous. There was no clear relationship between MVD measurement and thyroid pathology.
C1 Hull Royal Infirm, Dept Otolaryngol, Kingston Upon Hull HU3 2JZ, N Humberside, England.
   Hull Royal Infirm, Kingston Upon Hull HU3 2JZ, N Humberside, England.
C3 University of Hull; University of Hull
RP Atkin, S (corresponding author), Michael White Diabet Ctr, Hull York Med Sch, Head Acad Endocrinol Diabet & Metab, 220-236 Anlaby Rd, Kingston Upon Hull HU3 2RW, N Humberside, England.
EM s.l.arkin@hull.ac.uk
RI Atkin, stephen/ABE-7047-2020; Atkin, Stephen/D-7400-2014
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NR 48
TC 75
Z9 89
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0959-9673
EI 1365-2613
J9 INT J EXP PATHOL
JI Int. J. Exp. Pathol.
PD AUG 7
PY 2007
VL 88
IS 4
BP 271
EP 277
DI 10.1111/j.1365-2613.2007.00533.x
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 203TZ
UT WOS:000248998200010
PM 17696908
OA Green Published
DA 2025-06-01
ER

PT J
AU Dugan, JP
   Coleman, CB
   Haverkos, B
AF Dugan, James P.
   Coleman, Carrie B.
   Haverkos, Bradley
TI Opportunities to Target the Life Cycle of Epstein-Barr Virus (EBV) in
   EBV-Associated Lymphoproliferative Disorders
SO FRONTIERS IN ONCOLOGY
LA English
DT Review
DE EBV (Epstein-Barr virus); EBV-associated cancers; Lymphoproliferative
   disease (LPD); EBV latency; viral life cycle inhibitors
ID POSITIVE GASTRIC-CARCINOMA; LATENT MEMBRANE PROTEIN-1; NK/T-CELL
   LYMPHOMA; NERVOUS-SYSTEM LYMPHOMA; TUMOR-SUPPRESSOR GENES; NF-KAPPA-B;
   T-CELL; BURKITTS-LYMPHOMA; PROMOTER HYPERMETHYLATION; TRANSCRIPTIONAL
   ANALYSIS
AB Many lymphoproliferative disorders (LPDs) are considered "EBV associated" based on detection of the virus in tumor tissue. EBV drives proliferation of LPDs via expression of the viral latent genes and many pre-clinical and clinical studies have shown EBV-associated LPDs can be treated by exploiting the viral life cycle. After a brief review of EBV virology and the natural life cycle within a host we will discuss the importance of the viral gene programs expressed during specific viral phases, as well as within immunocompetent vs. immunocompromised hosts and corresponding EBV-associated LPDs. We will then review established and emerging treatment approaches for EBV-associated LPDs based on EBV gene expression programs. Patients with EBV-associated LPDs can have a poor performance status, multiple comorbidities, and/or are immunocompromised from organ transplantation, autoimmune disease, or other congenital or acquired immunodeficiency making them poor candidates to receive intensive cytotoxic chemotherapy. With the emergence of EBV-directed therapy there is hope that we can devise more effective therapies that confer milder toxicity.
C1 [Dugan, James P.; Haverkos, Bradley] Univ Colorado, Div Hematol, Aurora, CO 80045 USA.
   [Coleman, Carrie B.] Univ Colorado, Div Immunol, Aurora, CO USA.
C3 University of Colorado System; University of Colorado Anschutz Medical
   Campus; University of Colorado System; University of Colorado Anschutz
   Medical Campus
RP Haverkos, B (corresponding author), Univ Colorado, Div Hematol, Aurora, CO 80045 USA.
EM bradley.haverkos@ucdenver.edu
FU National Cancer Institute of the National Institutes of Health [L30
   CA189070]
FX BH was supported by the National Cancer Institute of the National
   Institutes of Health grant L30 CA189070.
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NR 145
TC 35
Z9 38
U1 1
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2234-943X
J9 FRONT ONCOL
JI Front. Oncol.
PD MAR 15
PY 2019
VL 9
AR 127
DI 10.3389/fonc.2019.00127
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA HP4LC
UT WOS:000461646500001
PM 30931253
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Zucca, E
   Bertoni, F
   Vannata, B
   Cavalli, F
AF Zucca, Emanuele
   Bertoni, Francesco
   Vannata, Barbara
   Cavalli, Franco
TI Emerging Role of Infectious Etiologies in the Pathogenesis of Marginal
   Zone B-cell Lymphomas
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HEPATITIS-C VIRUS; GASTRIC MALT LYMPHOMA; HELICOBACTER-PYLORI
   ERADICATION; NON-HODGKINS-LYMPHOMA; HCV INFECTION; CHLAMYDIA-PSITTACI;
   TISSUE LYMPHOMA; VILLOUS LYMPHOCYTES; NUCLEAR EXPRESSION; SPLENIC
   LYMPHOMA
AB Extranodal marginal zone B-cell lymphomas of the mucosa-associated lymphoid tissue (MALT) arise from lymphoid populations that are induced by chronic inflammation in extranodal sites. The most frequently affected organ is the stomach, where MALT lymphoma is incontrovertibly associated with a chronic gastritis induced by a microbial pathogen, Helicobacter pylori. Gastric MALT lymphoma therefore represents a paradigm for evaluating inflammation-associated lymphomagenesis, which may lead to a deeper understanding of a possible etiologic association between other microorganisms and nongastric marginal zone lymphomas. Besides infectious etiology, chronic inflammation caused by autoimmune diseases, such as Sjogren syndrome or Hashimoto thyroiditis, can also carry a significant risk factor for the development of marginal zone lymphoma. In addition to the continuous antigenic drive, additional oncogenic events play a relevant role in lymphoma growth and progression to the point at which the lymphoproliferative process may eventually become independent of antigenic stimulation. Recent studies on MALT lymphomas have in fact demonstrated genetic alterations affecting the NF-kappa B) pathway, a major signaling pathway involved in many cancers. This review aims to present marginal zone lymphoma as an example of the close pathogenetic link between chronic inflammation and tumor development, with particular attention to the role of infectious agents and the integration of these observations into everyday clinical practice. (C)2014 AACR.
C1 [Zucca, Emanuele; Bertoni, Francesco; Vannata, Barbara; Cavalli, Franco] Oncol Inst Southem Switzerland, Div Res, Lymphoma Unit, Bellinzona, Switzerland.
   [Bertoni, Francesco] IOR, Lymphoma & Genom Res Program, Bellinzona, Switzerland.
C3 Institute of Oncology Research (IOR); Institute of Oncology Research
   (IOR); Universita della Svizzera Italiana
RP Zucca, E (corresponding author), Osped San Giovanni Bellinzona, Oncol Inst Southem Switzerland IOSI, CH-6500 Bellinzona, Switzerland.
EM ielsg@ticino.com
RI Bertoni, Francesco/G-6922-2014
OI Bertoni, Francesco/0000-0001-5637-8983; Zucca,
   Emanuele/0000-0002-5522-6109
FU Oncosuisse-Swiss Federation Against Cancer [ICP OCS 02062-03-2007]
FX This work was supported in part by a grant from Oncosuisse-Swiss
   Federation Against Cancer (ICP OCS 02062-03-2007; to E. Zucca and F.
   Cavalli).
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NR 109
TC 75
Z9 77
U1 0
U2 15
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD OCT 15
PY 2014
VL 20
IS 20
BP 5207
EP 5216
DI 10.1158/1078-0432.CCR-14-0496
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AR9DW
UT WOS:000343873100008
PM 25320370
DA 2025-06-01
ER

PT J
AU Annibale, B
   Esposito, G
   Lahner, E
AF Annibale, Bruno
   Esposito, Gianluca
   Lahner, Edith
TI A current clinical overview of atrophic gastritis
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE Atrophic gastritis; iron deficiency anemia; vitamin B-12 deficiency;
   dyspepsia; Helicobacter pylori; chromoendoscopy; narrow-band imaging;
   gastric cancer
ID HELICOBACTER-PYLORI INFECTION; UPPER GASTROINTESTINAL ENDOSCOPY;
   AUTOIMMUNE THYROID-DISEASE; PARIETAL-CELL ANTIBODIES; INTESTINAL
   METAPLASIA; BODY GASTRITIS; FOLLOW-UP; IRON-DEFICIENCY; CANCER PATIENTS;
   GASTROESOPHAGEAL-REFLUX
AB Introduction: Atrophic gastritis (AG) is a complex syndrome which arises as a consequence of H. pylori infection or in the context of gastric autoimmunity. It often deserves a benign course but may lead to potentially life-threatening complications: cancer and anemia. This review aims to address traditional and innovative knowledge on this often under-diagnosed disorder. Areas covered: This review covers clinical presentation, risk factors, diagnosis, and management of AG and provides an updated resource for clinicians to get insight into this challenging disorder. Updated literature was searched in PubMed. Manual search from reference lists of publications was performed. Expert opinion: A case-finding strategy may be beneficial in individuals with anemia, dyspepsia, autoimmune thyropaties and type 1 diabetes, and family history of gastric cancer. AG is linked to gastric cancer risk and endoscopic surveillance is indicated according to topography of gastric atrophy and risk factors. The direction for future research in AG is summarized.
C1 [Annibale, Bruno; Esposito, Gianluca; Lahner, Edith] Sapienza Univ Rome, St Andrea Hosp, Dept Med Surg Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea
RP Annibale, B (corresponding author), Sapienza Univ Rome, St Andrea Hosp, Dept Med Surg Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM bruno.annibale@uniroma1.it
RI Esposito, Gianluca/J-7200-2019; Annibale, Bruno/A-5372-2008; Lahner,
   Edith/AAM-1039-2021
OI Esposito, Gianluca/0000-0002-2242-5048
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NR 134
TC 48
Z9 51
U1 3
U2 36
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD FEB 1
PY 2020
VL 14
IS 2
BP 93
EP 102
DI 10.1080/17474124.2020.1718491
EA JAN 2020
PG 10
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA KS2KU
UT WOS:000509024100001
PM 31951768
DA 2025-06-01
ER

PT J
AU Meindl, A
   Rao, MS
   Yang, GY
AF Meindl, Amanda
   Rao, M. Sambasiva
   Yang, Guang-Yu
TI Extranodal Rosai-Dorfman Disease With Mucosal Involvement of the Stomach
   in a Background of Autoimmune Atrophic Gastritis
SO INTERNATIONAL JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE Rosai-Dorfman disease; extranodal disease; gastrointestinal tract;
   autoimmune atrophic gastritis; carcinoid tumor
ID OF-THE-LITERATURE; MASSIVE LYMPHADENOPATHY; SINUS HISTIOCYTOSIS; TUMOR
AB Rosai-Dorfman disease (RDD), or sinus histiocytosis with massive lymphadenopathy, has been described involving both lymph nodes and extranodal sites, but extranodal RDD rarely involves the gastrointestinal tract. Although the etiology is unclear, several risk factors have been shown to be highly associated with this disease process, including viral infection and immune alterations. In this article, we present a case of a 79-year-old male with a history of autoimmune atrophic gastritis and multiple carcinoid tumors of the stomach presenting with a new stomach mass. An additional large sigmoid colon mass and adjacent enlarged lymph node was identified through imaging, prior to surgery. Through extensive pathologic analysis, we identified the first case of predominant extranodal RDD involving gastric mucosa and submucosa in a background of atrophic gastritis, with additional involvement of the sigmoid colon. Based on this case and literature review, we further discuss possible risk factors and pathogenesis of this disease process.
C1 [Meindl, Amanda; Rao, M. Sambasiva; Yang, Guang-Yu] Northwestern Mem Hosp, Chicago, IL 60611 USA.
C3 Northwestern Memorial Hospital
RP Yang, GY (corresponding author), Northwestern Univ, Dept Pathol, Feinberg Sch Med, 303 E Chicago Ave,Ward 4-115, Chicago, IL 60611 USA.
EM g-yang@northwestern.edu
OI Meindl, Amanda/0000-0003-4513-7919; Yang, Guang-Yu/0000-0002-5987-7750
FU NIH [DKI107767]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This
   research was supported by NIH (DKI107767).
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NR 15
TC 2
Z9 2
U1 1
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1066-8969
EI 1940-2465
J9 INT J SURG PATHOL
JI Int. J. Surg. Pathol.
PD OCT
PY 2018
VL 26
IS 7
BP 671
EP 675
DI 10.1177/1066896918773399
PG 5
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA GS5TF
UT WOS:000443733000018
PM 29720012
DA 2025-06-01
ER

PT J
AU Fornasarig, M
   Capuano, A
   Maiero, S
   Pivetta, E
   Guarnieri, G
   Canzonieri, V
   Zucchetto, A
   Mongiat, M
   Cannizzaro, R
   Spessotto, P
AF Fornasarig, Mara
   Capuano, Alessandra
   Maiero, Stefania
   Pivetta, Eliana
   Guarnieri, Giovanni
   Canzonieri, Vincenzo
   Zucchetto, Antonella
   Mongiat, Maurizio
   Cannizzaro, Renato
   Spessotto, Paola
TI pCLE highlights distinctive vascular patterns in early gastric cancer
   and in gastric diseases with high risk of malignant complications
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CONFOCAL LASER ENDOMICROSCOPY; DIAGNOSIS; CLASSIFICATION; METAPLASIA;
   WESTERN; ATROPHY
AB Endoscopy is widely used to detect and diagnose precancerous lesions and gastric cancer (GC). The probe-based Confocal Laser Endomicroscopy (pCLE) is an endoscopic technique suitable for subcellular resolution and for microvasculature analyses. The aim of this study was to use pCLE to identify specific vascular patterns in high-risk and early stage GC. Mucosal architecture, vessel tortuosity, enlargements and leakage were assessed in patients with autoimmune gastritis and early gastric cancer (EGC). We were able to stratify gastritis patients by identifying distinct vascular profiles: gastritis was usually associated with increased vascularization characterized by a high number of tortuous vessels, which were also found in atrophic autoimmune disease. Leaky and tortuous vessels, distributed in a spatially irregular network, characterized the atrophic metaplastic mucosa. The mucosal vasculature of EGC patients displayed tortuous vessels, but unlike what detected in atrophic gastritis, they appeared patchy, as is in neoplastic gastric tissue. Very importantly, we detected vascular changes even in areas without lesions, supporting the contention that vascular alterations may provide a favorable microenvironment for carcinogenesis. This report confirms that pCLE is a valid endoscopic approach to improve the definition of patients with malignant lesions or at increased risk for GC by assessing vascular changes.
C1 [Fornasarig, Mara; Maiero, Stefania; Guarnieri, Giovanni; Cannizzaro, Renato] IRCCS, Ctr Riferimento Oncol Aviano CRO, Oncol Gastroenterol, Aviano, Italy.
   [Capuano, Alessandra; Pivetta, Eliana; Mongiat, Maurizio; Spessotto, Paola] IRCCS, Ctr Riferimento Oncol Aviano CRO, Mol Oncol, Aviano, Italy.
   [Canzonieri, Vincenzo] IRCCS, Pathol Ctr Riferimento Oncol Aviano CRO, Aviano, Italy.
   [Canzonieri, Vincenzo] Univ Trieste, Dept Med Surg & Hlth Sci, Trieste, Italy.
   [Zucchetto, Antonella] IRCCS, Ctr Riferimento Oncol Aviano CRO, Unit Canc Epidemiol, Aviano, Italy.
C3 IRCCS Aviano (CRO); IRCCS Aviano (CRO); University of Trieste; IRCCS
   Aviano (CRO)
RP Fornasarig, M (corresponding author), IRCCS, Ctr Riferimento Oncol Aviano CRO, Oncol Gastroenterol, Aviano, Italy.
EM mfornasarig@cro.it
RI Guarnieri, Gabriella/O-2537-2016; Pivetta, Eliana/AAE-7969-2022;
   Mongiat, Maurizio/H-8297-2018; Maiero, Stefania/ABD-6092-2020;
   Fornasarig, Mara/ABD-5093-2020; Zucchetto, Antonella/ABC-8649-2020;
   Capuano, Alessandra/AAC-2129-2020; Canzonieri, Vincenzo/K-3141-2018;
   Cannizzaro, Renato/V-3804-2018; Spessotto, Paola/K-5005-2012
OI Zucchetto, Antonella/0000-0003-2812-6345; Capuano,
   Alessandra/0000-0002-5443-0570; Canzonieri,
   Vincenzo/0000-0001-6010-0976; Cannizzaro, Renato/0000-0002-2020-222X;
   Spessotto, Paola/0000-0002-3033-404X
FU Italian Ministry of Health [RF-2016-02361525]
FX This research was funded by the Italian Ministry of Health; Grant No.
   RF-2016-02361525.
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NR 37
TC 4
Z9 8
U1 1
U2 12
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 26
PY 2021
VL 11
IS 1
AR 21053
DI 10.1038/s41598-021-00550-w
PG 11
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA WN2SB
UT WOS:000711622600078
PM 34702885
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Vrkljan, AM
   Grasic, D
   Kruljac, I
   Nikolic, M
   Filipovic-Cugura, J
   Ulamec, M
   Kovacic, K
   Babic, N
   Ljubicic, N
AF Vrkljan, Ana Marija
   Grasic, David
   Kruljac, Ivan
   Nikolic, Marko
   Filipovic-Cugura, Jaksa
   Ulamec, Monika
   Kovacic, Ksenija
   Babic, Nenad
   Ljubicic, Neven
TI GASTRIC CARCINOID TYPE 1 IN A PATIENT WITH AUTOIMMUNE POLYGLANDULAR
   SYNDROME: ADDITIONAL ENDOCRINOLOGICAL EVALUATION REQUIRED
SO ACTA CLINICA CROATICA
LA English
DT Article
DE Stomach neoplasms; Carcinoid tumor; Polyendocrinopathies; autoimmune;
   Anemia, pernicious; Glucose intolerance; Diagnosis; differential; Case
   reports
ID CELL; MANAGEMENT; PREDICT; ADULTS
AB Autoimmune polyglandular syndrome by definition consists of two or more endocrinological insufficiencies or two organ specific autoimmune diseases. There are no stringent criteria for endocrinological evaluation of patients with one endocrine insufficiency. However, detailed endocrinological evaluation should be undertaken in patients with two autoimmune diseases. Additionally, follow up thereafter should be a must in these patients in order to avoid the possibility of not diagnosing subsequent autoimmune diseases that can occur. The aim of this case report is to point to the necessity of endocrinological screening to be made in patients presenting with gastric carcinoid type 1. We report on a 62-year-old woman who was diagnosed with primary hypothyroidism in 1993. In 2011, she was re-admitted to the hospital due to increasing fatigue. Macrocytic anemia, low vitamin B12 levels and positive parietal antibodies confirmed pernicious anemia. Furthermore, she underwent gastroscopy, which revealed two polyps in the corpus of the stomach and one in the fornix. Endoscopic mucosal resection was performed and histopathologic analysis confirmed three G1 gastric carcinoids (Ki67 2%). Additional endocrinological evaluation disclosed positive glutamic acid decarboxylase antibodies, but normal fasting and postprandial glucose and HbA1c. In 2013, she was diagnosed with glucose intolerance and subsequently with latent autoimmune diabetes of adulthood. Plasma glucose and HbA1c normalized after dietary intervention. Due to the increase of serum chromogranin A, prophylactic antrectomy was performed in 2014. The patient is still followed-up and has normal chromogranin A, gastrin and HbA1c levels.
C1 [Vrkljan, Ana Marija; Grasic, David; Kruljac, Ivan] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Mladen Sekso Clin Dept Endocrinol Diabetol & Meta, Zagreb 41001, Croatia.
   [Nikolic, Marko; Ljubicic, Neven] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Clin Dept Gastroenterol & Hepatol, Zagreb 41001, Croatia.
   [Filipovic-Cugura, Jaksa] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Clin Dept Surg, Zagreb 41001, Croatia.
   [Ulamec, Monika] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Ljudevit Jurak Clin Dept Pathol, Zagreb 41001, Croatia.
   [Kovacic, Ksenija] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Clin Dept Oncol & Nucl Med, Zagreb 41001, Croatia.
   [Babic, Nenad] Univ Zagreb, Sch Med, Sestre Milosrdnice Univ Hosp Ctr, Clin Dept Diagnost & Intervent Radiol, Zagreb 41001, Croatia.
C3 University of Zagreb; University of Zagreb; University of Zagreb;
   University of Zagreb; University of Zagreb; University of Zagreb
RP Kruljac, I (corresponding author), Sestre Milosrdnice Univ Hosp Ctr, Mladen Sekso Clin Dept Endocrinol Diabetol & Meta, Vinogradska C 29, HR-10000 Zagreb, Croatia.
EM ivkruljac@gmail.com
RI Ulamec, Monika/C-6299-2018
OI Ulamec, Monika/0000-0002-4843-8154
CR AHONEN P, 1990, NEW ENGL J MED, V322, P1829, DOI 10.1056/NEJM199006283222601
   Annibale B, 2001, EUR J GASTROEN HEPAT, V13, P1449, DOI 10.1097/00042737-200112000-00008
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NR 14
TC 0
Z9 0
U1 0
U2 2
PU SESTRE MILOSRDNICE UNIV HOSPITAL
PI ZAGREB
PA VINOGRADSKA C 29, ZAGREB, HR-10000, CROATIA
SN 0353-9466
EI 1333-9451
J9 ACTA CLIN CROAT
JI Acta Clin. Croat.
PD DEC
PY 2015
VL 54
IS 4
BP 525
EP 530
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA DE9ZD
UT WOS:000370997500020
PM 27017730
DA 2025-06-01
ER

PT J
AU Modica, R
   Liccardi, A
   Minotta, R
   Cannavale, G
   Benevento, E
   Colao, A
AF Modica, Roberta
   Liccardi, Alessia
   Minotta, Roberto
   Cannavale, Giuseppe
   Benevento, Elio
   Colao, Annamaria
TI Current understanding of pathogenetic mechanisms in neuroendocrine
   neoplasms
SO EXPERT REVIEW OF ENDOCRINOLOGY & METABOLISM
LA English
DT Review
DE Cancer; gastroenteropancreatic; medullary thyroid carcinoma; Merkel cell
   carcinoma; neuroendocrine neoplasm; neuroendocrine tumor; pathogenetic
   mechanism
ID MULTIPLE ENDOCRINE NEOPLASIA; PULMONARY NEUROEPITHELIAL BODIES;
   ZOLLINGER-ELLISON-SYNDROME; ATROPHIC BODY GASTRITIS; LONG-TERM USE;
   CARCINOID-TUMORS; CELL HYPERPLASIA; AUTOIMMUNE GASTRITIS; EXPRESSION
   PROFILES; THYMIC CARCINOIDS
AB IntroductionDespite the fact that important advances in research on neuroendocrine neoplasms (NENs) have been made, consistent data about their pathogenetic mechanism are still lacking. Furthermore, different primary sites may recognize different pathogenetic mechanisms.Areas coveredThis review analyzes the possible biological and molecular mechanisms that may lead to NEN onset and progression in different organs. Through extensive research of the literature, risk factors including hypercholesterolemia, inflammatory bowel disease, chronic atrophic gastritis are evaluated as potential pathogenetic mechanisms. Consistent evidence is available regarding sporadic gastric NENs and MEN1 related duodenopancreatic NENs precursor lesions, and genetic-epigenetic mutations may play a pivotal role in tumor development and bone metastases onset. In lung neuroendocrine tumors (NETs), diffuse proliferation of neuroendocrine cells on the bronchial wall (DIPNECH) has been proposed as a premalignant lesion, while in lung neuroendocrine carcinoma nicotine and smoke could be responsible for carcinogenic processes. Also, rare primary NENs such as thymic (T-NENs) and Merkel cell carcinoma (MCC) have been analyzed, finding different possible pathogenetic mechanisms.Expert opinionNew technologies in genomics and epigenomics are bringing new light to the pathogenetic landscape of NENs, but further studies are needed to improve both prevention and treatment in these heterogeneous neoplasms.
C1 [Modica, Roberta; Liccardi, Alessia; Minotta, Roberto; Cannavale, Giuseppe; Benevento, Elio; Colao, Annamaria] Univ Naples Federico II, Dept Clin Med & Surg, Endocrinol Unit, Naples, Italy.
   [Colao, Annamaria] Univ Naples Federico II, UNESCO Chair Educ Hlth & Sustainable Dev, Naples, Italy.
C3 University of Naples Federico II; University of Naples Federico II
RP Modica, R (corresponding author), Univ Naples Federico II, Dept Clin Med & Surg, Endocrinol Unit, Naples, Italy.
EM robertamodica@libero.it
RI Minotta, Roberto/JAX-3551-2023; Liccardi, Alessia/IAQ-9500-2023; Colao,
   Annamaria/A-7671-2011; Benevento, Elio/LWK-5716-2024; Modica,
   Roberta/AAX-5392-2021
OI Cannavale, Giuseppe/0000-0002-8524-1131; Minotta,
   Roberto/0000-0002-8823-0702; Benevento, Elio/0000-0002-4489-3651;
   Liccardi, Alessia/0000-0003-1784-5491; Colao,
   Annamaria/0000-0003-4049-2559; Modica, Roberta/0000-0002-3768-5803
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NR 166
TC 8
Z9 8
U1 1
U2 5
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 1744-6651
EI 1744-8417
J9 EXPERT REV ENDOCRINO
JI Expert Rev. Endocrinol. Metab.
PD JAN 2
PY 2024
VL 19
IS 1
BP 49
EP 61
DI 10.1080/17446651.2023.2279540
EA NOV 2023
PG 13
WC Endocrinology & Metabolism
WE Emerging Sources Citation Index (ESCI)
SC Endocrinology & Metabolism
GA DO6O6
UT WOS:001099005400001
PM 37936421
OA Bronze
DA 2025-06-01
ER

PT J
AU Saito, M
   Ogasawara, R
   Izumiyama, K
   Mori, A
   Kondo, T
   Tanaka, M
   Morioka, M
   Ieko, M
AF Saito, Makoto
   Ogasawara, Reiki
   Izumiyama, Koh
   Mori, Akio
   Kondo, Takeshi
   Tanaka, Masanori
   Morioka, Masanobu
   Ieko, Masahiro
TI Acquired hemophilia A in solid cancer: Two case reports and review of
   the literature
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Review
DE Acquired hemophilia A; Coagulation factor VIII; Solid cancer; Gastric
   cancer; Hepatocellular carcinoma; Case report
ID FACTOR-VIII; INHIBITORS; PATIENT
AB Acquired hemophilia A (AHA) is a rare, hemorrhagic autoimmune disease, whose pathogenesis involves reduced coagulation factor VIII (FVIII) activity related to the appearance of inhibitors against FVIII. Common etiological factors include autoimmune diseases, malignancy, and pregnancy. We report two cases of AHA in solid cancer. The first case is a 63-year-old man who developed peritoneal and intestinal bleeding after gastrectomy for gastric cancer. He was diagnosed with AHA, and was treated with prednisone, followed by cyclophosphamide. In the second case, a 68-year-old man developed a subcutaneous hemorrhage. He was diagnosed with AHA in hepatocellular carcinoma on CT imaging, and treated with rituximab alone. Hemostasis was achieved for both patients without bypassing agents as the amount of inhibitors was reduced and eradicated. However, both patients died within 1 year due to cancer progression. Successful treatment for AHA in solid cancer can be difficult because treatment of the underlying malignancy is also required.
C1 [Saito, Makoto; Ogasawara, Reiki; Izumiyama, Koh; Mori, Akio; Kondo, Takeshi; Tanaka, Masanori; Morioka, Masanobu] Aiiku Hosp, Dept Internal Med & Hematol, Sapporo, Hokkaido 0640804, Japan.
   [Ieko, Masahiro] Hlth Sci Univ Hokkaido, Dept Internal Med, Toubetsu 0610293, Japan.
C3 Health Sciences University of Hokkaido
RP Saito, M (corresponding author), Aiiku Hosp, Dept Internal Med & Hematol, Chuo Ku, Minami 4 Nishi 25, Sapporo, Hokkaido 0640804, Japan.
EM ikyoku@aiiku-hp.or.jp
RI Kondo, Takeshi/G-2103-2012
OI Kondo, Takeshi/0000-0001-7455-5824
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NR 22
TC 7
Z9 7
U1 0
U2 2
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD NOV 26
PY 2018
VL 6
IS 14
BP 781
EP 785
DI 10.12998/wjcc.v6.i14.781
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HB7TV
UT WOS:000451284700008
PM 30510943
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Soltész, P
   Szekanecz, Z
   Végh, J
   Lakos, G
   Tóth, L
   Szakáll, S
   Veres, K
   Szegedi, G
AF Soltész, P
   Szekanecz, Z
   Végh, J
   Lakos, G
   Tóth, L
   Szakáll, S
   Veres, K
   Szegedi, G
TI Catastrophic antiphospholipid syndrome in cancer
SO HAEMATOLOGIA
LA English
DT Article
DE antiphospholipid syndrome; anti-cardiolipin antibodies; beta 2
   glycorotein I; gastric cancer
ID RHEUMATOID-ARTHRITIS; ANTIBODIES; THROMBOSIS
AB Antiphospholipid syndrome is characterized by the presence of antiphospholipid antibodies resulting in arterial and venous thromboembolism. Apart from primary cases, this syndrome is often associated with autoimmune diseases. Around 50 cases of catastrophic antiphospholipid antibody syndrome have been reported as yet. Authors describe the first case of catastrophic antiphospholipid syndrome associated with gastric cancer. Apart from presenting the clinical case, authors also discuss the possible pathomechanism of this associated disorder including the role of immunological factors, as well as antiphospholipid antibodies.
C1 Univ Debrecen, Sch Med, Dept Med 3, H-4004 Debrecen, Hungary.
C3 University of Debrecen
RP Soltész, P (corresponding author), Univ Debrecen, Sch Med, Dept Med 3, 22 Morizc Str, H-4004 Debrecen, Hungary.
EM soltesz@iiibel.dote.hu
RI Szekanecz, Zoltán/GXN-0235-2022; Veres, Katalin/JED-3774-2023
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NR 21
TC 19
Z9 19
U1 0
U2 0
PU VSP BV
PI LEIDEN
PA BRILL ACADEMIC PUBLISHERS, PO BOX 9000, 2300 PA LEIDEN, NETHERLANDS
SN 0017-6559
J9 HAEMATOLOGIA
JI Haematologia
PY 2000
VL 30
IS 4
BP 303
EP 311
DI 10.1163/156855900300109549
PG 9
WC Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology
GA 394PM
UT WOS:000166532500006
PM 11204029
DA 2025-06-01
ER

PT J
AU Khan, M
   Arooj, S
   Wang, H
AF Khan, Muhammad
   Arooj, Sumbal
   Wang, Hua
TI Soluble B7-CD28 Family Inhibitory Immune Checkpoint Proteins and
   Anti-Cancer Immunotherapy
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE soluble immune checkpoints (SIC); alternative splice variants (ASV);
   immunotherapy (IT); immune checkpoint blockade (ICB); gene therapy;
   cancer vaccination (CVax)
ID DEATH-LIGAND 1; T-LYMPHOCYTE ATTENUATOR; ENHANCES ANTITUMOR IMMUNITY;
   CELL LUNG-CANCER; B7 FAMILY; COSTIMULATORY MOLECULE;
   HEPATOCELLULAR-CARCINOMA; PD-L1 EXPRESSION; SPLICE VARIANT;
   GASTRIC-CANCER
AB Co-inhibitory B7-CD28 family member proteins negatively regulate T cell responses and are extensively involved in tumor immune evasion. Blockade of classical CTLA-4 (cytotoxic T lymphocyte-associated antigen-4) and PD-1 (programmed cell death protein-1) checkpoint pathways have become the cornerstone of anti-cancer immunotherapy. New inhibitory checkpoint proteins such as B7-H3, B7-H4, and BTLA (B and T lymphocyte attenuator) are being discovered and investigated for their potential in anti-cancer immunotherapy. In addition, soluble forms of these molecules also exist in sera of healthy individuals and elevated levels are found in chronic infections, autoimmune diseases, and cancers. Soluble forms are generated by proteolytic shedding or alternative splicing. Elevated circulating levels of these inhibitory soluble checkpoint molecules in cancer have been correlated with advance stage, metastatic status, and prognosis which underscore their broader involvement in immune regulation. In addition to their potential as biomarker, understanding their mechanism of production, biological activity, and pathological interactions may also pave the way for their clinical use as a therapeutic target. Here we review these aspects of soluble checkpoint molecules and elucidate on their potential for anti-cancer immunotherapy.</p>
C1 [Khan, Muhammad; Wang, Hua] Anhui Med Univ, Dept Oncol, Affiliated Hosp 1, Hefei, Peoples R China.
   [Khan, Muhammad; Wang, Hua] Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.
   [Arooj, Sumbal] Univ Sialkot, Dept Biochem, Sialkot, Pakistan.
C3 Anhui Medical University; Anhui Medical University
RP Wang, H (corresponding author), Anhui Med Univ, Dept Oncol, Affiliated Hosp 1, Hefei, Peoples R China.; Wang, H (corresponding author), Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Hefei, Peoples R China.
EM wanghua@ahmu.edu.cn
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NR 259
TC 67
Z9 74
U1 3
U2 28
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 31
PY 2021
VL 12
AR 651634
DI 10.3389/fimmu.2021.651634
PG 21
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA UU1NM
UT WOS:000698569800001
PM 34531847
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Cho, MJ
   Moon, HS
   Lee, HS
   Park, JH
   Kim, JS
   Kang, SH
   Lee, ES
   Kim, SH
   Sung, JK
   Lee, BS
   Jeong, HY
AF Cho, Min Ji
   Moon, Hee Seok
   Lee, Hyeon Seok
   Park, Jae Ho
   Kim, Ju Seok
   Kang, Sun Hyung
   Lee, Eaum Seok
   Kim, Seok Hyun
   Sung, Jae Kyu
   Lee, Byung Seok
   Jeong, Hyun Yong
TI Immunoglobulin G4-related disease in the stomach presenting as a gastric
   subepithelial tumor Case report
SO MEDICINE
LA English
DT Article
DE asymptomatic subepithelial tumor; gastrointestinal tract; immunoglobulin
   G4-related disease
ID IGG4-RELATED SYSTEMIC-DISEASE; AUTOIMMUNE PANCREATITIS; IGG4
AB Introduction: Immunoglobulin G4-related disease (IgG4-RD) is an immune-mediated fibroinflammatory disorder characterized by specific pathologic findings and often, but not in all cases, elevated serum IgG4 concentration. Although it can virtually involve every organ system, cases involving the gastrointestinal tract and especially gastric mass lesions have rarely been reported. Patient concerns: A 45-year-old man, who was incidentally discovered asymptomatic subepithelial tumor (SET), by endoscopy, on the greater curvature of the upper gastric body, was referred to our hospital for further evaluation. Diagnosis: The patient was postoperatively diagnosed with IgG4-RD by histopathologic results. Interventions: The patient underwent laparoscopic wedge resection. Outcomes: The patient is presently followed up annually in our clinic and had no problems and showed no signs of recurrence in examination. Conclusion: We reported a rare case of IgG4-RD presenting as a gastric SET. The first line treatment of IgG4-RD is glucocorticoid administration. However, because pathologic examination is challenging owing to the lesion location, preoperative diagnosis is difficult and may lead to unnecessary gastric resection. Thus, using alternative preoperative diagnostic methods such as endoscopic ultrasound-guided fine-needle biopsy or the biopsy unroofing technique could spare the patient from unnecessary surgical treatment.
C1 [Cho, Min Ji; Moon, Hee Seok; Lee, Hyeon Seok; Park, Jae Ho; Kim, Ju Seok; Kang, Sun Hyung; Lee, Eaum Seok; Kim, Seok Hyun; Sung, Jae Kyu; Lee, Byung Seok; Jeong, Hyun Yong] Chungnam Natl Univ, Chungnam Natl Univ Hosp, Sch Med, Div Gastroenterol,Dept Internal Med, 282 Munhwa Ro, Daejeon 35015, South Korea.
C3 Chungnam National University; Chungnam National University Hospital
RP Moon, HS (corresponding author), Chungnam Natl Univ, Chungnam Natl Univ Hosp, Sch Med, Div Gastroenterol,Dept Internal Med, 282 Munhwa Ro, Daejeon 35015, South Korea.
EM mhs1357@cnuh.co.kr
RI Moon, Hee Seok/AAC-6951-2022; CHO, MINJI/MCO-3520-2025; Lee,
   Youngil/AAX-2787-2021
OI Kang, Sun Hyung/0000-0002-1913-4346; Kim, Ju Seok/0000-0002-6190-6506
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NR 21
TC 2
Z9 2
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD SEP 4
PY 2020
VL 99
IS 36
AR e22078
DI 10.1097/MD.0000000000022078
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA OC8ZH
UT WOS:000579444200091
PM 32899079
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Kamisawa, T
   Horiguchi, SI
   Hayashi, Y
   Yun, XQ
   Yamaguchi, T
   Tsuruta, K
   Sasaki, T
AF Kamisawa, Terumi
   Horiguchi, Shin-Ichirou
   Hayashi, Yukiko
   Yun, Xiaoqing
   Yamaguchi, Toshikazu
   Tsuruta, Koji
   Sasaki, Tsuneo
TI K-ras mutation in the major duodenal papilla and gastric and colonic
   mucosa in patients with autoimmune pancreatitis
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune pancreatitis; K-ras; IgG4; Foxp3
ID T-CELLS; CANCER; GALLBLADDER; FREQUENT; RISK; DUCT
AB Pancreatic cancer occurs in some patients with autoimmune pancreatitis (AIP). Significant K-ras mutations are frequently detected in the pancreas of AIP patients. AIP may be a pancreatic lesion of IgG4-related systemic disease. Gastric and colonic cancer can occur during the follow up of AIP patients. We examined K-ras mutations in the major duodenal papilla and gastric and colonic mucosa of AIP patients.
   K-ras analysis and/or immunohistochemical study was performed on the tissues of the major duodenal papilla (n = 8), gastric mucosa (n = 5), colonic mucosa (n = 3), pancreas (n = 5), common bile duct (n = 5), and gallbladder (n = 4) of 12 AIP patients.
   Significant K-ras mutations were detected in the major duodenal papilla of 4 of 8 cases [GAT (n = 4)], in the gastric mucosa of 2 of 4 cases [AGT (n = 2)], and in the colonic mucosa of 2 of 3 cases [GAT (n = 2)]. Significant K-ras mutations were detected in the pancreas of all 5 cases [GAT (n = 5), in the common bile duct of 4 cases (GAT (n = 2), TGT (n = 1), and GCT/TGT (n = 1)], and in the gallbladder epithelium of 3 cases [GAT (n = 1), GCT (n = 1), and GTT (n = 1)]. K-ras mutations were detected in the organs associated with IgG4-related fibroinflammation with abundant infiltration of T lymphocytes and forkhead box P3-positive cells.
   Significant K-ras mutations were frequently detected in the major duodenal papilla and gastric and colonic mucosa of AIP patients. AIP patients may have risk factors for gastric and colonic cancer, but the mechanisms of K-ras mutation and its clinical implications are not clear.
C1 [Kamisawa, Terumi] Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Bunkyo Ku, Tokyo 1138677, Japan.
   [Horiguchi, Shin-Ichirou; Hayashi, Yukiko] Tokyo Metropolitan Komagome Hosp, Dept Pathol, Tokyo 1138677, Japan.
   [Yun, Xiaoqing; Yamaguchi, Toshikazu] Biomed Labs, Div Clin Dev, Saitama, Japan.
   [Tsuruta, Koji] Tokyo Metropolitan Komagome Hosp, Dept Surg, Tokyo 1138677, Japan.
   [Sasaki, Tsuneo] Tokyo Metropolitan Komagome Hosp, Dept Chemotherapy, Tokyo 1138677, Japan.
C3 Tokyo Metropolitan Cancer & Infectious Diseases Center Komagome
   Hospital; Tokyo Metropolitan Cancer & Infectious Diseases Center
   Komagome Hospital; Tokyo Metropolitan Cancer & Infectious Diseases
   Center Komagome Hospital; Tokyo Metropolitan Cancer & Infectious
   Diseases Center Komagome Hospital
RP Kamisawa, T (corresponding author), Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Bunkyo Ku, 3-18-22 Honkomagome, Tokyo 1138677, Japan.
EM kamisawa@cick.jp
FU Ministry of Health, Labour, and Welfare of Japan
FX This work was partly supported by The Research Committee on Intractable
   Pancreatic Diseases provided by Ministry of Health, Labour, and Welfare
   of Japan.
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NR 32
TC 18
Z9 21
U1 0
U2 0
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUL
PY 2010
VL 45
IS 7
BP 771
EP 778
DI 10.1007/s00535-010-0211-y
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 622RW
UT WOS:000279684100012
PM 20157749
DA 2025-06-01
ER

PT J
AU Okamoto, A
   Watanabe, T
   Kamata, K
   Minaga, K
   Kudo, M
AF Okamoto, Ayana
   Watanabe, Tomohiro
   Kamata, Ken
   Minaga, Kosuke
   Kudo, Masatoshi
TI Recent Updates on the Relationship between Cancer and Autoimmune
   Pancreatitis
SO INTERNAL MEDICINE
LA English
DT Review
DE autoimmunc pancreatitis; IgG4-related disease; cancer
ID RISK; ASSOCIATION; DISEASE; MALIGNANCIES; MECHANISMS; TYPE-1
AB Autoimmune pancreatitis (AIP) is now considered a pancreatic manifestation of a newly proposed disease condition, IgG4-related disease (IgG4-RD). IgG4-RD is characterized by enhanced IgG4 antibody responses and multiple organ involvements. Recent epidemiological studies have addressed the incidence of cancer in patients with AIP and/or IgG4-RD. Surprisingly, a significant number of AIP patients were detected with cancer at or within one year of the diagnosis of AIP. Furthermore, around 50% of all cancers detected in AIP patients comprised mainly 3 types (gastric, lung, and prostate cancer). Thus, AIP appears to be associated with cancer of other organs rather than the pancreas itself, which suggests that AIP is not a pre-cancerous condition of the pancreas. Moreover, the simultaneous occurrence of cancer and AIP in many patients has led to the establishment of an attractive concept that AIP might sometimes arise from co-existing cancers as a paraneoplastic syndrome.
C1 [Okamoto, Ayana; Watanabe, Tomohiro; Kamata, Ken; Minaga, Kosuke; Kudo, Masatoshi] Kindai Univ, Dept Gastroenterol & Hepatol, Fac Med, Higashiosaka, Osaka, Japan.
C3 Kindai University (Kinki University)
RP Watanabe, T (corresponding author), Kindai Univ, Dept Gastroenterol & Hepatol, Fac Med, Higashiosaka, Osaka, Japan.
EM tomohiro@med.kindai.ac.jp
RI Minaga, Kosuke/AAD-2107-2020; Kudo, Masatoshi/AAA-9744-2019; Watanabe,
   Tomohiro/ABA-4712-2021
OI Watanabe, Tomohiro/0000-0002-6175-8064
FU Naito Foundation; SENSHIN Medical Research Foundation; Yakult
   Bio-Science Foundation; Smoking Research Foundation; Takeda Science
   Foundation; Japan Agency for Medical Research and Development (AMED);
   Kobayashi Foundation for Cancer Research
FX This work was supported by the Naito Foundation, SENSHIN Medical
   Research Foundation, Yakult Bio-Science Foundation, Smoking Research
   Foundation, Kobayashi Foundation for Cancer Research, Takeda Science
   Foundation, and Japan Agency for Medical Research and Development (AMED)
   Grants for Research on Intractable Diseases.
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NR 28
TC 33
Z9 35
U1 1
U2 4
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2019
VL 58
IS 11
BP 1533
EP 1539
DI 10.2169/internalmedicine.2210-18
PG 7
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IB4MV
UT WOS:000470247600002
PM 30713326
OA gold, Green Submitted, Green Published
DA 2025-06-01
ER

PT J
AU Gu, DQ
   Zhang, M
   Wang, YT
   Bai, Y
   Wang, X
   Deng, GH
AF Gu, Dongqing
   Zhang, Min
   Wang, Yutong
   Bai, Ye
   Wang, Xin
   Deng, Guohong
TI Causal effect of autoimmune liver diseases on cancer: Meta-analyses of
   cohort studies and Mendelian randomization study
SO LIVER INTERNATIONAL
LA English
DT Article
DE autoimmune hepatitis; autoimmune liver diseases; cancer; Mendelian
   randomization; primary biliary cholangitis; primary sclerosing
   cholangitis
ID PRIMARY SCLEROSING CHOLANGITIS; INFLAMMATORY-BOWEL-DISEASE; PRIMARY
   BILIARY-CIRRHOSIS; HEPATOCELLULAR-CARCINOMA; RISK LOCI; FOLLOW-UP;
   MALIGNANCY; SURVIVAL; EPIDEMIOLOGY; PANCREATITIS
AB Background and Aims Prior studies suggested that patients with autoimmune liver diseases (AiLDs) had an increased risk of cancer, whereas the causal effect remained unclear. Methods Meta-analyses concerning the relationship between AiLD and cancer risk were performed to calculate the pooled relative risk (RR) and corresponding 95% confidence intervals (CIs). Then, the associations with a p value of A total of 37 cohort studies covering more than 34 558 patients were included, and we observed an increased risk of overall cancers (pooled RR = 3.64, 95% CI: 2.64-5.03, p < .001) and cancer-related death (pooled RR = 2.48, 95% CI: 1.73-3.53, p < .001) for patients with AiLD. Besides, overall and several site-specific cancers risk were found in patients with primary biliary cholangitis (PBC), autoimmune hepatitis (AIH), and primary sclerosing cholangitis (PSC) (p < .05). However, associations between genetically predisposed AIH, PBC, and PSC and the risk of specific cancers did not reach a significant level, except for PBC and gastric cancer (OR = 0.96, 95% CI: 0.93-0.99; p = .02). Conclusions In addition to hepatobiliary cancer, results from the meta-analyses suggest that patients with AiLD might have an increased risk of several extrahepatobiliary cancers. However, the causal role of AiLD in cancer development needs to be further investigated.
C1 [Gu, Dongqing; Deng, Guohong] Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, 30 Gaotanyan St, Chongqing 400038, Peoples R China.
   [Zhang, Min; Bai, Ye] Chongqing Med Univ, Sch Publ Hlth & Management, Chongqing, Peoples R China.
   [Wang, Yutong; Wang, Xin] Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
C3 Army Medical University; Chongqing Medical University; Sichuan
   University
RP Deng, GH (corresponding author), Army Med Univ, Affiliated Hosp 1, Dept Infect Dis, 30 Gaotanyan St, Chongqing 400038, Peoples R China.; Wang, X (corresponding author), Sichuan Univ, West China Sch Publ Hlth, Dept Epidemiol & Biostat, South Renmin Rd, Chengdu 610041, Sichuan, Peoples R China.
EM wangxinmarine@126.com; gh_deng@hotmail.com
RI Wang, Xin/N-8865-2018
OI Wang, Xin/0000-0001-9325-3194; Deng, Guo-Hong/0000-0003-1263-7220
FU Chongqing Natural Science Foundation Program [cstc2020jcyj--msxmX0021,
   cstc2019jcyj--msxmX0466]; Chongqing Postdoctoral Science Special
   Foundation [XmT2018068]; National Natural Science Foundation of China
   [81903393, 81903398]
FX Chongqing Natural Science Foundation Program, Grant/Award Number:
   cstc2020jcyj--msxmX0021 and cstc2019jcyj--msxmX0466; Chongqing
   Postdoctoral Science Special Foundation, Grant/Award Number: XmT2018068;
   National Natural Science Foundation of China, Grant/Award Number:
   81903393 and 81903398
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NR 49
TC 6
Z9 6
U1 0
U2 22
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1478-3223
EI 1478-3231
J9 LIVER INT
JI Liver Int.
PD OCT
PY 2022
VL 42
IS 10
BP 2216
EP 2226
DI 10.1111/liv.15355
EA JUL 2022
PG 11
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 4D6VK
UT WOS:000825843700001
PM 35775855
DA 2025-06-01
ER

PT J
AU Melcescu, E
   Hogan, RB
   Brown, K
   Boyd, SA
   Abell, TL
   Koch, CA
AF Melcescu, Eugen
   Hogan, Reed B., II
   Brown, Keith
   Boyd, Stewart A.
   Abell, Thomas L.
   Koch, Christian A.
TI The various faces of autoimmune endocrinopathies: Non-tumoral
   hypergastrinemia in a patient with lymphocytic colitis and chronic
   autoimmune gastritis
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE Gastrin; Gastrinoma; Neuroendocrine tumor; Colitis; Gastritis;
   Polyglandular syndrome
ID ZOLLINGER-ELLISON-SYNDROME; TOLL-LIKE RECEPTORS; COLLAGENOUS COLITIS;
   MICROSCOPIC COLITIS; SERUM GASTRIN; CLINICAL PRESENTATION;
   PERNICIOUS-ANEMIA; CHRONIC DIARRHEA; TUMORS; DISEASES
AB Serum gastrin levels exceeding 1000 pg/ml (normal, <100) usually raise the suspicion for a neuroendocrine tumor (NET) that secretes gastrin. Rarely, such elevated gastrin levels are seen in patients with pernicious anemia which most commonly is associated with autoimmune gastritis (AG). AG can occur concomitantly with other autoimmune disorders including lymphocytic colitis (LC). Gastrin stimulates enterochromaffin-like cells which increase histamine secretion. Histamine excess can cause diarrhea as can bacterial overgrowth or LC. We present a 57-year-old woman with diarrhea, sporadic epigastric pain, and bloating. She also had a history of interstitial cystitis and took pentosan polysulfate and cetirizine. She had no history of ulcers, renal impairment or carcinoid syndrome. Fasting serum gastrin was 1846 pg/ml. Esophagoduodenal gastroscopy and biopsies revealed chronic gastritis and a pH of 7 with low stomach acid. Serum gastrin and plasma chromogranin A were suggestive of a gastrinoma or NET. Pernicious anemia was unlikely. Imaging studies did not reveal any tumor. Random colonic biopsy was compatible with LC, possibly explaining her diarrhea, although we also considered excessive histamine from elevated gastrin, bacterial overgrowth, and pentosan polysulfate which can cause diarrhea and be misleading in this setting, pointing to the diagnosis of gastrinoma. At 4 year follow-up in 2012, fasting serum gastrin was 1097 pg/ml and the patient asymptomatic taking only cetirizine for nasal allergies. This case illustrates that diarrhea may be associated with very high serum gastrin levels in the setting of chronic gastritis, LC. and interstitial cystitis (pentosan use), without clear evidence for a gastrinoma or NET. If no history of ulcers or liver metastases is present in such cases, watchful observation rather than an extensive/invasive and costly search for a NET may be justified. Considering the various forms of polyglandular syndrome, this may represent a variant and we here provide an algorithm for working up such patients, while also reviewing literature on the intertwined relationship between the immune and endocrine systems. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Koch, Christian A.] Univ Mississippi, Med Ctr, Div Endocrinol, Dept Med, Jackson, MS 39216 USA.
   [Hogan, Reed B., II; Brown, Keith] Gastrointestinal Associates, Jackson, MS 39202 USA.
   [Koch, Christian A.] GV Sonny Montgomery VA Med Ctr, Med Serv, Jackson, MS USA.
   [Koch, Christian A.] Univ Dresden, Dept Med, Dresden, Germany.
   [Hogan, Reed B., II; Brown, Keith] Endoscopy Ctr, Jackson, MS 39202 USA.
C3 University of Mississippi; University of Mississippi Medical Center;
   Technische Universitat Dresden
RP Koch, CA (corresponding author), Univ Mississippi, Med Ctr, Div Endocrinol, Dept Med, 2500 N State St, Jackson, MS 39216 USA.
EM ckoch@umc.edu
RI Koch, Christian/A-4699-2008; Boyd, Stephen/G-5819-2010
OI Koch, Christian/0000-0003-0678-1242
FU NIDDK NIH HHS [U01 DK074007] Funding Source: Medline
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NR 84
TC 11
Z9 14
U1 0
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2012
VL 93
IS 3
SI SI
BP 434
EP 440
DI 10.1016/j.yexmp.2012.09.025
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 056CN
UT WOS:000312466100024
PM 23043903
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Lahner, E
   Zagari, RM
   Zullo, A
   Di Sabatino, A
   Meggio, A
   Cesaro, P
   Lenti, MV
   Annibale, B
   Corazza, GR
AF Lahner, Edith
   Zagari, Rocco Maurizio
   Zullo, Angelo
   Di Sabatino, Antonio
   Meggio, Alberto
   Cesaro, Paola
   Lenti, Marco Vincenzo
   Annibale, Bruno
   Corazza, Gino Roberto
TI Chronic atrophic gastritis: Natural history, diagnosis and therapeutic
   management. A position paper by the Italian Society of Hospital
   Gastroenterologists and Digestive Endoscopists [AIGO], the Italian
   Society of Digestive Endoscopy [SIED], the Italian Society of
   Gastroenterology [SIGE], and the Italian Society of Internal Medicine
   [SIMI]
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Atrophic gastritis; Autoimmune gastritis; Diagnosis; H. pylori;
   Histology; Vitamin B-12
ID HELICOBACTER-PYLORI INFECTION; AUTOIMMUNE THYROID-DISEASE; PARIETAL-CELL
   ANTIBODIES; INTESTINAL METAPLASIA; FOLLOW-UP; IRON-DEFICIENCY;
   PRECANCEROUS CONDITIONS; CANCER PATIENTS; BODY GASTRITIS;
   GASTROESOPHAGEAL-REFLUX
AB Chronic atrophic gastritis (CAG) is an underdiagnosed condition characterised by translational features going beyond the strict field of gastroenterology as it may manifest itself by a variable spectrum of gastric and extra-gastric symptoms and signs. It is relatively common among older adults in different parts of the world, but large variations exist. Helicobacter pylori-related CAG [multifocal] and autoimmune CAG (corpus-restricted) are apparently two different diseases, but they display overlapping features. Patients with cobalamin and/or iron deficiency anaemia or autoimmune disorders, including autoimmune thyroiditis and type 1 diabetes mellitus, should be offered screening for CAG. Pepsinogens, gastrin-17, and anti-H. pylori antibodies serum assays seem to be reliable non-invasive screening tools for the presence of CAG, helpful to identify individuals to refer to gastroscopy with five standard gastric biopsies in order to obtain histological confirmation of diagnosis. Patients with CAG are at increased risk of developing gastric cancer, and they should be estimated with histological staging systems (OLGA or OLGIM). H. pylori eradication may be beneficial by modifying the natural history of atrophy, but not that of intestinal metaplasia. Patients with advanced stages of CAG (Stage III/IV OLGA or OLGIM) should undergo endoscopic surveillance every three years, those with autoimmune CAG every three-five years. In patients with CAG, a screening for autoimmune thyroid disease and micronutrient deficiencies, including iron and vitamin B-12, should be performed. The optimal treatment for dyspeptic symptoms in patients with CAG remains to be defined. Proton pump inhibitors are not indicated in hypochlorhydric CAG patients. (c) 2019 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Lahner, Edith; Annibale, Bruno] Sapienza Univ Rome, St Andrea Hosp, Digest & Liver Dis Unit, Dept Surg Med Sci & Translat Med, Rome, Italy.
   [Zagari, Rocco Maurizio] Univ Bologna, Dept Med & Surg Sci, Bologna, Italy.
   [Zullo, Angelo] Nuovo Regina Margherita Hosp, Gastroenterol & Digest Endoscopy, Rome, Italy.
   [Di Sabatino, Antonio; Lenti, Marco Vincenzo; Corazza, Gino Roberto] Univ Pavia, IRCCS San Matteo Hosp Fdn, Dept Internal Med 1, Pavia, Italy.
   [Zullo, Angelo; Meggio, Alberto] Dept Gastroenterol, Trento, Italy.
   [Zullo, Angelo; Meggio, Alberto] Rovereto Hosp, Trento, Italy.
   [Cesaro, Paola] Fdn Poliambulanza, Digest Endoscopy Unit, Brescia, Italy.
   [Cesaro, Paola] Fdn Poliambulanza, Gastroenterol, Brescia, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; University of
   Bologna; Poliambulatorio Nuovo Regina Margherita; University of Pavia;
   IRCCS Fondazione San Matteo
RP Lahner, E (corresponding author), Sapienza Univ Rome, Med Surg Dept Clin Sci & Translat Med, Via Grottarossa 1035, I-00189 Rome, Italy.
EM edith.lahner@uniroma1.it
RI Di Sabatino, Antonio/K-8015-2016; Zullo, Angelo/AAV-7092-2020; Zagari,
   Rocco/AAA-1836-2021; Corazza, Gino/K-8500-2016; Annibale,
   Bruno/A-5372-2008; Lahner, Edith/AAM-1039-2021; Lenti, Marco
   Vincenzo/F-9044-2018
OI Lenti, Marco Vincenzo/0000-0002-6654-4911; annibale,
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NR 170
TC 123
Z9 135
U1 2
U2 42
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD DEC
PY 2019
VL 51
IS 12
BP 1621
EP 1632
DI 10.1016/j.dld.2019.09.016
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA JQ2VL
UT WOS:000498808400001
PM 31635944
DA 2025-06-01
ER

PT J
AU Boutzios, G
   Koukoulioti, E
   Goules, AV
   Kalliakmanis, I
   Giovannopoulos, I
   Vlachoyiannopoulos, P
   Moutsopoulos, HM
   Tzioufas, AG
AF Boutzios, Georgios
   Koukoulioti, Eleni
   Goules, Andreas V.
   Kalliakmanis, Ioannis
   Giovannopoulos, Ilias
   Vlachoyiannopoulos, Panayiotis
   Moutsopoulos, Haralampos M.
   Tzioufas, Athanasios G.
TI Hashimoto Thyroiditis, Anti-Parietal Cell Antibodies: Associations With
   Autoimmune Diseases and Malignancies
SO FRONTIERS IN ENDOCRINOLOGY
LA English
DT Article
DE Hashimoto thyroiditis; anti-parietal cell antibodies; organ-specific
   autoimmunity; systemic autoimmunity; gastric malignancies
ID ATROPHIC BODY GASTRITIS; RISK; AUTOANTIBODIES; CANCER
AB BackgroundHashimoto thyroiditis (HT) is an autoimmune disease which may result in extensive damage of the thyroid gland. Chronic atrophic gastritis (CAG), is the most frequent HT-associated disorder, with anti-parietal cell autoantibodies (APCA) being a screening test for autoimmune CAG. The aim of this study was to investigate, in a cohort of HT patients: a) the prevalence of APCA in an attempt to define their clinical phenotype and b) any possible associations of APCA with other autoimmune diseases and malignancies. MethodsThis is a single-center, case-control study, conducted at a University Hospital. The study included patients with HT diagnosed between November 2017 and November 2020. Excluded were patients <18 years old, with sonographic features of HT but negative thyroid peroxidase (TPOAbs) or thyroglobulin autoantibodies (TgAbs), Graves' disease, Down or Turner's syndrome. ResultsA total of 840 patients with HT were included in the study, from whom 180 (21.4%) had positive APCA. A total of 79 patients (9.4%) had one or more organ-specific autoimmune diseases and 61 (7.3%) had a systemic autoimmune disease. Autoimmune diseases were more frequent in female than in male patients (17.9% versus 10.9%, p = 0.05). APCA-positive patients were older than APCA-negative (54.1 +/- 13.5 versus 49.0 +/- 14.6, p <0.001) and had more often positive TPOAbs (93.3% versus 83.9%, p=0.001). Gastric neoplasms were documented only in APCA-positive patients (p <0.001). A higher frequency of organ-specific autoimmune diseases was observed in the APCA-positive group (14.4% versus 8%, p = 0.024). In the subgroup of patients with additional autoimmune diseases (n = 140), younger age and positive APCA were independently associated with the presence of organ-specific autoimmunity (OR 0.954, 95% CI 0.927-0.982 and OR 3.100, 95% CI 1.256-7.652, respectively). Papillary thyroid cancer (PTC) occurred in 3.5% of patients (26/29 women). Positive family history for thyroid autoimmunity and negative TPOAbs were the only independent risk factors for PTC among women (OR 3.228, 95% CI 1.173-8.887 and 0.315, 95% 0.113-0.881, respectively). ConclusionThis study reveals for the first time an association of APCA with organ-specific autoimmunity in HT patients. APCA together with patient age were independently associated with the presence of organ-specific autoimmunity. Finally, this study showed an association between APCA and gastric neoplasms in these patients.
RI TZIOUFAS, ATHANASIOS/A-1690-2008
OI Tzioufas, Athanasios/0000-0001-6666-8642
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NR 29
TC 11
Z9 11
U1 3
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-2392
J9 FRONT ENDOCRINOL
JI Front. Endocrinol.
PD APR 22
PY 2022
VL 13
AR 860880
DI 10.3389/fendo.2022.860880
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 5T9LN
UT WOS:000876178300001
PM 35528009
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Steinbuss, G
   Kriegsmann, K
   Kriegsmann, M
AF Steinbuss, Georg
   Kriegsmann, Katharina
   Kriegsmann, Mark
TI Identification of Gastritis Subtypes by Convolutional Neuronal Networks
   on Histological Images of Antrum and Corpus Biopsies
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE deep learning; digital image analysis; convolutional neural networks;
   artificial intelligence
ID CANCER; CLASSIFICATION; RISK; CARCINOMA; DIAGNOSIS
AB Background: Gastritis is a prevalent disease and commonly classified into autoimmune (A), bacterial (B), and chemical (C) type gastritis. While the former two subtypes are associated with an increased risk of developing gastric intestinal adenocarcinoma, the latter subtype is not. In this study, we evaluated the capability to classify common gastritis subtypes using convolutional neuronal networks on a small dataset of antrum and corpus biopsies. Methods: 1230 representative 500 x 500 mu m images of 135 patients with type A, type B, and type C gastritis were extracted from scanned histological slides. Patients were allocated randomly into a training set (60%), a validation set (20%), and a test set (20%). One classifier for antrum and one classifier for corpus were trained and optimized. After optimization, the test set was analyzed using a joint result from both classifiers. Results: Overall accuracy in the test set was 84% and was particularly high for type B gastritis with a sensitivity of 100% and a specificity of 93%. Conclusions: Classification of gastritis subtypes is possible using convolutional neural networks on a small dataset of histopathological images of antrum and corpus biopsies. Deep learning strategies to support routine diagnostic pathology merit further evaluation.
C1 [Steinbuss, Georg; Kriegsmann, Katharina] Univ Hosp Heidelberg, Dept Hematol Oncol & Rheumatol, D-69120 Heidelberg, Germany.
   [Steinbuss, Georg; Kriegsmann, Mark] Univ Hosp Heidelberg, Inst Pathol, D-69120 Heidelberg, Germany.
C3 Ruprecht Karls University Heidelberg; Ruprecht Karls University
   Heidelberg
RP Kriegsmann, M (corresponding author), Univ Hosp Heidelberg, Inst Pathol, D-69120 Heidelberg, Germany.
EM georg.steinbuss@med.uni-heidelberg.de;
   katharina.kriegsmann@med.uni-heidelberg.de;
   mark.kriegsmann@med.uni-heidelberg.de
OI Kriegsmann, Mark/0000-0002-7319-3646
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NR 52
TC 20
Z9 20
U1 1
U2 18
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD SEP
PY 2020
VL 21
IS 18
AR 6652
DI 10.3390/ijms21186652
PG 16
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OD7GK
UT WOS:000580017400001
PM 32932860
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Zhang, XH
   Jin, X
   Guan, L
   Lin, XY
   Li, XD
   Li, YL
AF Zhang, Xinhe
   Jin, Xing
   Guan, Lin
   Lin, Xuyong
   Li, Xuedan
   Li, Yiling
TI IgG4-Related Disease With Gastrointestinal Involvement: Case Reports and
   Literature Review
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE IgG4-related disease; IgG4-related gastric disease; IgG4-related
   sclerosing cholangitis; atrophic gastritis; autoimmune diseases
ID IGG4; DIAGNOSIS; STOMACH; LESION
AB IgG4-related disease is an immune-mediated chronic, systemic, and autoinflammatory disease that can affect various organs throughout the body. The most commonly affected areas are the pancreas and biliary system. Due to the diverse clinical manifestations of the disease, it affects widely distributed organs. Thus, it is often easy to misdiagnose or miss. The digestive tract is a rarely affected system, and most IgG4-related gastric diseases manifest as tumors detected by endoscopy. This article reports two special cases with IgG4-related disease involving atrophic gastritis and intestinal polyps to provide a more empirical and theoretical basis for clinical diagnosis and treatment.
C1 [Zhang, Xinhe; Jin, Xing; Guan, Lin; Li, Yiling] China Med Univ, Gastroenterol Dept, Affiliated Hosp 1, Shenyang, Peoples R China.
   [Lin, Xuyong] China Med Univ, Affiliated Hosp 1, Dept Pathol, Shenyang, Peoples R China.
   [Li, Xuedan] China Med Univ, Affiliated Hosp 1, Radiol Dept, Shenyang, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University
RP Li, YL (corresponding author), China Med Univ, Gastroenterol Dept, Affiliated Hosp 1, Shenyang, Peoples R China.
EM lyl-72@163.com
RI li, xinke/JTU-3633-2023; Yu, Yanfang/KGK-4081-2024
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NR 30
TC 4
Z9 5
U1 2
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAR 10
PY 2022
VL 13
AR 816830
DI 10.3389/fimmu.2022.816830
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 0H3IB
UT WOS:000778628300001
PM 35359937
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Cicone, F
   Papa, A
   Lauri, C
   Tofani, A
   Virili, C
   Centanni, M
   Scopinaro, F
   Annibale, B
AF Cicone, Francesco
   Papa, Annalisa
   Lauri, Chiara
   Tofani, Anna
   Virili, Camilla
   Centanni, Marco
   Scopinaro, Francesco
   Annibale, Bruno
TI Thyro-gastric autoimmunity in patients with differentiated thyroid
   cancer: a prospective study
SO ENDOCRINE
LA English
DT Article
DE Autoimmune thyroid disease; Differentiated thyroid cancer; Autoimmune
   gastritis; Atrophy body gastritis; Iron deficiency anemia; Pernicious
   anemia
ID HELICOBACTER-PYLORI INFECTION; ATROPHIC BODY GASTRITIS; CHRONIC
   LYMPHOCYTIC THYROIDITIS; PARIETAL-CELL ANTIBODIES; ANTIGASTRIC
   AUTOANTIBODIES; HASHIMOTOS-THYROIDITIS; CARCINOMA; DISEASE; ASSOCIATION;
   TYPE-1
AB Thyro-gastric autoimmunity has not been previously evaluated in patients with differentiated thyroid cancer (DTC), although its long-term complications may be relevant for the management of DTC patients. We assessed the prevalence of gastric autoimmunity and autoimmune gastritis (AG) in patients with Hashimoto's thyroiditis (HT) and concomitant DTC. Prevalence of parietal cell antibody (PCA) positivity, iron deficiency anemia (IDA), and pernicious anemia (PA) were prospectively assessed in 150 DTC patients referred for radioiodine ablation after total thyroidectomy. Patients were classified as HT (n = 31) and non-HT (n = 119) based on a combination of serological, ultrasonographic, and histological findings. Patients with PCA positivity were subsequently addressed to endoscopy for confirmation of atrophy body gastritis, required for the diagnosis of AG. For all the variables under study, a comparison between groups was made using Fisher's exact test and appropriate parametric and non-parametric tests. PCA positivity was significantly more prevalent in HT than in non-HT patients (12.9 vs 1.6 %, p = 0.017). After Hp eradication, a reversal of PCA positivity was observed in 3/4 patients in the HT group. IDA and PA did not differ significantly between groups. In the HT group, only one patient had endoscopical confirmation of mild gastric corporal atrophy. Gastric autoimmunity shows higher prevalence in patients with DTC and concomitant HT than in patients with DTC alone; however, in most cases, PCA positivity was associated with Hp infection. Furthermore, although previous reports found up to one-third of patients with HT to have associated AG, in our cohort AG was extremely rare.
C1 [Cicone, Francesco; Papa, Annalisa; Lauri, Chiara; Scopinaro, Francesco; Annibale, Bruno] Univ Roma La Sapienza, Fac Med & Psychol, Dept Surg & Med Sci & Translat Med, I-00185 Rome, Italy.
   [Cicone, Francesco; Papa, Annalisa; Lauri, Chiara; Tofani, Anna; Scopinaro, Francesco] St Andrea Hosp, Nucl Med Unit, Rome, Italy.
   [Virili, Camilla; Centanni, Marco] AUSL Latina, Unit Endocrinol, Latina, Italy.
   [Virili, Camilla; Centanni, Marco] Univ Roma La Sapienza, Dept Medicosurg Sci & Biotechnol, I-00185 Rome, Italy.
   [Annibale, Bruno] St Andrea Hosp, Gastroenterol Unit, Rome, Italy.
C3 Sapienza University Rome; Sapienza University Rome; Azienda Ospedaliera
   Sant'Andrea; Sapienza University Rome; Sapienza University Rome; Azienda
   Ospedaliera Sant'Andrea
RP Cicone, F (corresponding author), Univ Roma La Sapienza, Fac Med & Psychol, Dept Surg & Med Sci & Translat Med, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
EM f.cicone@iol.it
RI Centanni, Marco/HPD-2477-2023; Annibale, Bruno/A-5372-2008; Lauri,
   C./AAH-1028-2019; Cicone, Francesco/W-9864-2019; Virili,
   Camilla/HRB-3894-2023
OI Lauri, Chiara/0000-0002-0314-5059; Cicone,
   Francesco/0000-0003-4664-1965; Scopinaro, Francesco/0000-0003-1924-3005;
   CENTANNI, Marco/0000-0003-0661-1649; annibale, bruno/0000-0001-9120-5957
FU "Sapienza" University of Rome (Progetto di Avvio alla Ricerca)
   [C26N13R29B]
FX This project was supported by a grant from the "Sapienza" University of
   Rome (Progetto di Avvio alla Ricerca 2013, Prot. Number: C26N13R29B). We
   are sincerely thankful to all the medical and non-medical staff of the
   Unit of Nuclear Medicine, Sant'Andrea Hospital of Rome, for taking care
   of the patients. Thanks also to Dr. Silvia Rigucci for statistical
   assistance.
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NR 33
TC 6
Z9 7
U1 0
U2 7
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1355-008X
EI 1559-0100
J9 ENDOCRINE
JI Endocrine
PD MAY
PY 2015
VL 49
IS 1
BP 163
EP 169
DI 10.1007/s12020-014-0424-6
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA CJ1GM
UT WOS:000355231900019
PM 25213471
DA 2025-06-01
ER

PT J
AU Elisei, R
   Vivaldi, A
   Pacini, F
AF Elisei, R
   Vivaldi, A
   Pacini, F
TI Biology and clinical application of the NIS gene
SO TUMORI
LA English
DT Article
DE active iodide transport; NIS expression; NIS therapy; sodium iodide;
   symporter (NIS); thyroid cancer
ID SODIUM-IODIDE SYMPORTER; PAPILLARY THYROID-CARCINOMA; RADIOIODIDE
   UPTAKE; BREAST-CANCER; CELL-LINES; EXPRESSION; MUTATIONS; TRANSPORT;
   GLAND
AB The sodium iodide symporter (NIS) is a plasma basolateral membrane protein that actively transports iodide to the thyroid follicular cells as the first step of thyroid hormone biosynthesis. NIS also mediates active iodide transport in other human tissues including the salivary glands, lactating mammary gland and gastric mucosa. NIS expression has been recently reported also in several other human tissues but its physiological role is still unclear. Cloning of the NIS gene and the development of specific NIS antibodies have allowed the characterization of the pathogenic role of NIS in thyroid cancer, thyroid autoimmune diseases, congenital hypothyroidism and other, non-thyroidal human diseases. The possibility to increase its levels of expression or to reinduce its expression in thyroid carcinomas that have lost the ability to take up radioiodine is one of the most promising clinically related fields of research. The recent discovery that more than 80% of human breast carcinomas endogenously express NIS protein has opened a very interesting new area of research into the possibility of using radioiodide in the diagnosis and treatment of breast cancer. In an attempt to make tumor cells susceptible to radioiodide destruction, several types of cancer cells have been transfected with the NIS gene. This has demonstrated the feasibility of the in vitro technique but also raised the problem of the absence of the iodide organification machinery in non-thyroidal cells, which, at the moment, represents the major limit of this strategy.
C1 Univ Siena, Dept Endocrinol & Metab, Policlin Le Scotte, I-53100 Siena, Italy.
   Univ Pisa, Dept Endocrinol & Metab, I-56100 Pisa, Italy.
C3 University of Siena; University of Pisa
RP Pacini, F (corresponding author), Univ Siena, Dept Endocrinol & Metab, Policlin Le Scotte, Via Bracci 16, I-53100 Siena, Italy.
OI ELISEI, ROSSELLA/0000-0002-5333-9257
CR [Anonymous], CLIN NUCL MED
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NR 20
TC 3
Z9 3
U1 0
U2 3
PU PENSIERO SCIENTIFICO EDITOR
PI ROME
PA VIA BRADANO 3/C, 00199 ROME, ITALY
SN 0300-8916
J9 TUMORI
JI Tumori
PD SEP-OCT
PY 2003
VL 89
IS 5
BP 523
EP 528
DI 10.1177/030089160308900513
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 747YZ
UT WOS:000186835400013
PM 14870777
DA 2025-06-01
ER

PT J
AU Kawashima, H
   Takatori, H
   Suzuki, K
   Iwata, A
   Yokota, M
   Suto, A
   Minamino, T
   Hirose, K
   Nakajima, H
AF Kawashima, Hirotoshi
   Takatori, Hiroaki
   Suzuki, Kotaro
   Iwata, Arifumi
   Yokota, Masaya
   Suto, Akira
   Minamino, Tohru
   Hirose, Koichi
   Nakajima, Hiroshi
TI Tumor Suppressor p53 Inhibits Systemic Autoimmune Diseases by Inducing
   Regulatory T Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID FOXP3 EXPRESSION; RHEUMATOID-ARTHRITIS; SELF-TOLERANCE; BREAST-CANCER;
   GENE; DNA; MICE; INTERLEUKIN-6; ACTIVATION; MUTATIONS
AB The tumor suppressor p53 plays a central role in tumor suppression by inducing apoptosis, cell cycle arrest, senescence, and DNA repair. In addition to the antitumor functions of p53, accumulating evidence using systemic p53-deficient mice suggests that p53 suppresses autoimmunity. However, it remains unknown how p53 suppresses autoimmunity. In this study, we generated T cell-specific p53-deficient mice (CD4-Cre p53(fl/fl) mice, or p53 conditional knockout [cKO] mice) and found that aged p53-cKO mice spontaneously developed inflammatory lesions in various organs, including lung, liver, stomach, thyroid gland, submandibular gland, and kidney. Additionally, anti-nuclear Abs and autoantibodies against gastric parietal cells were detected in p53-cKO mice but not in control p53(fl/fl) mice (p53 wild-type mice). Importantly, the number of Foxp3(+)CD4(+) regulatory T cells (Tregs) in the spleen and lung as well as in vitro differentiation of induced Tregs was significantly reduced in p53-cKO mice as compared with that in p53 wild-type mice. Regarding the mechanisms underlying p53-mediated Treg induction, p53 enhanced the transcription of Foxp3 by binding to the promoter and the conserved noncoding DNA sequence-2 of the Foxp3 gene. Taken together, these results suggest that p53 expressed in T cells functions as a suppressor for autoimmunity by inducing Treg differentiation.
C1 [Kawashima, Hirotoshi; Takatori, Hiroaki; Suzuki, Kotaro; Iwata, Arifumi; Yokota, Masaya; Suto, Akira; Hirose, Koichi; Nakajima, Hiroshi] Chiba Univ, Grad Sch Med, Dept Allergy & Clin Immunol, Chiba 2608670, Japan.
   [Minamino, Tohru] Niigata Univ, Grad Sch Med & Dent Sci, Dept Cardiovasc Biol & Med, Niigata 9518510, Japan.
C3 Chiba University; Niigata University
RP Takatori, H (corresponding author), Chiba Univ, Grad Sch Med, Dept Allergy & Clin Immunol, Chuo Ku, 1-8-1 Inohana, Chiba 2608670, Japan.
EM takatorih@faculty.chiba-u.jp; nakajimh@faculty.chiba-u.jp
RI Nakajima, Hiroshi/AFU-9313-2022; Hirose, Koichi/I-1506-2017; Minamino,
   Tohru/P-8145-2018
OI Nakajima, Hiroshi/0000-0001-8595-9381; Minamino,
   Tohru/0000-0003-1627-6151; Suto, Akira/0000-0002-2593-565X
FU Ministry of Education, Culture, Sports, Science and Technology; Japanese
   Government; Global Centers of Excellence Program (Global Center for
   Education and Research in Immune System Regulation and Treatment) of the
   Ministry of Education, Culture, Sports, Science and Technology, Japan;
   Grants-in-Aid for Scientific Research [24390207, 24790989, 23591113,
   23591458, 23591432] Funding Source: KAKEN
FX This work was supported in part by grants-in-aids for scientific
   research from the Ministry of Education, Culture, Sports, Science and
   Technology, the Japanese Government, and by the Global Centers of
   Excellence Program (Global Center for Education and Research in Immune
   System Regulation and Treatment) of the Ministry of Education, Culture,
   Sports, Science and Technology, Japan.
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NR 45
TC 73
Z9 82
U1 0
U2 22
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2013
VL 191
IS 7
BP 3614
EP 3623
DI 10.4049/jimmunol.1300509
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 221CH
UT WOS:000324634500017
PM 24006461
DA 2025-06-01
ER

PT J
AU Dawson, RE
   Deswaerte, V
   West, AC
   Sun, EKM
   Wray-McCann, G
   Livis, T
   Kumar, B
   Rodriguez, E
   Gabay, C
   Ferrero, RL
   Jenkins, BJ
AF Dawson, Ruby E.
   Deswaerte, Virginie
   West, Alison C.
   Sun, Ekimei
   Wray-McCann, Georgie
   Livis, Thaleia
   Kumar, Beena
   Rodriguez, Emiliana
   Gabay, Cem
   Ferrero, Richard L.
   Jenkins, Brendan J.
TI The cytosolic DNA sensor AIM2 promotes Helicobacter-induced
   gastric pathology via the inflammasome
SO IMMUNOLOGY AND CELL BIOLOGY
LA English
DT Article
DE Absent in melanoma 2 (AIM2); gastritis; Helicobacter; inflammasome
ID INTESTINAL HOMEOSTASIS; ADAPTER ASC; TUMORIGENESIS; CANCER; CELLS;
   PHOSPHORYLATION; ACTIVATION; COLON; LIFE
AB Helicobacter pylori (H. pylori) infection can trigger chronic gastric inflammation perpetuated by overactivation of the innate immune system, leading to a cascade of precancerous lesions culminating in gastric cancer. However, key regulators of innate immunity that promote H. pylori-induced gastric pathology remain ill-defined. The innate immune cytosolic DNA sensor absent in melanoma 2 (AIM2) contributes to the pathogenesis of numerous autoimmune and chronic inflammatory diseases, as well as cancers including gastric cancer. We therefore investigated whether AIM2 contributed to the pathogenesis of Helicobacter-induced gastric disease. Here, we reveal that AIM2 messenger RNA and protein expression levels are elevated in H. pylori-positive versus H. pylori-negative human gastric biopsies. Similarly, chronic Helicobacter felis infection in wild-type mice augmented Aim2 gene expression levels compared with uninfected controls. Notably, gastric inflammation and hyperplasia were less severe in H. felis-infected Aim2(-/-) versus wild-type mice, evidenced by reductions in gastric immune cell infiltrates, mucosal thickness and proinflammatory cytokine and chemokine release. In addition, H. felis-driven proliferation and apoptosis in both gastric epithelial and immune cells were largely attenuated in Aim2(-/-) stomachs. These observations in Aim2(-/-) mouse stomachs correlated with decreased levels of inflammasome activity (caspase-1 cleavage) and the mature inflammasome effector cytokine, interleukin-1 beta. Taken together, this work uncovers a pathogenic role for the AIM2 inflammasome in Helicobacter-induced gastric disease, and furthers our understanding of the host immune response to a common pathogen and the complex and varying roles of AIM2 at different stages of cancerous and precancerous gastric disease.
C1 [Dawson, Ruby E.; Deswaerte, Virginie; West, Alison C.; Sun, Ekimei; Wray-McCann, Georgie; Livis, Thaleia; Ferrero, Richard L.; Jenkins, Brendan J.] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
   [Dawson, Ruby E.; Deswaerte, Virginie; West, Alison C.; Sun, Ekimei; Wray-McCann, Georgie; Livis, Thaleia; Ferrero, Richard L.; Jenkins, Brendan J.] Monash Univ, Fac Med, Dept Mol & Translat Sci, Nursing & Hlth Sci, Clayton, Vic, Australia.
   [Kumar, Beena] Monash Hlth, Dept Anat Pathol, Clayton, Vic, Australia.
   [Rodriguez, Emiliana; Gabay, Cem] Univ Geneva, Pathol & Immunol Dept, CMU, Geneva, Switzerland.
   [Ferrero, Richard L.] Monash Univ, Biomed Discovery Inst, Dept Microbiol, Clayton, Vic, Australia.
C3 Hudson Institute of Medical Research; Monash University; Monash Health;
   University of Geneva; Monash University
RP Jenkins, BJ (corresponding author), Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
EM brendan.jenkins@hudson.org.au
RI jenkins, brendan/J-7854-2012; Gabay, Cem/LJM-4539-2024; Ferrero,
   Richard/U-1332-2017
OI Ferrero, Richard/0000-0001-6817-6211; Wray-McCann,
   Georgie/0009-0005-3156-9392
FU United States Department of Defense [CA210128]; Victorian Government of
   Australia; National Health and Medical Research Council (NHMRC) of
   Australia [APP1139371]; NHMRC Senior Research Fellowships
FX This work was funded by a Peer Reviewed Cancer Research Program Idea
   Award (CA210128) from the United States Department of Defense (BJJ).
   This work was also supported by the Operational Infrastructure Support
   Program by the Victorian Government of Australia, and a Project
   Grant(APP1139371) from the National Health and Medical Research Council
   (NHMRC) of Australia (BJJ). BJJ and RLF were supported by NHMRC Senior
   Research Fellowships.
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NR 51
TC 7
Z9 7
U1 0
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0818-9641
EI 1440-1711
J9 IMMUNOL CELL BIOL
JI Immunol. Cell Biol.
PD MAY
PY 2023
VL 101
IS 5
BP 444
EP 457
DI 10.1111/imcb.12641
EA APR 2023
PG 14
WC Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology
GA E5FV4
UT WOS:000971860800001
PM 36967659
OA hybrid
DA 2025-06-01
ER

PT J
AU Bai, X
   Guo, YR
   Zhu, XM
   Dai, DQ
AF Bai, Xiao
   Guo, Yunran
   Zhu, Xinmao
   Dai, Dongqiu
TI Autoimmune diseases and risk of gastrointestinal cancer: an umbrella
   review of meta-analyses of observational studies
SO INTERNATIONAL JOURNAL OF SURGERY
LA English
DT Article
DE autoimmune diseases; gastrointestinal cancer; risk factor; umbrella
   review
ID INFLAMMATORY-BOWEL-DISEASE; CLINICAL-PRACTICE UPDATE; PERNICIOUS-ANEMIA;
   COLORECTAL-CANCER; SURVEILLANCE; COLONOSCOPY; MANAGEMENT; INHIBITORS;
   DYSPLASIA; NETWORKS
AB Background:Several autoimmune diseases (ADs) are considered risk factors for gastrointestinal (GI) cancers. This study pooled and appraised the evidence associating ADs with GI cancer risks.Methods:Three databases were examined from initiation through 26 January 2024. Evidence was determined by the criteria including the P-value of random-effects, small-study effects, excess significance bias, heterogeneity, and 95% prediction interval.Results:Fourteen meta-analyses including 211 primary studies describing 31 associations were selected. Inflammatory bowel disease (IBD) and Crohn's disease (CD) are strong risk factors (with effect sizes of 10.33 and 12.12, respectively) for small bowel cancer (SBC), as indicated by highly suggestive evidence. Another highly suggestive evidence is that gastric cancer (GC) risk was elevated in individuals suffering from pernicious anemia (PA, effect size: 2.80). Suggestive evidence emerged that the risks of colorectal cancer (CRC) were decreased in patients with rheumatoid arthritis (RA, effect size: 0.79) but increased in patients with IBD (effect size: 1.82).Conclusions:This study finds three highly suggestive pieces of evidence of IBD and CD patients with higher SBC risk and PA patients with higher GC risk. Future studies should identify these associations to provide more personalized cancer screenings for patients with ADs.
C1 [Bai, Xiao; Zhu, Xinmao; Dai, Dongqiu] China Med Univ, Dept Surg Oncol, Affiliated Hosp 4, 4 Chongshan East Rd, Shenyang 110032, Peoples R China.
   [Guo, Yunran] China Med Univ, Hlth Sci Inst, Shenyang, Peoples R China.
   [Dai, Dongqiu] China Med Univ, Canc Ctr, Affiliated Hosp 4, 4 Chongshan East Rd, Shenyang 110032, Peoples R China.
C3 China Medical University; China Medical University; China Medical
   University
RP Dai, DQ (corresponding author), China Med Univ, Dept Surg Oncol, Affiliated Hosp 4, 4 Chongshan East Rd, Shenyang 110032, Peoples R China.; Dai, DQ (corresponding author), China Med Univ, Canc Ctr, Affiliated Hosp 4, 4 Chongshan East Rd, Shenyang 110032, Peoples R China.
EM dqdai@cmu.edu.cn
OI Guo, Yunran/0000-0002-3951-483X; Bai, Xiao/0000-0001-5964-0289
FU National Natural Science Foundation of China [81972322]
FX This work was supported by the National Natural Science Foundation of
   China (Grant No. 81972322).
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NR 97
TC 0
Z9 0
U1 4
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1743-9191
EI 1743-9159
J9 INT J SURG
JI Int. J. Surg.
PD FEB
PY 2025
VL 111
IS 2
BP 2273
EP 2282
DI 10.1097/JS9.0000000000002219
PG 10
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA W9C7Q
UT WOS:001421468300008
PM 39764592
OA gold
DA 2025-06-01
ER

PT J
AU Zeuzem, S
AF Zeuzem, S
TI Gut-liver axis
SO INTERNATIONAL JOURNAL OF COLORECTAL DISEASE
LA English
DT Review
DE enterohepatic circulation; bile acids; motility; portal system;
   inflammatory bowel disease
ID PRIMARY SCLEROSING CHOLANGITIS; SPONTANEOUS BACTERIAL PERITONITIS;
   TUMOR-NECROSIS-FACTOR; BILE-ACID MALABSORPTION; NITRIC-OXIDE SYNTHASE;
   INFLAMMATORY-BOWEL-DISEASE; ACQUIRED IMMUNODEFICIENCY SYNDROME;
   INTERCELLULAR-ADHESION MOLECULE-1; PORTAL HYPERTENSIVE GASTROPATHY;
   PROTEIN-CALORIE MALNUTRITION
AB The gut and the liver are the key organs in nutrient absorption and metabolism. Bile acids, drugs, and toxins undergo extensive enterohepatic circulation. Bile acids play a major role in several hepatic and intestinal diseases. Endotoxins deriving from intestinal Gram-negative bacteria are important in the pathogenesis of liver and systemic diseases. Chronic liver diseases can influence gastrointestinal motility, which together with other factors may contribute to bacterial overgrowth and in patients with ascites to an increased risk of spontaneous bacterial peritonitis. Patients with end-stage liver disease frequently develop portal hypertension leading to varices, gastric vascular ectasia, and portal hypertensive gastroenteropathy. Several liver and biliary abnormalities are observed in patients with inflammatory bowel disease (primary sclerosing cholangitis, autoimmune hepatitis, cholelithiasis). The primary defect in hemochromatosis is located in the intestine, causing an inappropriate increase in iron absorption, and the liver is the site of earliest and heaviest iron deposition. Elevated transaminases are observed in many patients with celiac disease, and steatohepatitis frequently develops in patients with jejunoileal bypass and short bowel syndrome. Furthermore, the liver is the primary organ for metastasis of intestinal cancer. Many viral, bacterial, fungal, and parasitic diseases affect the intestine as well as the liver and the biliary tract.
C1 Univ Frankfurt Klinikum, Zentrum Inneren Med, Med Klin 2, D-60590 Frankfurt, Germany.
C3 Goethe University Frankfurt; Goethe University Frankfurt Hospital
RP Univ Frankfurt Klinikum, Zentrum Inneren Med, Med Klin 2, Theodor Stern Kai 7, D-60590 Frankfurt, Germany.
EM Zeuzem@em.uni-frankfurt.de
RI Zeuzem, Stefan/AAE-7435-2019
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NR 300
TC 92
Z9 102
U1 1
U2 32
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0179-1958
EI 1432-1262
J9 INT J COLORECTAL DIS
JI Int. J. Colorectal Dis.
PD APR
PY 2000
VL 15
IS 2
BP 59
EP 82
DI 10.1007/s003840050236
PG 24
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA 320GH
UT WOS:000087393100001
PM 10855547
DA 2025-06-01
ER

PT J
AU Mohamed, AH
   Obeid, RA
   Fadhil, AA
   Amir, AA
   Adhab, ZH
   Jabouri, EA
   Ahmad, I
   Alshahrani, MY
AF Mohamed, Asma 'a H.
   Obeid, Ruaa Ali
   Fadhil, Ali Abdulhussain
   Amir, Ahmed Ali
   Adhab, Zainab H.
   Jabouri, Enaam Anad
   Ahmad, Irfan
   Alshahrani, Mohammad Y.
TI BTLA and HVEM: Emerging players in the tumor microenvironment and cancer
   progression
SO CYTOKINE
LA English
DT Review
DE BTLA; HEVM; Neoplasm; TNFR superfamily; Inhibitory Receptor Checkpoint;
   Immune checkpoint Inhibitors
ID T-LYMPHOCYTE ATTENUATOR; VIRUS ENTRY MEDIATOR; B-CELL LYMPHOMA;
   INHIBITORY RECEPTOR BTLA; HIGH EXPRESSION; CLINICAL-SIGNIFICANCE;
   POOR-PROGNOSIS; IMMUNE ESCAPE; LUNG-CANCER; PROLIFERATION
AB Immunotherapy has emerged as a revolutionary cancer treatment, particularly with the introduction of immune checkpoint inhibitors (ICIs). ICIs target specific proteins that restrain the immune system from attacking cancer cells. Prominent examples of checkpoint proteins that ICIs block include PD-1, PD-L1, and CTLA-4. The success of PD-1/L1 and CTLA-4 blockade has prompted further research on other inhibitory mechanisms that could aid in the treatment of cancer. One such mechanism is the BTLA/HVEM checkpoint, which regulates immune responses in a similar manner to CTLA-4 and PD-1. BTLA, a member of the Ig superfamily, binds to HVEM, a member of the TNF receptor superfamily. While BTLA is essential for maintaining immunological self-tolerance and preventing autoimmune diseases, overexpression of BTLA and HVEM has been observed in various malignancies such as lung, ovarian, glioblastoma, gastric cancer, and non-Hodgkin's lymphoma. The function of the BTLA/HVEM checkpoint in various malignancies has been extensively studied, revealing its significant role in immunotherapy for cancer. This review study aims to explain the BTLA/HVEM checkpoint and its functions in different types of cancers. In conclusion, the development of new immunotherapies such as ICIs has revolutionized cancer treatment. The discovery of the BTLA/HVEM checkpoint and its role in various malignancies provides opportunities for advancing cancer treatment through immunotherapy.
C1 [Mohamed, Asma 'a H.] Al Mustaqbal Univ Coll, Intelligent Med Syst Dept, Hilla 51001, Babylon, Iraq.
   [Obeid, Ruaa Ali] Univ Al Ameed, Coll Pharm, Dept Pharmaceut, Karbala, Iraq.
   [Fadhil, Ali Abdulhussain] Al Farahidi Univ, Coll Med Technol, Med Lab Tech, Baghdad, Iraq.
   [Amir, Ahmed Ali] AL Nisour Univ Coll, Dept Med Labs Technol, Baghdad, Iraq.
   [Adhab, Zainab H.] Al Zahrawi Univ Coll, Dept Pharm, Karbala, Iraq.
   [Jabouri, Enaam Anad] AlNoor Univ Coll, Dept Med Lab Tech, Nineveh, Iraq.
   [Ahmad, Irfan; Alshahrani, Mohammad Y.] King Khalid Univ, Coll Appl Med Sci, Dept Clin Lab Sci, POB 960, Abha 62529, Saudi Arabia.
C3 Al-Mustaqbal University College; University of Al-Ameed; Al-Farahidi
   University; Al-Nisour University College; Al-Zahrawi University College;
   Alnoor University; King Khalid University
RP Ahmad, I (corresponding author), King Khalid Univ, Coll Appl Med Sci, Dept Clin Lab Sci, POB 960, Abha 62529, Saudi Arabia.
EM irfancsmmu@gmail.com
RI Alshahrani, M/AAX-9276-2020; Ahmad, I/AFO-5220-2022; ABDUL-HUSSEIN,
   ALI/GOK-1196-2022; , Al-Zahrawi University College/KEE-9430-2024
OI , Al-Zahrawi University College/0009-0006-0211-3887; Alshahrani,
   Mohammad Y./0009-0006-9288-2523; Ahmad, Irfan/0009-0005-0251-0922
FU Deanship of Scientific Research at King Khalid University
   [RGP.02/339/44]
FX The authors express their gratitude to the Deanship of Scientific
   Research at King Khalid University for funding this work through the
   Large Research Group Project under grant number RGP.02/339/44.
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NR 89
TC 4
Z9 5
U1 0
U2 9
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD DEC
PY 2023
VL 172
AR 156412
DI 10.1016/j.cyto.2023.156412
EA NOV 2023
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA Y6ES8
UT WOS:001106177500001
PM 39492110
DA 2025-06-01
ER

PT J
AU Grant, WB
AF Grant, William B.
TI Hypothesis-ultraviolet-B irradiance and vitamin D reduce the risk of
   viral infections and thus their sequelae, including autoimmune diseases
   and some cancers
SO PHOTOCHEMISTRY AND PHOTOBIOLOGY
LA English
DT Review
ID EPSTEIN-BARR-VIRUS; ENVIRONMENTAL TOBACCO-SMOKE;
   INFLAMMATORY-BOWEL-DISEASE; PROSTATE-CANCER; MULTIPLE-SCLEROSIS;
   HUMAN-PAPILLOMAVIRUS; D-RECEPTOR; ANTIMICROBIAL PEPTIDES; D
   SUPPLEMENTATION; UNITED-STATES
AB Many viral infections reach clinical significance in winter, when it is cold, relative humidity is lowest and vitamin D production from solar ultraviolet-B irradiation is at its nadir. Several autoimmune diseases, such as multiple sclerosis, type I diabetes mellitus and asthma, are linked to viral infections. Vitamin D, through induction of cathelicidin, which effectively combats both bacterial and viral infections, may reduce the risk of several autoimmune diseases and cancers by reducing the development of viral infections. Some types of cancer are also linked to viral infections. The cancers with seemingly important risk from viral infections important in winter, based on correlations with increasing latitude in the United States, an index of wintertime solar ultraviolet-B dose and vitamin D, are bladder, prostate, testicular and thyroid cancer, Hodgkin's and non-Hodgkin's lymphoma, and, perhaps, gastric cancer. The evidence examined includes the role of viruses in the etiology of these diseases, the geographic and seasonal variation of these diseases, and the time of life when vitamin D is effective in reducing the risk of disease. In general, the evidence supports the hypothesis. However, further work is required to evaluate this hypothesis.
C1 Sunlight Nutr & Hlth Res Ctr SUNARC, San Francisco, CA USA.
RP Grant, WB (corresponding author), Sunlight Nutr & Hlth Res Ctr SUNARC, San Francisco, CA USA.
EM wgrant@infionline.net
RI Grant, William/B-8311-2009
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NR 177
TC 64
Z9 69
U1 0
U2 14
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0031-8655
EI 1751-1097
J9 PHOTOCHEM PHOTOBIOL
JI Photochem. Photobiol.
PD MAR-APR
PY 2008
VL 84
IS 2
BP 356
EP 365
DI 10.1111/j.1751-1097.2007.00266.x
PG 10
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA 270UZ
UT WOS:000253747000013
PM 18179620
DA 2025-06-01
ER

PT J
AU Eleftheriadis, T
   Antoniadi, G
   Liakopoulos, V
   Kortsaris, A
AF Eleftheriadis, Theodoros
   Antoniadi, Georgia
   Liakopoulos, Vassihos
   Kortsaris, Alexandros
TI T-Cell zeta chain expression, phosphorylation and degradation and their
   role in T-cell signal transduction and immune response regulation in
   health and disease
SO CURRENT SIGNAL TRANSDUCTION THERAPY
LA English
DT Review
DE T-cell receptor; zeta chain; cancer; autoimmune disease; infection;
   inflammation
ID PROTEIN-TYROSINE-PHOSPHATASE; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
   TUMOR-INFILTRATING LYMPHOCYTES; PERIPHERAL-BLOOD LYMPHOCYTES; WEIGHT
   PHOSPHOTYROSINE PHOSPHATASE; SEVERE COMBINED IMMUNODEFICIENCY;
   GASTRIC-CARCINOMA PATIENTS; LEUKOCYTE-COMMON ANTIGEN; MYELOID
   SUPPRESSOR-CELLS; OVARIAN-CANCER PATIENTS
AB T-cell zeta chain expression, phosphorylation and degradation and their role in T-cell signal transduction and immune response regulation in health and disease.
   Zeta chain is a stable constituent of the antigen specific T-cell receptor and its phosphorylation is one of the earliest and key events in the T-cell signal transduction. Zeta chain phosphorylation is strictly controlled by the action of sarcoma-family kinases and also by phosphatases, indicating its crucial role in antigen specific T-cell activation. Furthermore, after its phosphorylation and T-cell activation, xi-chain is ubiquitylated and degraded, a fact suggesting that its level on T-cell surface is also under control and contribute to the regulation of an initiated immune response.
   Zeta chain expression and/or phosphorylation seems to be of great importance in many clinical conditions from the pathogenesis of various types of cancer to the immunosuppressive state in dialysis patients. Its levels are also affected by chronic inflammation.
   In addition to its role in the antigen specific signal transduction, xi-chain is present only in T-cells and natural killer cells, making it a possible target for immunotherapeutic applications. The recent discovery of specific inhibitors of xi-chain phosphorylation opens new horizons for future research and for possible therapeutic interventions in various clinical conditions.
C1 Univ Thessaly, Dept Nephrol, Larisa, Greece.
   Democritus Univ Thrace, Biochem Lab, Alexandroupolis, Greece.
C3 University of Thessaly; Democritus University of Thrace
RP Eleftheriadis, T (corresponding author), Kriezotou 17, GR-54645 Thessaloniki, Greece.
EM elefthe@otenet.gr
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NR 194
TC 10
Z9 10
U1 0
U2 5
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-3624
EI 2212-389X
J9 CURR SIGNAL TRANSD T
JI Curr. Signal Transduct. Ther.
PD MAY
PY 2006
VL 1
IS 2
BP 191
EP 208
DI 10.2174/157436206777012039
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 168FH
UT WOS:000246508000005
DA 2025-06-01
ER

PT J
AU Tsang, KW
   Lam, SK
AF Tsang, KW
   Lam, SK
TI Helicobacter pylori and extra-digestive diseases
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Review
DE Helicobacter pylori; infection; inflammation; seroprevalence
ID CORONARY HEART-DISEASE; HUMAN RESPIRATORY MUCOSA; TUMOR-NECROSIS-FACTOR;
   PEPTIC-ULCERATION; CAMPYLOBACTER-PYLORIDIS; PSEUDOMONAS-AERUGINOSA;
   HAEMOPHILUS-INFLUENZAE; HIGH SEROPREVALENCE; GASTRIC LYMPHOMA;
   RISK-FACTORS
AB Helicobacter pylori is a recently rediscovered Gram-negative bacteria that causes peptic ulcer disease, gastric lymphoma and gastric carcinoma. Helicobacter pylori achieves its pathogenetic role by triggering an intense leucocyte infiltration of the gastric submucosa which is mediated by proinflammatory cytokines. This pathogenetic mechanism is common to many other diseases and therefore, Helicobacter pylori seroprevalence has also been investigated in other diseases. It is now known that H. pylori seropositivity is associated with an increasing number of cardiovascular, respiratory extra-gastroduodenal digestive, neurological, skin, autoimmune, growth and miscellaneous disorders. Although the precise role for H. pylori is unknown in these diseases, it is of tremendous interest to most clinicians and scientists as H. pylori is amenable to eradication therapy using simple and reliable drug regimens. The conditions associated with H. pylori seropositivity are highlighted in this concise article. (C) 1999 Blackwell Science Asia Pty Ltd.
C1 Univ Hong Kong, Queen Mary Hosp, Univ Dept Med, Hong Kong, Peoples R China.
C3 University of Hong Kong
RP Univ Hong Kong, Queen Mary Hosp, Univ Dept Med, Hong Kong, Peoples R China.
EM kwtt@hkucc.hku.hk
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NR 68
TC 55
Z9 68
U1 1
U2 5
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0815-9319
EI 1440-1746
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD SEP
PY 1999
VL 14
IS 9
BP 844
EP 850
DI 10.1046/j.1440-1746.1999.01974.x
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 240UR
UT WOS:000082845500003
PM 10535464
OA Bronze
DA 2025-06-01
ER

PT J
AU Zhang, Y
   Ma, DX
   Zhang, Y
   Tian, YJ
   Wang, XP
   Qiao, YB
   Cui, BX
AF Zhang, Yan
   Ma, Daoxin
   Zhang, Yong
   Tian, Yongju
   Wang, Xuping
   Qiao, Yunbo
   Cui, Baoxia
TI The imbalance of Th17/Treg in patients with uterine cervical cancer
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Uterine cervical cancer; Cervical intraepithelial neoplasia; T helper
   17; CD4(+)CD25(+)Foxp3(+) regulatory T cells; Immune imbalance
ID REGULATORY T-CELLS; TH17 CELLS; TUMOR-IMMUNITY; INFILTRATING
   LYMPHOCYTES; IL-17-PRODUCING CELLS; PERIPHERAL-BLOOD; GASTRIC-CANCER;
   ROR-GAMMA; DIFFERENTIATION; CARCINOMA
AB Background: Th17/Treg was reported to play critical roles in immunoregulation, and its imbalance may lead to autoimmune diseases and allergic reactions. Information on Th17/Treg in cancer bearing hosts is still limited.
   Methods: We examined the expression of IL-17, Foxp3 and IL-10 in uterine cervical cancer (UCC) patients, cervical intraepithelial neoplasia (GIN) patients and healthy controls by flow cytometry and enzyme-linked immunosorbent assay. Interleukin (IL)-17-producing CD4(+) cells as Th17 and CD4(+)CD25(+)Foxp3(+) cells as Treg were expressed as a percentage of the total CD4(+) cells.
   Results: Compared with controls, patients with UCC or GIN had a higher proportion of Th17 cells. UCC patients also revealed a significant increase in Treg number and IL-17 and IL-10 concentrations in plasma, while CIN patients did not. Notably, in UCC patients, the increased Th17 prevalence was associated with clinical stage, lymph node metastases and vasoinvasion, while the increased Treg frequency was associated with tumor differentiation. Remarkably, an attractive imbalance of Th17/Treg was observed in UUC and CIN patients. Furthermore. in UCC patients with lymph node metastases or vasoinvasion, the ratio of Th17/Treg was significantly higher than that in negative patients respectively.
   Conclusions: Our results indicated a possible role of Th17 in UCC patients correlated to Treg cells, and the imbalance of Th17/Treg may be involved in the development and progression of UCC. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Zhang, Yan; Tian, Yongju; Qiao, Yunbo; Cui, Baoxia] Shandong Univ, Qilu Hosp, Dept Obstet & Gynecol, Jinan 250012, Shandong, Peoples R China.
   [Zhang, Yan; Ma, Daoxin; Tian, Yongju; Wang, Xuping; Cui, Baoxia] Shandong Univ, Qilu Hosp, Chinese Minist Hlth, Jinan 250012, Shandong, Peoples R China.
   [Zhang, Yan; Ma, Daoxin; Tian, Yongju; Wang, Xuping; Cui, Baoxia] Chinese Minist Educ, Key Lab Cardiovasc Remodeling & Funct Res, Jinan, Peoples R China.
   [Ma, Daoxin] Shandong Univ, Qilu Hosp, Haematol Oncol Ctr, Jinan 250012, Shandong, Peoples R China.
   [Zhang, Yong] Peoples Hosp, Weifang City 262500, Shandong, Peoples R China.
C3 Shandong University; Shandong University; Ministry of Education - China;
   Shandong University
RP Cui, BX (corresponding author), Shandong Univ, Qilu Hosp, Dept Obstet & Gynecol, 107 WenhuaXi Rd, Jinan 250012, Shandong, Peoples R China.
EM baoxiacui@hotmail.com
FU National Natural Science Foundation of China [30400475, 81070407];
   Shandong Technological Development Project [2006BS03060, Q2008C07,
   BS2009SW014]; Scientific Research Foundation (SRF) for the Returned
   Overseas Chinese Scholars (ROCS); State Education Ministry (SEM);
   Independent Innovation Foundation of Shandong University [2009TS063]
FX This study was supported by grants from the National Natural Science
   Foundation of China (Nos. 30400475 and 81070407), the Shandong
   Technological Development Project (Nos. 2006BS03060, Q2008C07 and
   BS2009SW014), the Scientific Research Foundation (SRF) for the Returned
   Overseas Chinese Scholars (ROCS), the State Education Ministry (SEM),
   and Independent Innovation Foundation of Shandong University
   (2009TS063).
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NR 37
TC 72
Z9 88
U1 0
U2 23
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0009-8981
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD MAY 12
PY 2011
VL 412
IS 11-12
BP 894
EP 900
DI 10.1016/j.cca.2011.01.015
PG 7
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA 770YU
UT WOS:000291125200015
PM 21255562
DA 2025-06-01
ER

PT J
AU Asl, MH
   Khelejani, FP
   Mahdavi, SZB
   Emrahi, L
   Jebelli, A
   Mokhtarzadeh, A
AF Asl, Mohammad Heydarnezhad
   Khelejani, Faezeh Pasban
   Mahdavi, Seyedeh Zahra Bahojb
   Emrahi, Leila
   Jebelli, Asiyeh
   Mokhtarzadeh, Ahad
TI The various regulatory functions of long noncoding RNAs in apoptosis,
   cell cycle, and cellular senescence
SO JOURNAL OF CELLULAR BIOCHEMISTRY
LA English
DT Review
DE apoptosis; cell cycle; cellular senescence; lncRNA
ID EPITHELIAL-MESENCHYMAL TRANSITION; MAMMALIAN MITOCHONDRIAL FISSION;
   COLORECTAL-CANCER; EMERGING ROLES; POOR-PROGNOSIS; GASTRIC-CANCER;
   TRANSCRIPTIONAL REGULATION; HEPATOCELLULAR-CARCINOMA; DOWN-REGULATION;
   OVARIAN-CANCER
AB Long noncoding RNAs (lncRNAs) are a group of noncoding cellular RNAs involved in significant biological phenomena such as differentiation, cell development, genomic imprinting, adjusting the enzymatic activity, regulating chromosome conformation, apoptosis, cell cycle, and cellular senescence. The misregulation of lncRNAs interrupting normal biological processes has been implicated in tumor formation and metastasis, resulting in cancer. Apoptosis and cell cycle, two main biological phenomena, are highly conserved and intimately coupled mechanisms. Hence, some cell cycle regulators can influence both programmed cell death and cell division. Apoptosis eliminates defective and unwanted cells, and the cell cycle enables cells to replicate themselves. The improper regulation of apoptosis and cell cycle contributes to numerous disorders such as neurodegenerative and autoimmune diseases, viral infection, anemia, and mainly cancer. Cellular senescence is a tumor-suppressing response initiated by environmental and internal stress factors. This phenomenon has recently attained more attention due to its therapeutic implications in the field of senotherapy. In this review, the regulatory roles of lncRNAs on apoptosis, cell cycle, and senescence will be discussed. First, the role of lncRNAs in mitochondrial dynamics and apoptosis is addressed. Next, the interaction between lncRNAs and caspases, pro/antiapoptotic proteins, and also EGFR/PI3K/PTEN/AKT/mTORC1 signaling pathway will be investigated. Furthermore, the effect of lncRNAs in the cell cycle is surveyed through interaction with cyclins, cdks, p21, and wnt/beta-catenin/c-myc pathway. Finally, the function of essential lncRNAs in cellular senescence is mentioned.
C1 [Asl, Mohammad Heydarnezhad] Univ Tabriz, Fac Nat Sci, Dept Biol, Tabriz, Iran.
   [Khelejani, Faezeh Pasban] Univ Maragheh, Fac Basic Sci, Dept Cell & Mol Biol, Maragheh, Iran.
   [Mahdavi, Seyedeh Zahra Bahojb] Azarbaijan Shahid Madani Univ, Fac Basic Sci, Dept Biol, Tabriz, Iran.
   [Emrahi, Leila] Tarbiat Modares Univ, Fac Med Sci, Dept Med Genet, Tehran, Iran.
   [Jebelli, Asiyeh] Higher Educ Inst Rab Rashid, Fac Basic Sci, Dept Biol Sci, Tabriz, Iran.
   [Jebelli, Asiyeh] Tabriz Univ Med Sci, TB & Lung Dis Res Ctr, Tabriz, Iran.
   [Mokhtarzadeh, Ahad] Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
C3 University of Tabriz; University of Maragheh; Azarbaijan Shahid Madani
   University; Tarbiat Modares University; Tabriz University of Medical
   Science; Tabriz University of Medical Science
RP Jebelli, A (corresponding author), Higher Educ Inst Rab Rashid, Fac Basic Sci, Dept Biol Sci, Tabriz, Iran.; Mokhtarzadeh, A (corresponding author), Tabriz Univ Med Sci, Immunol Res Ctr, Tabriz, Iran.
EM jebelli.a@raberashidi.ac.ir; mokhtarzadehah@tbzmed.ac.ir
RI Jebelli, Asiyeh/IAP-3359-2023; Mokhtarzadeh, Ahad/V-3748-2017
OI jebelli, asiyeh/0000-0001-9494-2207
FU Immunology Research Center, Tabriz University of Medical Sciences
   [67252, 67255]
FX The authors are grateful for the financial support from the Immunology
   Research Center, Tabriz University of Medical Sciences (Grant numbers:
   67252 and 67255).
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NR 209
TC 40
Z9 41
U1 1
U2 29
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0730-2312
EI 1097-4644
J9 J CELL BIOCHEM
JI J. Cell. Biochem.
PD JUN
PY 2022
VL 123
IS 6
BP 995
EP 1024
DI 10.1002/jcb.30221
EA FEB 2022
PG 30
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 2C9JI
UT WOS:000749470100001
PM 35106829
DA 2025-06-01
ER

PT J
AU Kishikawa, H
   Ojiro, K
   Nakamura, K
   Katayama, T
   Arahata, K
   Takarabe, S
   Miura, S
   Kanai, T
   Nishida, J
AF Kishikawa, Hiroshi
   Ojiro, Keisuke
   Nakamura, Kenji
   Katayama, Tadashi
   Arahata, Kyoko
   Takarabe, Sakiko
   Miura, Soichiro
   Kanai, Takanori
   Nishida, Jiro
TI Previous Helicobacter pylori infection-induced atrophic
   gastritis: A distinct disease entity in an understudied
   population without a history of eradication
SO HELICOBACTER
LA English
DT Review
DE chronic atrophic gastritis; endoscopy; eradication; gastric autoimmune
   diseases; Helicobacter pylori diagnosis; Helicobacter pylori infection
ID SERUM PEPSINOGEN LEVELS; PROTON PUMP INHIBITORS; GASTROINTESTINAL
   ENDOSCOPY; INTESTINAL METAPLASIA; NEGATIVE GASTRITIS; MUCOSAL ATROPHY;
   IGG ANTIBODIES; COMBINED ASSAY; CANCER RISK; CLASSIFICATION
AB Individuals with chronic atrophic gastritis who are negative for active H. pylori infection with no history of eradication therapy have been identified in clinical practice. By excluding false-negative and autoimmune gastritis cases, it can be surmised that most of these patients have experienced unintentional eradication of H. pylori after antibiotic treatment for other infectious disease, unreported successful eradication, or H. pylori that spontaneously disappeared. These patients are considered to have previous H. pylori infection-induced atrophic gastritis. In this work, we define these cases based on the following criteria: absence of previous H. pylori eradication; atrophic changes on endoscopy or histologic confirmation of glandular atrophy; negative for a current H. pylori infection diagnosed in the absence of proton-pump inhibitors or antibiotics; and absence of localized corpus atrophy, positivity for autoantibodies, or characteristic histologic findings suggestive of autoimmune gastritis. The risk of developing gastric cancer depends on the atrophic grade. The reported rate of developing gastric cancer is 0.31%-0.62% per year for successfully eradicated severely atrophic cases (pathophysiologically equal to unintentionally eradicated cases and unreported eradicated cases), and 0.53%-0.87% per year for spontaneously resolved cases due to severe atrophy. Therefore, for previous H. pylori infection-induced atrophic gastritis cases, we recommend endoscopic surveillance every 3 years for high-risk patients, including those with endoscopically severe atrophy or intestinal metaplasia. Because of the difficulty involved in the endoscopic diagnosis of gastric cancer in cases of previous infection, appropriate monitoring of the high-risk subgroup of this understudied population is especially important.
C1 [Kishikawa, Hiroshi; Ojiro, Keisuke; Nakamura, Kenji; Katayama, Tadashi; Arahata, Kyoko; Takarabe, Sakiko; Nishida, Jiro] Tokyo Dent Coll, Ichikawa Gen Hosp, Dept Gastroenterol, 5-11-13 Sugano, Ichikawa, Chiba 2728513, Japan.
   [Miura, Soichiro] Int Univ Hlth & Welf, Grad Sch, Minato Ku, Tokyo, Japan.
   [Kanai, Takanori] Keio Univ, Dept Internal Med, Div Gastroenterol & Hepatol, Shinjyuku Ku, Tokyo, Japan.
C3 Tokyo Dental College; International University of Health & Welfare; Keio
   University
RP Kishikawa, H (corresponding author), Tokyo Dent Coll, Ichikawa Gen Hosp, Dept Gastroenterol, 5-11-13 Sugano, Ichikawa, Chiba 2728513, Japan.
EM kisikawa@tdc.ac.jp
RI Kishikawa, Hiroshi/AAU-5977-2021; Kanai, Takanori/JPA-0539-2023
OI Kishikawa, Hiroshi/0000-0003-3689-2517
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NR 86
TC 54
Z9 63
U1 0
U2 15
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PD FEB
PY 2020
VL 25
IS 1
AR e12669
DI 10.1111/hel.12669
EA NOV 2019
PG 10
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Microbiology
GA KA1AB
UT WOS:000493710500001
PM 31680399
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Torne, AS
   Robertson, ES
AF Torne, Atharva S.
   Robertson, Erle S.
TI Epigenetic Mechanisms in Latent Epstein-Barr Virus Infection and
   Associated Cancers
SO CANCERS
LA English
DT Review
DE Epstein-Barr virus; tumor viruses; viral epigenetics; host virus
   interactions; microRNAs; EBV-associated cancers
ID MEMBRANE-PROTEIN 1; EPITHELIAL-MESENCHYMAL TRANSITION; NASOPHARYNGEAL
   CARCINOMA-CELLS; POSITIVE GASTRIC-CARCINOMA; NF-KAPPA-B;
   GENE-EXPRESSION; TRANSCRIPTIONAL ACTIVATION; ABERRANT METHYLATION;
   GLYCOPROTEIN GP340; VIRAL LATENCY
AB Simple Summary Epstein-Barr virus (EBV) was first isolated in 1964 and has since become an important human tumor virus. With an estimated 90% of the human population infected with the virus, EBV has also been shown to cause several types of cancers. The virus has evolved numerous epigenetic mechanisms by which it can affect its host and contribute to the development and progression of cancer. In this review, we introduce four prominent epigenetic regulatory mechanisms that result in host-virus interactions for the purpose of EBV infection, persistence, and contribution to EBV-associated diseases. We then look at how epigenetic profiles of the host are altered in EBV-associated cancers to understand the precise ways EBV interacts with its host to cause disease. This work explores the viral epigenetics of EBV and provides insights into the knowns and unknowns of research into EBV and EBV-associated cancers.Abstract The Epstein-Barr Virus (EBV) is a double-stranded DNA-based human tumor virus that was first isolated in 1964 from lymphoma biopsies. Since its initial discovery, EBV has been identified as a major contributor to numerous cancers and chronic autoimmune disorders. The virus is particularly efficient at infecting B-cells but can also infect epithelial cells, utilizing an array of epigenetic strategies to establish long-term latent infection. The association with histone modifications, alteration of DNA methylation patterns in host and viral genomes, and microRNA targeting of host cell factors are core epigenetic strategies that drive interactions between host and virus, which are necessary for viral persistence and progression of EBV-associated diseases. Therefore, understanding epigenetic regulation and its role in post-entry viral dynamics is an elusive area of EBV research. Here, we present current outlooks of EBV epigenetic regulation as it pertains to viral interactions with its host during latent infection and its propensity to induce tumorigenesis. We review the important epigenetic regulators of EBV latency and explore how the strategies involved during latent infection drive differential epigenetic profiles and host-virus interactions in EBV-associated cancers.
C1 [Torne, Atharva S.; Robertson, Erle S.] Univ Penn, Dept Otorhinolaryngol Head & Neck Surg, Tumor Virol Program, Perelman Sch Med, Philadelphia, PA 19104 USA.
C3 University of Pennsylvania
RP Robertson, ES (corresponding author), Univ Penn, Dept Otorhinolaryngol Head & Neck Surg, Tumor Virol Program, Perelman Sch Med, Philadelphia, PA 19104 USA.
EM atharva.torne@pennmedicine.upenn.edu; erle@pennmedicine.upenn.edu
OI Torne, Atharva/0009-0006-1692-8913; Robertson, Erle/0000-0002-6088-2979
FU National Cancer Institute
FX We sincerely apologize to the authors whose work could not be cited or
   discussed.
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NR 202
TC 10
Z9 11
U1 1
U2 5
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAR
PY 2024
VL 16
IS 5
AR 991
DI 10.3390/cancers16050991
PG 28
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA KV2N6
UT WOS:001182674400001
PM 38473352
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Jain, K
   Barve, K
   Bhatt, LK
AF Jain, Kripa
   Barve, Kalyani
   Bhatt, Lokesh Kumar
TI Gasdermins: Pore-forming Proteins as a Potential Therapeutic Target
SO CURRENT PROTEIN & PEPTIDE SCIENCE
LA English
DT Review
DE Gasdermins; pyroptosis; autoimmune disease; kidney diseases; CNS
   diseases; gasdermin mediated necrosis
ID NLRP3 INFLAMMASOME ACTIVATION; CELL-DEATH; PARKINSONS-DISEASE;
   GASTROINTESTINAL-TRACT; REGULATES PYROPTOSIS; DIABETIC-NEPHROPATHY;
   CYTOSOLIC BACTERIA; OXIDATIVE STRESS; LUPUS NEPHRITIS; GASTRIC-CANCER
AB Gasdermins are novel pore forming proteins that comprise Gasdermin A, Gasdermin B, Gasdermin C, Gasdermin D, Gasdermin E and Pejvakin (DFNB59). Recently, pyroptosis has been redefined as "Gasdermin mediated necrosis", as gasdermins are key regulators of apoptosis, necrosis, and pyroptosis. The discovery of the gasdermin family has broadened the field of pyroptosis studies. Studies have correlated gasdermins with several diseases. This review summarizes the physiological roles and signal transduction of gasdermins. It further highlights the role of gasdermins in pathological conditions like autoimmune disease, kidney diseases, and central nervous system diseases.
C1 [Jain, Kripa; Bhatt, Lokesh Kumar] Dr Bhanuben Nanavati Coll Pharm, Dept Pharmacol, Mumbai 400056, Maharashtra, India.
   [Jain, Kripa; Bhatt, Lokesh Kumar] SVKMs Dr Bhanuben Nanavati Coll Pharm, Dept Pharmacol, Mumbai, Maharashtra, India.
   [Barve, Kalyani] NMIMS Univ, SPP Sch Pharm & Technol Management, Dept Pharmacol, Mumbai, Maharashtra, India.
C3 SVKM's NMIMS (Deemed to be University)
RP Bhatt, LK (corresponding author), Dr Bhanuben Nanavati Coll Pharm, Dept Pharmacol, Mumbai 400056, Maharashtra, India.
EM Lokesh.bhatt@bncp.ac.in
RI Bhatt, Lokesh Kumar/O-3277-2015; , kalyani/I-1155-2019
OI Bhatt, Lokesh Kumar/0000-0002-4302-9300; , kalyani/0000-0003-4166-3380
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PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-2037
EI 1875-5550
J9 CURR PROTEIN PEPT SC
JI Curr. Protein Pept. Sci.
PY 2022
VL 23
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BP 133
EP 151
DI 10.2174/1389203723666220510123740
PG 19
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA 3I7TU
UT WOS:000832914900002
PM 35538820
DA 2025-06-01
ER

PT J
AU Yuzhalin, AE
   Kutikhin, AG
AF Yuzhalin, Arseniy E.
   Kutikhin, Anton G.
TI Interleukin-12: Clinical usage and molecular markers of cancer
   susceptibility
SO GROWTH FACTORS
LA English
DT Article
DE Interleukin-12; IL-12; SNP; cancer; carcinogenesis
ID RECOMBINANT HUMAN INTERLEUKIN-12; RENAL-CELL CARCINOMA;
   NON-HODGKINS-LYMPHOMA; VASOACTIVE-INTESTINAL-PEPTIDE; IFN-GAMMA
   PRODUCTION; PHASE-II TRIAL; HUMAN T-CELLS; GASTRIC-CANCER;
   HEPATOCELLULAR-CARCINOMA; MAMMARY CARCINOGENESIS
AB The last decade has seen the emergence of immunomodulators as therapeutic agents in cancer treatment. Interleukins (ILs) are a category of small cell-signaling molecules that organize communication and interaction between immune cells and therefore they could be used as perfect immunomodulators. IL-12 is a promising candidate for cancer immunotherapy since it plays a major role in development of antitumor immune response. Numerous studies report that IL-12 promotes an effective destruction of cancer cells both in vivo and in vitro. In addition, IL-12 has anti-angiogenic activity and it is able to dramatically decrease tumor-supportive activities of tumor-associated macrophages. The first part of the review is devoted to immunobiology of IL-12. Signaling pathways of IL-12 as well as clinical trials of this cytokine are discussed. The second part of the review is concerned on the inherited variations in IL-12A and IL-12B genes that could modulate cancer susceptibility, and as a consequence, possess predictive, therapeutic, or prognostic significance. It is known that functional single nucleotide polymorphisms (SNPs) in IL-12A and IL-12B genes may dramatically affect on protein expression level, or alter its functions, which may lead to immune disorders, autoimmune diseases, and eventually contribute to cancer occurrence. The list of genetic polymorphisms for further investigations might include the following: IL-12B_ + 1188A/C (rs3212227), IL-12A_ + 277G/A (rs568408), IL-12A_-798T/A (rs582054), IL-12A_-504T/G (rs190533), IL-12A_-1148T/C (rs2243123), and IL-12B_ + 16974 A/C. Perhaps, some of these SNPs may become an attractive target for oncogenomics and possibly could be used in programs of early cancer diagnosis as well as cancer prevention in the nearest future.
C1 [Yuzhalin, Arseniy E.] Kemerovo State Univ, Dept Genet, Kemerovo 650000, Russia.
   [Yuzhalin, Arseniy E.; Kutikhin, Anton G.] Kemerovo State Med Acad, Cent Res Lab, Kemerovo, Russia.
   [Kutikhin, Anton G.] Kemerovo State Med Acad, Dept Epidemiol, Kemerovo, Russia.
C3 Kemerovo State University; Kemerovo State Medical Academy; Kemerovo
   State Medical Academy
RP Yuzhalin, AE (corresponding author), Kemerovo State Univ, Dept Genet, Krasnaya Str 6, Kemerovo 650000, Russia.
EM yuzhalin@gmail.com; antonkutikhin@gmail.com
RI Kutikhin, Anton/B-9397-2012; Yuzhalin, Arseniy/J-3951-2013
OI Yuzhalin, Arseniy/0000-0001-7454-6653; Kutikhin, Anton
   G/0000-0001-8679-4857
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NR 127
TC 61
Z9 68
U1 0
U2 24
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0897-7194
EI 1029-2292
J9 GROWTH FACTORS
JI Growth Factors
PD JUN
PY 2012
VL 30
IS 3
BP 176
EP 191
DI 10.3109/08977194.2012.678843
PG 16
WC Cell Biology; Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Endocrinology & Metabolism
GA 945IC
UT WOS:000304265300005
PM 22515181
DA 2025-06-01
ER

PT J
AU Mukherjee, S
   Patra, R
   Behzadi, P
   Masotti, A
   Paolini, A
   Sarshar, M
AF Mukherjee, Suprabhat
   Patra, Ritwik
   Behzadi, Payam
   Masotti, Andrea
   Paolini, Alessandro
   Sarshar, Meysam
TI Toll-like receptor-guided therapeutic intervention of human cancers:
   molecular and immunological perspectives
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE toll-like receptors (TLRs); human cancers; therapeutic interventions;
   immunotherapy; chemotherapy; agonists; antagonists
ID NF-KAPPA-B; PLASMACYTOID DENDRITIC CELLS; WORLD-HEALTH-ORGANIZATION;
   BACILLUS-CALMETTE-GUERIN; HEPATOCELLULAR-CARCINOMA; TUMOR
   MICROENVIRONMENT; COLORECTAL-CANCER; GASTRIC-CANCER; X-CHROMOSOME;
   INFLAMMATORY RESPONSES
AB Toll-like receptors (TLRs) serve as the body's first line of defense, recognizing both pathogen-expressed molecules and host-derived molecules released from damaged or dying cells. The wide distribution of different cell types, ranging from epithelial to immune cells, highlights the crucial roles of TLRs in linking innate and adaptive immunity. Upon stimulation, TLRs binding mediates the expression of several adapter proteins and downstream kinases, that lead to the induction of several other signaling molecules such as key pro-inflammatory mediators. Indeed, extraordinary progress in immunobiological research has suggested that TLRs could represent promising targets for the therapeutic intervention of inflammation-associated diseases, autoimmune diseases, microbial infections as well as human cancers. So far, for the prevention and possible treatment of inflammatory diseases, various TLR antagonists/inhibitors have shown to be efficacious at several stages from pre-clinical evaluation to clinical trials. Therefore, the fascinating role of TLRs in modulating the human immune responses at innate as well as adaptive levels directed the scientists to opt for these immune sensor proteins as suitable targets for developing chemotherapeutics and immunotherapeutics against cancer. Hitherto, several TLR-targeting small molecules (e.g., Pam3CSK4, Poly (I:C), Poly (A:U)), chemical compounds, phytocompounds (e.g., Curcumin), peptides, and antibodies have been found to confer protection against several types of cancers. However, administration of inappropriate doses of such TLR-modulating therapeutics or a wrong infusion administration is reported to induce detrimental outcomes. This review summarizes the current findings on the molecular and structural biology of TLRs and gives an overview of the potency and promises of TLR-directed therapeutic strategies against cancers by discussing the findings from established and pipeline discoveries.
C1 [Mukherjee, Suprabhat; Patra, Ritwik] Kazi Nazrul Univ, Dept Anim Sci, Integrat Biochem & Immunol Lab, Asansol, West Bengal, India.
   [Behzadi, Payam] Islamic Azad Univ, Dept Microbiol, Shahr E Qods Branch, Tehran, Iran.
   [Masotti, Andrea; Paolini, Alessandro; Sarshar, Meysam] Bambino Gesu Childrens Hosp IRCCS, Res Labs, Rome, Italy.
C3 Islamic Azad University; IRCCS Bambino Gesu
RP Mukherjee, S (corresponding author), Kazi Nazrul Univ, Dept Anim Sci, Integrat Biochem & Immunol Lab, Asansol, West Bengal, India.; Behzadi, P (corresponding author), Islamic Azad Univ, Dept Microbiol, Shahr E Qods Branch, Tehran, Iran.; Sarshar, M (corresponding author), Bambino Gesu Childrens Hosp IRCCS, Res Labs, Rome, Italy.
EM suprabhat.mukherjee@knu.ac.in; behzadipayam@yahoo.com;
   meysam.sarshar@uniroma1.it
RI BEHZADI, Payam/GPW-6289-2022; Patra, Ritwik/AAN-7386-2021; Sarshar,
   Meysam/K-4347-2018; Paolini, Alessandro/H-2905-2016
OI Sarshar, Meysam/0000-0002-5726-2090; Paolini,
   Alessandro/0000-0003-4354-9100; Patra, Ritwik/0000-0003-1450-1589
FU DST-SERB-CRG; Italian Ministry of Health with Current Research funds [5
   x 1,000, SG-2018-12365432]; Italian Ministry of Health
FX SM and RP acknowledge DST-SERB-CRG, Govt. of India (Sanction no.
   CRG/2021/002605) for awarding the research grant to SM and Junior
   Research Fellowship to RP. This work was supported by the Italian
   Ministry of Health with Current Research funds. We would also like to
   thank the Italian Ministry of Health for funding (Ricerca 5 x 1,000 to
   AM and AP and Ricerca Finalizzata Starting Grant SG-2018-12365432 to
   MS).
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NR 349
TC 59
Z9 62
U1 2
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 26
PY 2023
VL 14
AR 1244345
DI 10.3389/fimmu.2023.1244345
PG 33
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA T4WM8
UT WOS:001078007600001
PM 37822929
OA Green Published, gold
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Su, ZL
   Sun, YK
   Zhu, HT
   Liu, YQ
   Lin, X
   Shen, HL
   Chen, JG
   Xu, WL
   Xu, HX
AF Su, Zhaoliang
   Sun, Yingkun
   Zhu, Haitao
   Liu, Yueqin
   Lin, Xin
   Shen, Huiling
   Chen, Jianguo
   Xu, Wenlin
   Xu, Huaxi
TI Th17 cell expansion in gastric cancer may contribute to cancer
   development and metastasis
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Th17; Gastric cancer; Th1
ID CLINICAL-RELEVANCE; TGF-BETA; T-CELLS; EPIDEMIOLOGY; DIFFERENTIATION;
   INFLAMMATION; GENERATION
AB Th0 cells differentiate into Th1 or Th2 depending on multiple transcription factors acting on specific time points to regulate gene expression. Th17 cells, a subset of IL-17-producing T cells distinct from Th1 or Th2 cells has been described as key players in inflammation and autoimmune diseases as well as cancer development. In the present study, 66 patients with gastric cancer were included; the expression level of Th1- and Th17-related IFN-gamma, IL-17, T-bet, ROR gamma t in gastric cancer tissues and peripheral blood mononuclear cell (PBMC) were detected, analyzed the relationship between Th17 or Th1 infiltration and metastasis and explored the possible mechanism. Our results showed that IL-17 and ROR gamma t expression were significantly increased in gastric cancer tissues and PBMC, especially, in metastasis patients; plasma IL-17 also increased; furthermore, the mRNA and protein levels of IL-1 beta, IL-21 and TGF-beta were up-regulated. All the data indicated that Th17 was infiltrated the cancer tissue; IL-1 beta, IL-21 and TGF-beta were also involved in gastric cancer development by promoting Th17 cell generation. From the above data, we speculated that Th17 cell expansion in gastric cancer may contribute to cancer development and metastasis.
C1 [Su, Zhaoliang; Liu, Yueqin; Lin, Xin; Xu, Wenlin; Xu, Huaxi] Jiangsu Univ, Affiliated Hosp 4, Cent Lab, Zhenjiang 212001, Peoples R China.
   [Su, Zhaoliang; Sun, Yingkun; Zhu, Haitao] Jiangsu Univ, Ctr Clin Med & Lab, Dept Immunol & Lab Immunol, Zhenjiang 212013, Peoples R China.
   [Shen, Huiling] Jiangsu Univ, Affiliated Peoples Hosp, Zhenjiang 212013, Jiangsu, Peoples R China.
   [Chen, Jianguo] Jiangsu Univ, Affiliated Peoples Hosp, Zhenjiang 212001, Peoples R China.
   [Xu, Huaxi] Jiangsu Univ, Ctr Clin Med & Lab, Dept Immunol, Zhenjiang 212013, Jiangsu, Peoples R China.
C3 Jiangsu University; Jiangsu University; Jiangsu University; Jiangsu
   University; Jiangsu University
RP Xu, WL (corresponding author), Jiangsu Univ, Affiliated Hosp 4, Cent Lab, Zhenjiang 212001, Peoples R China.
EM szl30@yeah.net; xuhx@ujs.edu.cn
RI zhu, HAITAO/GVL-0589-2022; SU, Zhaoliang/ABD-9062-2021; Chen,
   Gang/G-2722-2010; Chen, Jian-Guo/ABG-3956-2020
OI Chen, Jian-Guo/0000-0003-4102-8934
FU National Natural Science Foundation of China [81370084, 81001319,
   81101677]; Postdoctoral foundation of China [2012M511705, 2013T60508];
   Postdoctoral foundation of Jiangsu Province [1102129C]; Natural Science
   Foundation of Colleges and Universities in Jiangsu Province
   [10KJB310003]; High-Tech of Jiangsu University [11JDG128]
FX This work was supported by National Natural Science Foundation of China
   (Grant No. 81370084, 81001319, 81101677), Postdoctoral foundation of
   China (2012M511705, 2013T60508), Postdoctoral foundation of Jiangsu
   Province (1102129C), Natural Science Foundation of Colleges and
   Universities in Jiangsu Province (Grant No. 10KJB310003) and High-Tech
   of Jiangsu University (Grant No. 11JDG128).
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NR 31
TC 43
Z9 53
U1 0
U2 10
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD JAN
PY 2014
VL 58
IS 1
BP 118
EP 124
DI 10.1007/s12026-013-8483-y
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA AA0OL
UT WOS:000330794400013
PM 24402773
DA 2025-06-01
ER

PT J
AU Lahner, E
   Galli, G
   Esposito, G
   Pilozzi, E
   Corleto, VD
   Annibale, B
AF Lahner, Edith
   Galli, Gloria
   Esposito, Gianluca
   Pilozzi, Emanuela
   Corleto, Vito D.
   Annibale, Bruno
TI Updated features associated with type 1 gastric carcinoids patients: a
   single-center study
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE atrophic gastritis; autoimmune gastritis; iron deficiency anemia;
   pernicious anemia; type 1 gastric carcinoids
ID ATROPHIC BODY GASTRITIS; ENTEROCHROMAFFIN-LIKE CELLS; AUTOIMMUNE
   THYROID-DISEASE; IRON-DEFICIENCY; MANAGEMENT; TUMORS; RISK; POLYPS;
   CLASSIFICATION; PATHOGENESIS
AB Objective. Data on clinical presentation and associated features of patients with type 1 gastric carcinoids (T1-GCs) are scanty. This study aimed to provide detailed data on a series of patients with T1-GCs. Material and Methods. Clinical, laboratory, endoscopic, and histological data were assessed from 31 T1-GCs patients (cross-sectional design), consecutively diagnosed in a tertiary center according to a standardized diagnostic protocol. T1-GCs were diagnosed at baseline or follow-up gastroscopy for atrophic gastritis in 74.2% and 25.8% of patients, respectively. Results. Seventy-one percent of T1-GC patients were female. Age ranged from 23 to 78 (median 58 years). T1-GCs were more frequently diagnosed between 40-49 years (35.5%) and 60-69 years (32.3%) (p = 0.0383). Thyroid disease was present in 54.8% (in 29% autoimmune). All 31 patients had either cobalamin or iron deficiency with or without anemia. Manifest pernicious anemia was present in 67.7% of patients and cobalamin deficiency without anemia in 9.7% patients. Iron deficiency anemia was present in 29% and iron deficiency without anemia in 12.9% of patients. In 48.4% of patients, T1-GCs appeared as polyps, which were single in all cases and had a median size of 4 mm (range 2-15 mm). In patients with polypoid T1-GCs, thyroid disease of autoimmune and nonautoimmune origin (p = 0.0181) was more frequently associated. Conclusion. This study shows that T1-GCs may be diagnosed at any age. Autoimmune features are frequently present as well as cobalamin and iron deficiency. The copresence of autoimmune diseases and micronutrient deficiencies should be accurately investigated, in particular in patients with polypoid T1-GCs.
C1 [Lahner, Edith; Galli, Gloria; Esposito, Gianluca; Annibale, Bruno] Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Digest & Liver Dis, I-00189 Rome, Italy.
   [Pilozzi, Emanuela] Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Pathol, I-00189 Rome, Italy.
   [Corleto, Vito D.] Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Digest Endoscopy, I-00189 Rome, Italy.
   [Corleto, Vito D.] Osped S Pietro, Ctr Ric S Pietro, Rome, Italy.
C3 Sapienza University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza
   University Rome; Azienda Ospedaliera Sant'Andrea; Sapienza University
   Rome; Azienda Ospedaliera Sant'Andrea
RP Annibale, B (corresponding author), Univ Roma La Sapienza, St Andrea Hosp, Sch Med, Dept Digest & Liver Dis, Via Grottarossa 1035-1039, I-00189 Rome, Italy.
EM bruno.annibale@uniroma1.it
RI Lahner, Edith/AAM-1039-2021; Annibale, Bruno/A-5372-2008; Esposito,
   Gianluca/J-7200-2019; PILOZZI, Emanuela/AAC-1854-2022
OI annibale, bruno/0000-0001-9120-5957; GALLI, GLORIA/0000-0003-3547-1067;
   Esposito, Gianluca/0000-0002-2242-5048
FU University Sapienza
FX This work was funded by grants from University Sapienza 2011-2013.
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NR 35
TC 11
Z9 11
U1 0
U2 1
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0036-5521
EI 1502-7708
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD DEC
PY 2014
VL 49
IS 12
BP 1447
EP 1455
DI 10.3109/00365521.2014.968859
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AU4TE
UT WOS:000345603500008
PM 25309981
DA 2025-06-01
ER

PT J
AU Testerman, TL
   Morris, J
AF Testerman, Traci L.
   Morris, James
TI Beyond the stomach: An updated view of Helicobacter pylori
   pathogenesis, diagnosis, and treatment
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Enterohepatic; Pathogenesis; Diagnosis; Treatment; Extragastric; CagA;
   Cancer; Autoimmune; Inflammation; Virulence factor
ID NEUTROPHIL-ACTIVATING PROTEIN; GAMMA-GLUTAMYL-TRANSPEPTIDASE;
   CYTOTOXIN-ASSOCIATED-GENE; IRON-DEFICIENCY ANEMIA; PEPTIC-ULCER DISEASE;
   IV SECRETION SYSTEM; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; IMMUNE
   THROMBOCYTOPENIC PURPURA; AUTOIMMUNE THYROID-DISEASES; SQUAMOUS-CELL
   CARCINOMA
AB Helicobacter pylori (H. pylori) is an extremely common, yet underappreciated, pathogen that is able to alter host physiology and subvert the host immune response, allowing it to persist for the life of the host. H. pylori is the primary cause of peptic ulcers and gastric cancer. In the United States, the annual cost associated with peptic ulcer disease is estimated to be $6 billion and gastric cancer kills over 700000 people per year globally. The prevalence of H. pylori infection remains high (>50%) in much of the world, although the infection rates are dropping in some developed nations. The drop in H. pylori prevalence could be a double-edged sword, reducing the incidence of gastric diseases while increasing the risk of allergies and esophageal diseases. The list of diseases potentially caused by H. pylori continues to grow; however, mechanistic explanations of how H. pylori could contribute to extragastric diseases lag far behind clinical studies. A number of host factors and H. pylori virulence factors act in concert to determine which individuals are at the highest risk of disease. These include bacterial cytotoxins and polymorphisms in host genes responsible for directing the immune response. This review discusses the latest advances in H. pylori pathogenesis, diagnosis, and treatment. Up-to-date information on correlations between H. pylori and extragastric diseases is also provided. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
C1 [Testerman, Traci L.] Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, Bethesda, MD 20814 USA.
   [Morris, James] Louisiana State Univ, Hlth Sci Ctr Shreveport, Dept Gastroenterol, Shreveport, LA 71130 USA.
C3 Uniformed Services University of the Health Sciences - USA; Louisiana
   State University System; Louisiana State University Health Sciences
   Center at Shreveport
RP Testerman, TL (corresponding author), Uniformed Serv Univ Hlth Sci, Dept Microbiol & Immunol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM t.testerman01@gmail.com
RI Testerman, Traci/AAI-1506-2020
OI Testerman, Traci/0000-0002-3883-6407
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NR 316
TC 219
Z9 248
U1 2
U2 53
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD SEP 28
PY 2014
VL 20
IS 36
BP 12781
EP 12808
DI 10.3748/wjg.v20.i36.12781
PG 28
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AR9GK
UT WOS:000343880900006
PM 25278678
OA Green Accepted, Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Lohoff, M
   Röllinghoff, M
   Sommer, F
AF Lohoff, M
   Röllinghoff, M
   Sommer, F
TI Helicobacter pylori gastritis:: a Th1 mediated disease?
SO JOURNAL OF BIOTECHNOLOGY
LA English
DT Article
DE Helicobacter pylori; Th1 cells; Th2 cells
ID EPITHELIAL-CELLS; IMMUNE-RESPONSES; MOUSE MODEL; INFECTION; EXPRESSION;
   MICE; LYMPHOCYTES; INTERFERON; PHENOTYPE; MUCOSA
AB Helicobacter pylori is now considered to be the main cause for most stomach diseases including ulcer, MALT lymphoma, adenocarcinoma and gastritis. The infection with this bacterium is chronic despite a local and systemic immune response towards it. Among the cellular infiltrate that arises during H, pylori-mediated gastritis, there is a considerable frequency of CD4 + Th1 cells producing IFN gamma, but not of Th2 cells producing IL-4. Since IFN gamma may induce binding of H. pylori to gastric epithelial cells followed by apoptosis of these cells, one may speculate that H. pylori-mediated diseases are in part autoimmune diseases initiated by H. pylori-specific Th1 cells infiltrating the gastric mucosa. Recent support for this hypothesis comes from an animal model in which mice are infected with H. pylori and display strongly reduced gastritis in the absence of IFN gamma. (C) 2000 Elsevier Science B.V. All rights reserved.
C1 Inst Klin Mikrobiol Immunol & Hyg, D-91054 Erlangen, Germany.
C3 University of Erlangen Nuremberg
RP Lohoff, M (corresponding author), Inst Klin Mikrobiol Immunol & Hyg, Wasserturmstr 3, D-91054 Erlangen, Germany.
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NR 22
TC 23
Z9 27
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-1656
J9 J BIOTECHNOL
JI J. Biotechnol.
PD SEP 29
PY 2000
VL 83
IS 1-2
BP 33
EP 36
DI 10.1016/S0168-1656(00)00295-9
PG 4
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA 360CM
UT WOS:000089648900006
PM 11000457
DA 2025-06-01
ER

PT J
AU Nakano, Y
   Nishida, K
   Okamoto, N
   Gohma, I
   Yasuhara, Y
AF Nakano, Yoshio
   Nishida, Koji
   Okamoto, Norio
   Gohma, Iwao
   Yasuhara, Yumiko
TI Anti-MDA5 Antibody-Positive Clinically Amyopathic Dermatomyositis
   Associated With Multiple Heterologous Carcinomas: A Case Report
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE heterochronous; cancer; interstitial lung disease; anti-mda5 antibody;
   dermatomyositis
ID INTERSTITIAL LUNG-DISEASE; MYOSITIS; CANCER
AB Dermatomyositis (DM), an autoimmune disorder, is linked to increased malignancy risk. A 53 -year -old man with anti -melanoma differentiation -associated gene 5 (MDA5)-positive clinically amyopathic dermatomyositis (CADM) and rapidly progressing interstitial lung disease (RP-ILD) developed heterochronous gastric and colorectal cancers. Early endoscopic screenings led to successful curative resections, preventing recurrence. Despite low cancer incidence assumptions in patients with anti-MDA5positive RP-ILD, this case advocates for reevaluation and periodic cancer screenings to enhance management, considering the improved survival with intensive therapy. Vigilance for multiple carcinomas at various time points is vital in CADM management.
C1 [Nakano, Yoshio; Nishida, Koji; Okamoto, Norio; Gohma, Iwao] Sakai City Med Ctr, Resp Med, Osaka, Japan.
   [Yasuhara, Yumiko] Sakai City Med Ctr, Pathol, Osaka, Japan.
RP Nakano, Y (corresponding author), Sakai City Med Ctr, Resp Med, Osaka, Japan.
EM methylemon@yahoo.co.jp
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PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD FEB 21
PY 2024
VL 16
IS 2
AR e54660
DI 10.7759/cureus.54660
PG 6
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA NI7S7
UT WOS:001199895600026
PM 38523968
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Khalilollah, S
   Soltanieh, SK
   Saleh, RO
   Alzahrani, AA
   Maabreh, HG
   Al-Hamdani, MM
   Dehghani-Ghorbi, M
   Khonachaei, MS
   Akhavan-Sigari, R
AF Khalilollah, Shayan
   Soltanieh, Sina Kalantari
   Saleh, Raed Obaid
   Alzahrani, Abdullah Ali
   Maabreh, Hatem Ghaleb
   Al-Hamdani, Mais Mazin
   Dehghani-Ghorbi, Mahmoud
   Khonachaei, Metanat Shafiei
   Akhavan-Sigari, Reza
TI LncRNAs involvement in pathogenesis of immune-related disease via
   regulation of T regulatory cells, an updated review
SO CYTOKINE
LA English
DT Review
DE LncRNAs; Autoimmune diseases; Treg cells; Immune cell differentiation
ID RECURRENT SPONTANEOUS-ABORTION; NONCODING RNA; GASTRIC-CANCER;
   PROLIFERATION; EXPRESSION; SUPPRESSION; DIFFERENTIATION; TOLERANCE;
   INVASION; GROWTH
AB The pathophysiology of several illnesses, including cancer and autoimmune diseases depends on human regulatory T cells (Tregs), and abnormalities in these cells may function as triggers for these conditions. Cancer and autoimmune, and gynecological diseases are associated with the differentiation of the proinflammatory T cell subset TH17 and its balance with the production of Treg. Recently, long non-coding RNAs (lncRNAs) have become important regulatory molecules in a wide range of illnesses. During epigenetic regulation, they can control the expression of important genes at several levels by affecting transcription, post-transcriptional actions, translation, and protein modification. They might connect with different molecules, such as proteins, DNA and RNA, and their structural composition is intricate. Because lncRNAs regulate biological processes, including cell division, death, and growth, they are linked to several diseases. A notable instance of this is the lncRNA NEAT1, which has been the subject of several investigations to ascertain its function in immune cell development. In the context of immune cell development, several additional lncRNAs have been connected to Treg cell differentiation. In this work, we summarize current findings about the diverse functions of lncRNAs in Treg cell differentiation and control of the Th17/Treg homeostasis in autoimmune disorders, cancers, as well as several gynecological diseases where Tregs are key players.
C1 [Khalilollah, Shayan] Islamic Azad Univ, Fac Med Tehran Med Sci, Dept Neurosurg, Tehran, Iran.
   [Soltanieh, Sina Kalantari] MVZ Lab Synlab Berlin, Berlin, Germany.
   [Saleh, Raed Obaid] Univ Fallujah, Coll Appl Sci, Dept Pathol Anal, Al Anbar, Iraq.
   [Alzahrani, Abdullah Ali] Taif Univ, Dept Surg, Taif, Saudi Arabia.
   [Maabreh, Hatem Ghaleb] Peoples Friendship Univ Russia, RUDN Univ, Dept Dermatovenerol Foreign Languages, Moscow, Russia.
   [Al-Hamdani, Mais Mazin] Al Ayen Univ, Coll Pharm, Pharmaceut Dept, Thi Qar, Iraq.
   [Dehghani-Ghorbi, Mahmoud] Shahid Beheshti Univ Med Sci, Imam Hossein Educ Hosp, Hematol Oncol Dept, Tehran, Iran.
   [Khonachaei, Metanat Shafiei] Univ Guilan, Fac Sci, Dept Biol, Guilan, Iran.
   [Akhavan-Sigari, Reza] Univ Med Ctr, Dept Neurosurg, Tubingen, Germany.
   [Akhavan-Sigari, Reza] Coll Humanum Warsaw Management Univ Warsaw, Dept Hlth Care Management & Clin Res, Warsaw, Poland.
C3 Islamic Azad University; University of Fallujah; Taif University;
   Peoples Friendship University of Russia; Al-Ayen University; Shahid
   Beheshti University Medical Sciences; University of Guilan; Eberhard
   Karls University of Tubingen; Eberhard Karls University Hospital
RP Dehghani-Ghorbi, M (corresponding author), Shahid Beheshti Univ Med Sci, Imam Hossein Educ Hosp, Hematol Oncol Dept, Tehran, Iran.; Khonachaei, MS (corresponding author), Univ Guilan, Fac Sci, Dept Biol, Guilan, Iran.
EM Shayan.1997@hotmail.com; sinakalantari@gmail.com;
   raed.obaid@uofallujah.edu.iq; Abdullazahrani@tu.edu.sa;
   Hatemmaabreh89@gmail.com; Mais.yahya@alayen.edu.iq;
   m.dehghanighorbi@sbmu.ac.ir; Metanat.shafiei7@gmail.com;
   rasigari@yahoo.de
RI Al-Hamdani, Mais/ADY-6838-2022; Saleh, Raed/AAM-3803-2020
FU Deanship of Scientific Research at Umm Al-Qura University
   [23UQU4331100DSR030]
FX The authors would like to thank the Deanship of Scientific Research at
   Umm Al-Qura University for supporting this work by Grant Code:
   23UQU4331100DSR030.
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NR 173
TC 3
Z9 3
U1 3
U2 21
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
EI 1096-0023
J9 CYTOKINE
JI Cytokine
PD JUL
PY 2024
VL 179
AR 156585
DI 10.1016/j.cyto.2024.156585
EA APR 2024
PG 11
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA QX9A2
UT WOS:001224272300001
PM 38579428
DA 2025-06-01
ER

PT J
AU Martinelli, TM
   vanDriel, IR
   Alderuccio, F
   Gleeson, PA
   Toh, BH
AF Martinelli, TM
   vanDriel, IR
   Alderuccio, F
   Gleeson, PA
   Toh, BH
TI Analysis of mononuclear cell infiltrate and cytokine production in
   murine autoimmune gastritis
SO GASTROENTEROLOGY
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; NEONATAL THYMECTOMY; LYMPHOCYTE SUBPOPULATIONS;
   EXPRESSION; MOUSE; ANTIGENS; MICE; THYROIDITIS; DISEASES; COMPLEX
AB Background & Aims: Murine autoimmune gastritis, induced by day-3 thymectomy, is characterized by cellular infiltrates and circulating autoantibodies to gastric hydrogen/potassium adenosine triphosphatase. The aim of this study was to analyze the cellular infiltrates and cytokines in autoimmune gastritis, Methods: Stomachs and blood samples from day-3 thymectomized BALB/c mice were obtained from 2 to 12 weeks after thymectomy for analysis, Results: At 4 weeks, the gastritic infiltrates were composed of macrophages and CD4(+) T cells, accompanied by major histocompatibility complex class II expression on gastric epithelial cells. Mucosal B cells, scant at 4 weeks, were abundant at 8 weeks, coincident with the peaking of autoantibodies to gastric hydrogen/potassium adenosine triphosphatase, CD8(+) T cells increased marginally during the 12 weeks, Mononuclear cells from diseased stomachs transferred gastritis to nu/nu recipients, At 4 weeks, interleukins 2, 3, 5, 6, and 10; interferon gamma; tumor necrosis factor alpha; and granulocyte-macrophage colony-stimulating factor were detected in gastritic mucosa, but interleukin 4 was not, Conclusions: The early lesion of autoimmune gastritis is composed of macrophages and CD4(+) T cells with major histocompatibility complex class II expression in gastric epithelial cells. Autoantibody production is a late event, Our results ave consistent with a lesion mediated by CD4(+) T cells producing a mix of Th1- and Th2-type cytokines.
C1 MONASH UNIV, ALFRED HOSP, SCH MED, DEPT PATHOL & IMMUNOL, MELBOURNE, VIC 3181, AUSTRALIA.
C3 Florey Institute of Neuroscience & Mental Health; Howard Florey
   Institute Affiliates; Monash University
RI Alderuccio, Frank/D-5808-2011
OI Alderuccio, Frank/0000-0003-4853-3394; van Driel,
   Ian/0000-0001-5371-120X; Gleeson, Paul/0000-0002-5336-6503
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NR 49
TC 80
Z9 83
U1 0
U2 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
EI 1528-0012
J9 GASTROENTEROLOGY
JI Gastroenterology
PD JUN
PY 1996
VL 110
IS 6
BP 1791
EP 1802
DI 10.1053/gast.1996.v110.pm8964405
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA UN831
UT WOS:A1996UN83100014
PM 8964405
OA Bronze
DA 2025-06-01
ER

PT J
AU Yamaguchi, T
   Bamba, K
   Kitayama, A
   Kuroiwa, Y
   Yoshimatsu, K
   Shimakawa, T
   Ogawa, K
   Sekine, T
   Shimizu, N
   Yamamoto, K
AF Yamaguchi, T
   Bamba, K
   Kitayama, A
   Kuroiwa, Y
   Yoshimatsu, K
   Shimakawa, T
   Ogawa, K
   Sekine, T
   Shimizu, N
   Yamamoto, K
TI Long-term intravenous administration of activated autologous lymphocytes
   for cancer patients does not induce antinuclear antibody and rheumatoid
   factor
SO ANTICANCER RESEARCH
LA English
DT Article
DE adoptive immunotherapy; autologous activated lymphocyte; antinuclear
   antibody; rheumatoid factor; autoimmune disease
ID ADOPTIVE IMMUNOTHERAPY; T-CELLS; INTERLEUKIN-2; CARCINOMA; THERAPY
AB The treatment of activated autologous lymphocyte can lead to a potent antitumor effect with destruction of autologous cancer cells, but potential adverse autoimmune effects due to destruction of autologous tissue must also be considered. This study was performed to evaluate whether administration of activated autologous lymphocytes induces autoimmune disease. Patients with advanced cancer, who underwent transfer therapy with activated autologous lymphocytes, were eligible for the study. Informed consent was obtained from 22 patients with hepatocelluler carcinoma, ovarian cancer, gastric cancer, etc. The variation in activated lymphocyte phenotypes was CD3(+)/HLA-DR+ activated T lymphocytes, 23% to 99%; including CD4(+) cells, 4% to 65%; CD8(+) cells, 10 to 91%; and CD16(+)/CD56(+) NK cells, 1% to 59%. Of the 22 patients, levels of antinuclear antibody and/or rheumatoid factor were above normal limits during the study in the following 5 patients: 3 patients showed no marked changes, one patient a slight decrease in rheumatoid factor and one patient a slight increase in antinuclear antibody during the course of treatment, respectively. The values for these markers of the other 17 patients varied within normal limits during treatment. Mild transient fever occurred in several patients as an adverse event. There were no other adverse reactions. No clinical symptoms or signs suggestive of autoimmune disease occurred in any patient during or after treatment. These results suggested that long-term administration of activated autologous lymphocytes does not induce autoimmune disease.
C1 Tokyo Womens Med Univ, Daini Hosp, Dept Surg, Arakawa Ku, Tokyo 1160011, Japan.
   Lymphotec Inc, Bunkyo Ku, Tokyo 1120001, Japan.
   Tokyo Med & Dent Univ, Dept Virol, Div Virol & Immunol, Med Res Inst,Bunkyo Ku, Tokyo 1010062, Japan.
C3 Tokyo Women's Medical University; Institute of Science Tokyo; Tokyo
   Medical & Dental University (TMDU)
RP Tokyo Womens Med Univ, Daini Hosp, Dept Surg, Arakawa Ku, 2-1-10 Nishiogu, Tokyo 1168567, Japan.
EM ogawasu@dnh.twmu.ac.jp
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NR 17
TC 3
Z9 4
U1 0
U2 0
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD JUL-AUG
PY 2004
VL 24
IS 4
BP 2423
EP 2429
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 852BY
UT WOS:000223731400043
PM 15330194
DA 2025-06-01
ER

PT J
AU Dohán, O
   De la Vieja, A
   Paroder, V
   Riedel, C
   Artani, M
   Reed, M
   Ginter, CS
   Carrasco, N
AF Dohán, O
   De la Vieja, A
   Paroder, V
   Riedel, C
   Artani, M
   Reed, M
   Ginter, CS
   Carrasco, N
TI The sodium/iodide symporter (NIS):: Characterization, regulation, and
   medical significance
SO ENDOCRINE REVIEWS
LA English
DT Review
ID SODIUM-IODIDE SYMPORTER; AUTOIMMUNE THYROID-DISEASE; HUMAN NA+/I
   SYMPORTER; PROTEIN-KINASE-A; AFFINITY CHOLINE TRANSPORTER;
   MESSENGER-RIBONUCLEIC-ACID; POLYMERASE-CHAIN-REACTION;
   TUMOR-NECROSIS-FACTOR; DENSE CORE VESICLES; CANCER CELL-LINES
AB The Na+/I- symporter (NIS) is an integral plasma membrane glycoprotein that mediates active I- transport into the thyroid follicular cells, the first step in thyroid hormone biosynthesis. NIS-mediated thyroidal I- transport from the bloodstream to the colloid is a vectorial process made possible by the selective targeting of NIS to the basolateral membrane. NIS also mediates active I- transport in other tissues, including salivary glands, gastric mucosa, and lactating mammary gland, in which it translocates I- into the milk for thyroid hormone biosynthesis by the nursing newborn. NIS provides the basis for the effective diagnostic and therapeutic management of thyroid cancer and its metastases with radioiodide. NIS research has proceeded at an astounding pace after the 1996 isolation of the rat NIS cDNA, comprising the elucidation of NIS secondary structure and topology, biogenesis and posttranslational modifications, transcriptional and posttranscriptional regulation, electrophysiological analysis, isolation of the human NIS cDNA, and determination of the human NIS genomic organization. Clinically related topics include the analysis of congenital I- transport defect-causing NIS mutations and the role of NIS in thyroid cancer. NIS has been transduced into various kinds of cancer cells to render them susceptible to destruction with radioiodide. Most dramatically, the discovery of endogenous NIS expression in more than 80% of human breast cancer samples has raised the possibility that radioiodide may be a valuable novel tool in breast cancer diagnosis and treatment.
C1 Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA.
C3 Montefiore Medical Center; Albert Einstein College of Medicine; Yeshiva
   University
RP Albert Einstein Coll Med, Dept Mol Pharmacol, Forchheimer Bldg,Room 209,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM carrasco@aecom.yu.edu
RI Paroder, Viktoriya/AGZ-3431-2022; Carrasco, Nancy/AAH-1053-2019; Dohan,
   Orsolya/B-3750-2012; De la Vieja, Antonio/I-4774-2013
OI Dohan, Orsolya/0000-0001-6235-5657; Paroder,
   Viktoriya/0000-0003-4356-8256; De la Vieja, Antonio/0000-0002-1187-1907;
   Riedel, Claudia/0000-0001-6168-8601
FU NIDDK NIH HHS [DK-41544] Funding Source: Medline; NIGMS NIH HHS [T32
   GM007288] Funding Source: Medline
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   THYROID
   WHONHD994
NR 242
TC 635
Z9 726
U1 2
U2 95
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD FEB
PY 2003
VL 24
IS 1
BP 48
EP 77
DI 10.1210/er.2001-0029
PG 30
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 645PU
UT WOS:000180988200003
PM 12588808
OA Bronze
DA 2025-06-01
ER

PT J
AU Huang, J
   Fan, XF
   Liu, WT
AF Huang, Jia
   Fan, Xiaofei
   Liu, Wentian
TI Applications and Prospects of Artificial Intelligence-Assisted
   Endoscopic Ultrasound in Digestive System Diseases
SO DIAGNOSTICS
LA English
DT Review
DE artificial intelligence; endoscopic ultrasound; machine learning; deep
   learning; digestive system diseases
ID PANCREATIC CYSTS; AUTOIMMUNE PANCREATITIS; MANAGEMENT; DIAGNOSIS; EUS;
   LESIONS; ENDOMICROSCOPY; ELASTOGRAPHY; VALIDATION; CANCER
AB Endoscopic ultrasound (EUS) has emerged as a widely utilized tool in the diagnosis of digestive diseases. In recent years, the potential of artificial intelligence (AI) in healthcare has been gradually recognized, and its superiority in the field of EUS is becoming apparent. Machine learning (ML) and deep learning (DL) are the two main AI algorithms. This paper aims to outline the applications and prospects of artificial intelligence-assisted endoscopic ultrasound (EUS-AI) in digestive diseases over the past decade. The results demonstrated that EUS-AI has shown superiority or at least equivalence to traditional methods in the diagnosis, prognosis, and quality control of subepithelial lesions, early esophageal cancer, early gastric cancer, and pancreatic diseases including pancreatic cystic lesions, autoimmune pancreatitis, and pancreatic cancer. The implementation of EUS-AI has opened up new avenues for individualized precision medicine and has introduced novel diagnostic and treatment approaches for digestive diseases.
C1 [Huang, Jia; Fan, Xiaofei; Liu, Wentian] Tianjin Med Univ Gen Hosp, Dept Gastroenterol & Hepatol, 154 Anshan Rd, Tianjin 300052, Peoples R China.
C3 Tianjin Medical University
RP Liu, WT (corresponding author), Tianjin Med Univ Gen Hosp, Dept Gastroenterol & Hepatol, 154 Anshan Rd, Tianjin 300052, Peoples R China.
EM helga@tmu.edu.cn; ffan@tmu.edu.cn; tliu01@tmu.edu.cn
FU Tianjin Medical University General Hospital Clinical Research Program
   [22ZYYLCCG09]
FX This work was supported by Tianjin Medical University General Hospital
   Clinical Research Program, grant number 22ZYYLCCG09.
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NR 81
TC 9
Z9 10
U1 8
U2 30
PU MDPI
PI BASEL
PA Gross-peteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD SEP
PY 2023
VL 13
IS 17
AR 2815
DI 10.3390/diagnostics13172815
PG 18
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Q9YJ7
UT WOS:001060996800001
PM 37685350
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Park, JS
   Lee, SJ
   Kim, TH
   Yeom, J
   Park, ES
   Seo, JH
   Jun, JS
   Lim, JY
   Park, CH
   Woo, HO
   Youn, HS
   Ko, GH
   Kang, HL
   Baik, SC
   Lee, WK
   Cho, MJ
   Rhee, KH
AF Park, Ji Sook
   Lee, Su-Jin
   Kim, Tae Hyo
   Yeom, Jeongsuk
   Park, Eun-Sil
   Seo, Ji-Hyun
   Jun, Jin-Su
   Lim, Jae-Young
   Park, Chan-Hoo
   Woo, Hyang-Ok
   Youn, Hee-Shang
   Ko, Gyung-Hyuck
   Kang, Hyung-Lyun
   Baik, Seung-Chul
   Lee, Woo-Kon
   Cho, Myung-Je
   Rhee, Kwang-Ho
TI Gastric Autoantigenic Proteins in Helicobacter Pylori Infection
SO YONSEI MEDICAL JOURNAL
LA English
DT Article
DE Helicobacter pylori; gastric atrophy; autoantigen; 2D immunoblotting
ID MOLECULAR MIMICRY; ANTIGASTRIC AUTOANTIBODIES; MONOCLONAL-ANTIBODIES;
   PEPTIC-ULCERATION; MUCOSA; IDENTIFICATION; AUTOIMMUNITY; ERADICATION;
   DISEASE; SERUM
AB Purpose: This study tried to identify novel gastric autoimmune antigens that might be involved in aggravating the atrophic gastritis among patients with Helicobacter pylori infection using two-dimensional immunoblotting analysis. Materials and Methods: Proteins from gastric mucosal antrectomy specimens and AGS cells (gastric adenocarcinoma cell lines derived from a Caucasian patient who had received no prior therapy) were 2-dimensionally immunoblotted separately with a pool of 300 sera from H. pylroi-infected patients at Gyeongsang National University Hospital. Results: Thirty-eight autoantigenic proteins including alcohol dehydrogenase [NADP+], alpha enolase, gastrokine-1, gastric triacylglycerol lipase, heat shock 70 kDa protein 1, and peroxiredoxin-2 were identified in the gastric mucosal tissue. Fourteen autoantigenic proteins including programmed cell death 6-interacting protein, serum albumin and T-complex protein 1 subunit gamma were identified in the AGS cells. Albumin, alpha-enolase, annexin A3, cytoplasmic actin 1, heat shock cognate 71 kDa protein and leukocyte elastase inhibitor were commonly observed autoantigenic proteins in both gastric mucosal tissue and AGS cells. Alpha-enolase, glutathione S-transferase P, heat shock cognate 71 kDa protein, heat shock 70 kDa protein 1, human mitochondrial adenosine triphosphate synthase (ATP) subunit beta, mitochondrial 60 kDa heat shock protein, peroxiredoxin-2, 78 kDa glucose-regulated protein precursor, tyrosine-protein phosphatase non-receptor type 11 and Tryptophan-Aspartic acid (WD) repeat-containing protein 1 showed 60% or higher amino acid positivity. Conclusion: These newly identified gastric autoimmune antigens might be useful in the control and prevention of gastroduodenal disorders, and might be valuable in breaking the vicious circle that exists in gastroduodenal disorders if their pathophysiological roles could be understood in the progress of chronic atrophic gastritis, gastroduodenal ulcers, intestinal metaplasia, and gastric carcinogenesis.
C1 [Park, Ji Sook; Lee, Su-Jin; Yeom, Jeongsuk; Park, Eun-Sil; Seo, Ji-Hyun; Jun, Jin-Su; Lim, Jae-Young; Park, Chan-Hoo; Woo, Hyang-Ok; Youn, Hee-Shang] Gyeongsang Natl Univ, Sch Med, Dept Pediat, Gyeongsang Inst Hlth Sci, Jinju 660702, South Korea.
   [Kim, Tae Hyo] Gyeongsang Natl Univ, Sch Med, Dept Internal Med, Gyeongsang Inst Hlth Sci, Jinju 660702, South Korea.
   [Ko, Gyung-Hyuck] Gyeongsang Natl Univ, Sch Med, Dept Pathol, Gyeongsang Inst Hlth Sci, Jinju 660702, South Korea.
   [Kang, Hyung-Lyun; Baik, Seung-Chul; Lee, Woo-Kon; Cho, Myung-Je; Rhee, Kwang-Ho] Gyeongsang Natl Univ, Sch Med, Dept Microbiol, Gyeongsang Inst Hlth Sci, Jinju 660702, South Korea.
C3 Gyeongsang National University; Gyeongsang National University;
   Gyeongsang National University; Gyeongsang National University
RP Youn, HS (corresponding author), Gyeongsang Natl Univ, Sch Med, Dept Pediat, 79 Gangnam Ro, Jinju 660702, South Korea.
EM hsyoun@gnu.ac.kr
OI Youn, Hee-Shang/0000-0002-5498-838X
FU Multi-year Clinical Research Fund of Gyeongsang National University
   Hospital; Ministry of Health Welfare
FX This study was supported by the Multi-year Clinical Research Fund of
   Gyeongsang National University Hospital in 2008-2009. Biospecimens were
   provided by the Gyeongsang National University Hospital, which is a
   member of the National Biobank of Korea supported by the Ministry of
   Health & Welfare.
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NR 36
TC 6
Z9 9
U1 0
U2 13
PU YONSEI UNIV COLLEGE MEDICINE
PI SEOUL
PA IN-HONG CHOI, M.D., PH D, 50 SEONGSAN-RO, SEODAEMUN-GU, SEOUL 120-752,
   SOUTH KOREA
SN 0513-5796
EI 1976-2437
J9 YONSEI MED J
JI Yonsei Med. J.
PD NOV 1
PY 2013
VL 54
IS 6
BP 1342
EP 1352
DI 10.3349/ymj.2013.54.6.1342
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 244UK
UT WOS:000326415500007
PM 24142637
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Franchini, M
   Vescovi, PP
   Garofano, M
   Veneri, D
AF Franchini, Massimo
   Vescovi, Pier Paolo
   Garofano, Massimo
   Veneri, Dino
TI Helicobacter Pylori-Associated Idiopathic Thrombocytopenic
   Purpura: A Narrative Review
SO SEMINARS IN THROMBOSIS AND HEMOSTASIS
LA English
DT Review
DE Helicobacter pylori; thrombocytopenia; bleeding; eradication therapy
ID INDUCE PLATELET RECOVERY; ERADICATION THERAPY; CAGA PROTEIN; CHRONIC
   ITP; INFECTION; CHILDREN; CHILDHOOD; COUNT; MANAGEMENT; RESPONSES
AB The Gram-negative bacterium Helicobacter pylori has a well-demonstrated role in several gastroduodenal diseases, including peptic ulcer disease, chronic active gastritis, mucosa-associated lymphoid tissue lymphoma, and gastric adenocarcinoma. In addition, more recently, several studies have focused on the possible causal role of H. pylori in various extragastric disorders, such as cardiovascular, respiratory, neurological, skin, and autoimmune conditions. The current status of the research on the pathogenesis, clinical and therapeutic aspects of H. pylori-associated idiopathic thrombocytopenic purpura in adults and children will be addressed in this narrative review.
C1 [Franchini, Massimo] Azienda Osped C Poma, Dipartimento Med Trasfus & Ematol, Mantua, Italy.
   [Vescovi, Pier Paolo; Garofano, Massimo] Azienda Osped C Poma, Div Med, Mantua, Italy.
   [Veneri, Dino] Azienda Osped Univ Integrata Verona, Dipartimento Med Sperimentale & Clin, Sez Ematol, Verona, Italy.
C3 Hospital Carlo Poma; Hospital Carlo Poma; University of Verona; Azienda
   Ospedaliera Universitaria Integrata Verona
RP Franchini, M (corresponding author), Azienda Osped C Poma, Dipartimento Med Trasfus & Ematol, Mantua, Italy.
EM massimo.franchini@aopoma.it
RI Franchini, Massimo/AAB-7345-2022
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NR 62
TC 19
Z9 22
U1 0
U2 10
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0094-6176
EI 1098-9064
J9 SEMIN THROMB HEMOST
JI Semin. Thromb. Hemost.
PD JUL
PY 2012
VL 38
IS 5
BP 463
EP 468
DI 10.1055/s-0032-1305781
PG 6
WC Hematology; Peripheral Vascular Disease
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Cardiovascular System & Cardiology
GA 969UX
UT WOS:000306086000006
PM 22753098
DA 2025-06-01
ER

PT J
AU Halusková, J
AF Haluskova, J.
TI Epigenetic Studies in Human Diseases
SO FOLIA BIOLOGICA
LA English
DT Review
DE epigenetics; humandiseases; methylation; histoneacetylation; miRNA;
   cancer
ID CELL LUNG-CANCER; DNA METHYLATION MARKERS; PROMOTER HYPERMETHYLATION;
   BREAST-CANCER; HISTONE MODIFICATION; COLORECTAL-CANCER; PROSTATE-CANCER;
   GASTRIC-CANCER; OVARIAN-CANCER; CPG ISLANDS
AB Irreversible genetic alterations underlying human diseases have been widely studied to date. However, it is evident that the potentially reversible epigenetic dysregulations may also have an important role in the disease origin. The studies of epigenetic mechanisms underlying disease onset, progression and pathogenesis have been performed in various human disorders. The epigenetic approaches may reveal useful markers for disease diagnostics, classification and prognostics as well as for progressive pharmacological treatment. This review summarizes the studies of epigenetic dysregulations including aberrant methylation, histone modifications and miRNA alterations in cancer as well as the studies of methylation changes and aberrant histone modifications in neurodegenerative, autoimmune, cardiovascular and other diseases. The imprinting disorders together with the emerging role of epigenetics in nutritional genomics, environment-organism interaction studies and in some other fields are also mentioned.
C1 PJ Safarik Univ Kosice, Fac Med, Dept Med Biol, Kosice 04066, Slovakia.
C3 University of Pavol Jozef Safarik Kosice
RP Halusková, J (corresponding author), PJ Safarik Univ Kosice, Fac Med, Dept Med Biol, Trieda SNP 1, Kosice 04066, Slovakia.
EM jana.haluskova@upjs.sk
RI Halušková, Jana/AAG-7326-2021
OI Haluskova, Jana/0000-0002-8137-1684
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NR 130
TC 36
Z9 40
U1 0
U2 7
PU CHARLES UNIV PRAGUE, FIRST FACULTY MEDICINE
PI PRAGUE 6
PA FLEMINGOVO NAM. 2, PRAGUE 6 166 37, CZECH REPUBLIC
SN 0015-5500
J9 FOLIA BIOL-PRAGUE
JI Folia Biol.-Prague
PY 2010
VL 56
IS 3
BP 83
EP 96
PG 14
WC Biochemistry & Molecular Biology; Biology; Oncology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Oncology; Cell Biology
GA 620IV
UT WOS:000279493800001
PM 20653993
DA 2025-06-01
ER

PT J
AU Faller, G
   Ruff, S
   Reiche, N
   Hochberger, J
   Hahn, EG
   Kirchner, T
AF Faller, G
   Ruff, S
   Reiche, N
   Hochberger, J
   Hahn, EG
   Kirchner, T
TI Mucosal production of antigastric autoantibodies in Helicobacter
   pylori gastritis
SO HELICOBACTER
LA English
DT Article
ID INFECTED PATIENTS; EPITHELIAL-CELLS; ANTIBODIES; IGA; DISEASE;
   LYMPHOCYTES; EXPRESSION; PHENOTYPE; PROTEIN; CANCER
AB Background. Apart form bacterial virulence factors of Helicobacter pylori, certain host factors influence the pathogenesis of H. pylori gastritis. In particular, antigastric autoantibodies that are detectable in the sera of a substantial proportion of H. pylori were shown to correlate with the development of gastric atrophy. The aim of this study was to analyze the possible antigastric autoimmune response in H. pylori gastritis at the site where the action is, i.e., in the gastric mucosa.
   Materials and Methods. Gastric biopsy specimens from antrum and corpus mucosa of 24 H. pylori-infected and of 33 noninfected patients were cultured for 3 days, and tissue culture supernatants were analyzed for the amount of locally produced IgA and IgG. Antigastric autoantibodies were screened in the sera and in the supernatants by means of immunohistochemistry.
   Results. The infected patients had significantly higher concentrations of locally produced IgA, whereas the IgG concentrations were virtually the same in infected and noninfected patients. IgG or IgA antigastric autoantibodies, or both, were detectable only in the sera (38%) and supernatants (17%) of infected patients. Interestingly, the patient with the strongest local autoimmune response showed body-predominant H. pylori gastritis, with destruction of gastric glands and atrophy of the body mucosa.
   Conclusions. These results demonstrate that antigastric autoimmune reactions are detectable at the site of the disease and might be relevant for the pathogenesis of gastric mucosa atrophy in H. pylori gastritis.
C1 Univ Erlangen Nurnberg, Inst Pathol, D-91054 Erlangen, Germany.
   Univ Erlangen Nurnberg, Dept Internal Med 1, D-91054 Erlangen, Germany.
C3 University of Erlangen Nuremberg; University of Erlangen Nuremberg
RP Univ Erlangen Nurnberg, Inst Pathol, Krankenhausstr 8-10, D-91054 Erlangen, Germany.
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NR 37
TC 14
Z9 16
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PD SEP
PY 2000
VL 5
IS 3
BP 129
EP 134
DI 10.1046/j.1523-5378.2000.00020.x
PG 6
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Microbiology
GA 349PE
UT WOS:000089054200002
PM 10971676
DA 2025-06-01
ER

PT J
AU Tam, C
   Wong, JH
   Tsui, SKW
   Zuo, T
   Chan, TF
   Ng, TB
AF Tam, Chit
   Wong, Jack Ho
   Tsui, Stephen Kwok Wing
   Zuo, Tao
   Chan, Ting Fung
   Ng, Tzi Bun
TI LncRNAs with miRNAs in regulation of gastric, liver, and colorectal
   cancers: updates in recent years
SO APPLIED MICROBIOLOGY AND BIOTECHNOLOGY
LA English
DT Review
DE lncRNA; miRNA; Epigenetic alteration; Microbiota meditation; Tumor
   proliferation; Metastasis; Targeted therapy design
ID LONG NONCODING RNA; PROMOTES CELL-PROLIFERATION; EPITHELIAL-MESENCHYMAL
   TRANSITION; HEPATOCELLULAR-CARCINOMA CELLS; PREDICTS POOR-PROGNOSIS;
   HELICOBACTER-PYLORI INFECTION; WNT/BETA-CATENIN PATHWAY; FACILITATES
   TUMOR-GROWTH; GENOME-WIDE ANALYSIS; COLON-CANCER
AB Long noncoding RNA (lncRNA) is a kind of RNAi molecule composed of hundreds to thousands of nucleotides. There are several major types of functional lncRNAs which participate in some important cellular pathways. LncRNA-RNA interaction controls mRNA translation and degradation or serves as a microRNA (miRNA) sponge for silencing. LncRNA-protein interaction regulates protein activity in transcriptional activation and silencing. LncRNA guide, decoy, and scaffold regulate transcription regulators of enhancer or repressor region of the coding genes for alteration of expression. LncRNA plays a role in cellular responses including the following activities: regulation of chromatin structural modification and gene expression for epigenetic and cell function control, promotion of hematopoiesis and maturation of immunity, cell programming in stem cell and somatic cell development, modulation of pathogen infection, switching glycolysis and lipid metabolism, and initiation of autoimmune diseases. LncRNA, together with miRNA, are considered the critical elements in cancer development. It has been demonstrated that tumorigenesis could be driven by homeostatic imbalance of lncRNA/miRNA/cancer regulatory factors resulting in biochemical and physiological alterations inside the cells. Cancer-driven lncRNAs with other cellular RNAs, epigenetic modulators, or protein effectors may change gene expression level and affect the viability, immortality, and motility of the cells that facilitate cancer cell cycle rearrangement, angiogenesis, proliferation, and metastasis. Molecular medicine will be the future trend for development. LncRNA/miRNA could be one of the potential candidates in this category. Continuous studies in lncRNA functional discrepancy between cancer cells and normal cells and regional and rational genetic differences of lncRNA profiles are critical for clinical research which is beneficial for clinical practice.
C1 [Tam, Chit; Wong, Jack Ho; Tsui, Stephen Kwok Wing; Ng, Tzi Bun] Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.
   [Zuo, Tao] Chinese Univ Hong Kong, Dept Med & Therapeut, Fac Med, Shatin, Hong Kong, Peoples R China.
   [Chan, Ting Fung] Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
C3 Chinese University of Hong Kong; Chinese University of Hong Kong;
   Chinese University of Hong Kong
RP Tam, C; Ng, TB (corresponding author), Chinese Univ Hong Kong, Sch Biomed Sci, Fac Med, Shatin, Lo Kwee Seong Integrated Biomed Sci Bldg,Area 39, Hong Kong, Peoples R China.; Chan, TF (corresponding author), Chinese Univ Hong Kong, Sch Life Sci, Fac Sci, Shatin, Run Run Shaw Sci Bldg, Hong Kong, Peoples R China.
EM 1155059540@link.cuhk.edu.hk; tf.chan@cuhk.edu.hk; tzibunng@cuhk.edu.hk
RI Zuo, Tao/AAB-9328-2020; TAM, Chit/IQU-3939-2023; Chan,
   TingFung/A-6161-2013; Tsui, Stephen Kwok-Wing/E-4385-2015
OI WONG, Jack/0000-0002-9732-986X; TAM, Chit/0000-0002-8719-1190; Chan,
   TingFung/0000-0002-0489-3884; Zuo, Tao/0000-0001-8450-5281; Tsui,
   Stephen Kwok-Wing/0000-0003-0686-4259
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NR 406
TC 114
Z9 122
U1 2
U2 53
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0175-7598
EI 1432-0614
J9 APPL MICROBIOL BIOT
JI Appl. Microbiol. Biotechnol.
PD JUN
PY 2019
VL 103
IS 12
BP 4649
EP 4677
DI 10.1007/s00253-019-09837-5
PG 29
WC Biotechnology & Applied Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology
GA HZ9QN
UT WOS:000469192100001
PM 31062053
DA 2025-06-01
ER

PT J
AU Lehy, T
   Roucayrol, AM
   Mignon, M
AF Lehy, T
   Roucayrol, AM
   Mignon, M
TI Histomorphological characteristics of gastric mucosa in patients with
   Zollinger-Ellison syndrome or autoimmune gastric atrophy: Role of
   gastrin and atrophying gastritis
SO MICROSCOPY RESEARCH AND TECHNIQUE
LA English
DT Article
ID ENTEROCHROMAFFIN-LIKE CELLS; MULTIPLE ENDOCRINE NEOPLASIA; ARGYROPHIL
   CARCINOID-TUMORS; SELF-REPLICATION RATE; PERNICIOUS-ANEMIA; OXYNTIC
   MUCOSA; FUNDIC MUCOSA; PARIETAL-CELL; HYPERGASTRINEMIC PATIENTS;
   ANTISECRETORY TREATMENT
AB The role of gastrin in the pathophysiology of two diseases affecting the human stomach, the Zollinger Ellison syndrome (ZES) and the pernicious anemia (PA), is reviewed. Both diseases present chronic hypergastrinemia but from different origins. The ZES is characterized by the occurrence of ectopic endocrine gastrin-secreting tumors and PA by a fundic atrophic gastritis leading to complete atrophy of fundus and resulting in achlorhydria. In PA, the lack of acid induces continuous gastrin cell activation and is responsible for the subsequent gastrin hypersynthesis and secretion. In ZES, hypergastrinemia causes hypertrophy of the oxyntic mucosa, which, in addition, displays hyperplasia of parietal and mucus cells. In both diseases, hypergastrinemia also induces the hyperproliferation of enterochromaffin-like endocrine cells in the fundic mucosa, which can offer all aspects from hyperplasia, then dysplasia, until true carcinoid tumor. The influence of antisecretory treaments and MEN 1 in the ZES as well as that of several other factors and antrectomy in PA on the behavior of the different gastric cells is evoked. Finally, the role that gastrin and its receptor play in the maintenance of the normal development of gastric mucosa and gastric acid secretion is emphasized by results observed in gene knockout models. (C) 2000 Wiley-Liss. Inc.
C1 Hop Bichat Claude Bernard, INSERM, U 10, F-75877 Paris 18, France.
   CHI Villeneuve St Georges, Dept Pathol, F-94195 Villeneuve St Georges, France.
   Hop Bichat Claude Bernard, Dept Hepato Gastroenterol, F-75877 Paris 18, France.
C3 Assistance Publique Hopitaux Paris (APHP); Universite Paris Cite;
   Hopital Universitaire Bichat-Claude Bernard - APHP; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Assistance Publique
   Hopitaux Paris (APHP); Universite Paris Cite; Hopital Universitaire
   Bichat-Claude Bernard - APHP
RP Fac Xavier Bichat, INSERM, Unite U410, 16 Rue Henri Huchard, Paris 18, France.
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NR 95
TC 28
Z9 30
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-910X
EI 1097-0029
J9 MICROSC RES TECHNIQ
JI Microsc. Res. Tech.
PD MAR 15
PY 2000
VL 48
IS 6
BP 327
EP 338
PG 12
WC Anatomy & Morphology; Biology; Microscopy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anatomy & Morphology; Life Sciences & Biomedicine - Other Topics;
   Microscopy
GA 300DW
UT WOS:000086238400003
PM 10738314
DA 2025-06-01
ER

PT J
AU Gu, JJ
   Su, CY
   Huang, F
   Zhao, YW
   Li, J
AF Gu, Junjie
   Su, Chongying
   Huang, Fei
   Zhao, Yuwei
   Li, Jing
TI Past, Present and Future: The Relationship Between Circular RNA and
   Immunity
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE circRNAs; immunity; immune-related diseases; autoimmune diseases; tumor;
   infectious diseases
ID MICROARRAY EXPRESSION PROFILE; BLOOD MONONUCLEAR-CELLS; MACROPHAGE
   ACTIVATION; HEPATOCELLULAR-CARCINOMA; ENHANCES RESISTANCE; DENDRITIC
   CELLS; GASTRIC-CANCER; PROLIFERATION; SUPPRESSION; PROGRESSION
AB The immune system has evolved since the birth of humans. However, immune-related diseases have not yet been overcome due to the lack of expected indicators and targeting specificity of current medical technology, subjecting patients to very uncomfortable physical and mental experiences and high medical costs. Therefore, the requirements for treatments with higher specificity and indicative ability are raised. Fortunately, the discovery of and continuous research investigating circular RNAs (circRNAs) represent a promising method among numerous methods. Although circRNAs wear regarded as metabolic wastes when discovered, as a type of noncoding RNA (ncRNA) with a ring structure and wide distribution range in the human body, circRNAs shine brilliantly in medical research by virtue of their special nature and structure-determined functions, such as high stability, wide distribution, high detection sensitivity, acceptable reproducibility and individual differences. Based on research investigating the role of circRNAs in immunity, we systematically discuss the hotspots of the roles of circRNAs in immune-related diseases, including expression profile analyses, potential biomarker research, ncRNA axis/network construction, impacts on phenotypes, therapeutic target seeking, maintenance of nucleic acid stability and protein binding research. In addition, we summarize the current situation of and problems associated with circRNAs in immune research, highlight the applications and prospects of circRNAs in the treatment of immune-related diseases, and provide new insight into future directions and new strategies for laboratory research and clinical applications.
C1 [Gu, Junjie; Su, Chongying; Huang, Fei; Li, Jing] Sichuan Univ, West China Hosp Stomatol, Chinese Acad Med Sci, Natl Clin Res Ctr Oral Dis,Res Unit Oral Carcinoge, Chengdu, Peoples R China.
   [Zhao, Yuwei] Chengdu Blood Ctr, Blood Res Lab, Chengdu, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Sichuan University
RP Li, J (corresponding author), Sichuan Univ, West China Hosp Stomatol, Chinese Acad Med Sci, Natl Clin Res Ctr Oral Dis,Res Unit Oral Carcinoge, Chengdu, Peoples R China.; Zhao, YW (corresponding author), Chengdu Blood Ctr, Blood Res Lab, Chengdu, Peoples R China.
EM cdbczyw@163.com; lijing1984@scu.edu.cn
RI LI, Jing/HNB-5575-2023
FU National Natural Science Foundation of China [81872211, 82072999];
   Sichuan Science and Technology Program [2020YJ0102]; Innovation Research
   Project of Sichuan University [2022SCUH0029]; CAMS Innovation Fund for
   Medical Sciences [2020-I2M-CT-A-023]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81872211 and 82072999), the Sichuan Science and
   Technology Program (2020YJ0102), the Innovation Research Project of
   Sichuan University (2022SCUH0029), and the CAMS Innovation Fund for
   Medical Sciences (2020-I2M-C&T-A-023).
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NR 167
TC 10
Z9 11
U1 0
U2 18
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 25
PY 2022
VL 13
AR 894707
DI 10.3389/fimmu.2022.894707
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 1Y1DN
UT WOS:000807884900001
PM 35693804
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Aditi, A
   Graham, DY
AF Aditi, Anupam
   Graham, David Y.
TI Vitamin C, Gastritis, and Gastric Disease: A Historical Review and
   Update
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Helicobacter pylori; Ascorbic acid; Vitamin C; Peptic ulcer; Gastritis;
   Pernicious anemia; Gastric cancer; Dehydroascorbic acid; Intestinal
   metaplasia; Gastrointestinal bleeding
ID HELICOBACTER-PYLORI INFECTION; ASCORBIC-ACID; CORPUS GASTRITIS; TRIPLE
   THERAPY; PEPTIC-ULCER; CANCER; OMEPRAZOLE; JUICE; ERADICATION; NITRITE
AB The discovery of Helicobacter pylori as the cause of gastritis and peptic ulcers ushered in the modern era of research into gastritis and into acid-peptic diseases and rekindled interest in the role of ascorbic acid in the pathophysiology and treatment of gastritis and peptic ulcer disease. Here, we review historic and modern studies on ascorbic acid and gastric diseases with an emphasis on H. pylori gastritis and its sequelae. The relationship of ascorbic acid and gastritis and peptic ulcer and its complications was extensively studied during the 1930s through the 1950s. Much of this extensive literature has been effectively "lost." Ascorbic acid deficiency was associated with all forms of gastritis (e.g., autoimmune, chemical, and infectious) due in varying degrees to insufficient intake, increased metabolic requirements, and destruction within the GI tract. Importantly, gastritis-associated abnormalities in gastric ascorbic acid metabolism are reversed by H. pylori-eradication and potentially worsened by proton pump inhibitor therapy. Diets rich in naturally occurring ascorbic acid are associated with protection of the gastric corpus from atrophy and a reduction in the incidence of gastric cancer possibly through the ability of ascorbic acid to reduce oxidative damage to the gastric mucosa by scavenging carcinogenic N-nitroso compounds and free radicals and attenuating the H. pylori-induced inflammatory cascade. Ascorbic acid supplementation was possibly associated with a decreased incidence of bleeding from peptic ulcer disease. Pharmacologic doses of ascorbic acid also may improve the effectiveness of H. pylori-eradication therapy. Occasionally, looking back can help plot the way forward.
C1 [Graham, David Y.] Michael E DeBakey VA Med Ctr, Houston, TX 77030 USA.
   [Aditi, Anupam] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   [Graham, David Y.] Baylor Coll Med, Houston, TX 77030 USA.
C3 Baylor College of Medicine; Baylor College Medical Hospital; Washington
   University (WUSTL); Baylor College of Medicine
RP Graham, DY (corresponding author), Michael E DeBakey VA Med Ctr, RM 3A-320 111D,2002 Holcombe Blvd, Houston, TX 77030 USA.
EM anupam.aditi@gmail.com; dgraham@bcm.edu
RI Graham, David/AAL-2165-2021
FU Office of Research and Development Medical Research Service Department
   of Veterans Affairs; Public Health Service [DK56338, DK067366,
   CA116845]; Baylor College of Medicine
FX Dr. Graham is an unpaid consultant for Novartis in relation to vaccine
   development for treatment or prevention of H. pylori infection. Dr.
   Graham is supported in part by the Office of Research and Development
   Medical Research Service Department of Veterans Affairs, Public Health
   Service grant DK56338, which funds the Texas Medical Center Digestive
   Diseases Center, DK067366 and CA116845. The authors thank Dr. Rassa
   Shahidzadeh for helping to get this project started.Dr. Graham is also a
   paid consultant for Otsuka Pharmaceuticals regarding diagnostic testing
   and has received royalties from the Baylor College of Medicine patent
   covering materials related to the <SUP>13</SUP>C-urea breath test. Dr.
   Aditi has no conflicts to declare.
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NR 86
TC 62
Z9 67
U1 1
U2 43
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD OCT
PY 2012
VL 57
IS 10
BP 2504
EP 2515
DI 10.1007/s10620-012-2203-7
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 012HQ
UT WOS:000309227300007
PM 22543844
OA Green Accepted, Bronze
DA 2025-06-01
ER

PT J
AU Sela, M
   Arnon, R
   Schechter, B
AF Sela, M
   Arnon, R
   Schechter, B
TI Therapeutic vaccines: realities of today and hopes for the future
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL
   MYASTHENIA-GRAVIS; ALTERED PEPTIDE LIGAND; REMITTING MULTIPLE-SCLEROSIS;
   MYELIN BASIC-PROTEIN; T-CELL EPITOPE; PHASE-II TRIAL;
   ALZHEIMERS-DISEASE; HELICOBACTER-PYLORI; METASTATIC MELANOMA
AB Vaccines are by definition prophylactic, but in recent years an interest has developed in therapeutic vaccines for infectious diseases such as AIDS and tuberculosis, as well as gastric ulcers, cancer (with different approaches to combat various types of malignancy) and autoimmune diseases (a definite success was the development of a vaccine against multiple sclerosis) and there are potential vaccines in development for myasthenia gravis, lupus and diabetes. Therapeutic vaccines are also being developed against cognitive diseases such as Alzheimer's disease, prion diseases and Huntington's disease, All of these efforts are based on the therapeutic vaccine being closely related chemically to the etiological agent that causes the disease.
C1 Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel.
C3 Weizmann Institute of Science
RP Weizmann Inst Sci, Dept Immunol, IL-76100 Rehovot, Israel.
EM michael.sela@weizmann.ac.il
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NR 74
TC 17
Z9 25
U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
EI 1878-5832
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD JUN 15
PY 2002
VL 7
IS 12
BP 664
EP 673
DI 10.1016/S1359-6446(02)02296-1
PG 10
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 565NU
UT WOS:000176377000008
PM 12110243
DA 2025-06-01
ER

PT J
AU Zhao, ZW
   Kang, WM
   Ma, ZQ
   Ye, X
   Yu, JC
AF Zhao, Zhe-Wei
   Kang, Wei-Ming
   Ma, Zhi-Qiang
   Ye, Xin
   Yu, Jian-Chun
TI Gastric cancer with severe immune thrombocytopenia: A case report
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Gastric cancer; Immune thrombocytopenia; Surgical treatment; Case report
ID LAPAROSCOPIC SPLENECTOMY; PLATELET TRANSFUSION; PURPURA ITP; OUTCOMES;
   JEJUNOSTOMY; PATIENT; COUNT
AB BACKGROUND
   Primary immune thrombocytopenia (ITP) is a rare autoimmune disease associated with a high bleeding risk. For those patients with gastric cancer, surgical treatment may be the only option for therapy. Here, we present the first case of gastric cancer with severe and medically refractory ITP treated by radical resection of the gastric cancer and splenectomy.
   CASE SUMMARY
   A 54-year-old female patient was admitted to our surgical department with a 2 mo history of decreased appetite, nausea, vomiting, and weight loss, which progressed to difficulty in feeding 3 d prior to her visit. According to her medical history, she was diagnosed with refractory ITP [platelets (PLT), 3000-8000/mu L] 10 years ago. After admission, the patient underwent a splenectomy and a distal subtotal gastrectomy (D2 radical resection) with Roux-en-Y reconstruction simultaneously. She had an uneventful postoperative course with a slight increase in her PLT count. This case is unique in terms of the patient's complication of severe and medically refractory ITP.
   CONCLUSION
   Simultaneous splenectomy, preoperative PLT transfusion, and early enteral nutrition were important treatment methods for helping this patient recover.
C1 [Zhao, Zhe-Wei; Kang, Wei-Ming; Ma, Zhi-Qiang; Ye, Xin; Yu, Jian-Chun] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, 1 Shuaifuyuan, Beijing 100730, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College Hospital
RP Yu, JC (corresponding author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Gen Surg, 1 Shuaifuyuan, Beijing 100730, Peoples R China.
EM yjcpumch@126.com
RI Ma, qiang/HZK-3874-2023
OI Kang, Weiming/0000-0002-6736-4728
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NR 26
TC 1
Z9 1
U1 0
U2 5
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD DEC 6
PY 2018
VL 6
IS 15
BP 1024
EP 1028
DI 10.12998/wjcc.v6.i15.1024
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HD3SE
UT WOS:000452438600018
PM 30568958
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Papamichael, K
   Konstantopoulos, P
   Mantzaris, GJ
AF Papamichael, Konstantinos
   Konstantopoulos, Panagiotis
   Mantzaris, Gerassimos J.
TI Helicobacter pylori infection and inflammatory bowel disease: Is
   there a link?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Helicobacter pylori; Inflammatory bowel disease; Ulcerative colitis;
   Crohn's disease; Colorectal cancer
ID REGULATORY T-CELLS; UPPER GASTROINTESTINAL LESIONS; FOCALLY ENHANCED
   GASTRITIS; TERM-FOLLOW-UP; CROHNS-DISEASE; LOW-PREVALENCE;
   ULCERATIVE-COLITIS; VACUOLATING CYTOTOXIN; RHEUMATOID-ARTHRITIS;
   CYTOKINE PRODUCTION
AB Helicobacter pylori (H. pylori) infection is one of the most widely spread infectious diseases in humans. It can cause chronic gastritis, peptic ulcer disease and gastric malignancies and has been associated with extra-gastric disorders. H. pylori elicit a chronic systemic inflammatory response which, under certain conditions, may trigger autoimmune reactions and may be implicated in the pathogenesis of autoimmune diseases. Although the pathogenesis of inflammatory bowel disease (IBD) is unknown, it is thought to result from complex interactions between environmental factors and microbiota in the gut of individuals who are genetically susceptible. Several bacterial and viral agents have been implicated in the aetiology of IBD. In theory, H. pylori infection could be involved in the pathogenesis of IBD by inducing alterations in gastric and/or intestinal permeability or by causing immunological derangements resulting in absorption of antigenic material and autoimmunity via various immunological pathways. Similar mechanisms may also be responsible for the co-existence of IBD with other autoimmune diseases and/or extra-intestinal manifestations. However, the epidemiological data fail to support this association. In fact, various studies indicate that the prevalence of H. pylori infection is low in patients with IBD, suggesting a protective role for this infection in the development of IBD. In this report, we aim to shed light on proposed mechanisms and confounding factors underlying the potential link between H. pylori infection and IBD. (C) 2014 Baishideng Publishing Group Inc. All rights reserved.
C1 [Papamichael, Konstantinos; Konstantopoulos, Panagiotis; Mantzaris, Gerassimos J.] Evaggelismos Hosp, Gastroenterol Clin 1, Athens 10676, Greece.
RP Papamichael, K (corresponding author), Evaggelismos Hosp, Gastroenterol Clin 1, 45-47 Ypsilantou St, Athens 10676, Greece.
EM kpapamdoc@yahoo.gr
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NR 147
TC 78
Z9 92
U1 4
U2 23
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD JUN 7
PY 2014
VL 20
IS 21
BP 6374
EP 6385
DI 10.3748/wjg.v20.i21.6374
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AK6BS
UT WOS:000338513200003
PM 24914359
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Kaku, N
   Yanagihara, K
   Morinaga, Y
   Sato, T
   Nakashima, M
   Sakai, T
   Tominaga, H
   Wakigawa, F
   Nagashima, S
   Fukuda, M
   Hashiguchi, K
   Kohno, S
AF Kaku, Norihito
   Yanagihara, Katsunori
   Morinaga, Yoshitomo
   Sato, Tsuyoshi
   Nakashima, Munetoshi
   Sakai, Takahiro
   Tominaga, Hiroo
   Wakigawa, Fumiko
   Nagashima, Seiji
   Fukuda, Minoru
   Hashiguchi, Kohji
   Kohno, Shigeru
TI Detection of Legionella pneumophila serogroup 1 in blood cultures
   from a patient treated with tumor necrosis factor-alpha inhibitor
SO JOURNAL OF INFECTION AND CHEMOTHERAPY
LA English
DT Article
DE Legionnaires' disease; Community-acquired pneumonia; Blood culture;
   Tumor necrosis factor-alpha inhibitor
ID COMMUNITY-ACQUIRED PNEUMONIA; TERM-CARE FACILITY; LEGIONNAIRES-DISEASE;
   RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES; UNITED-STATES; RISK;
   OUTBREAK; THERAPY; HOSPITALIZATION
AB A 65-year-old man was admitted to our hospital with a temperature of 39.3 A degrees C, cough, sputum, and pharyngeal discomfort that had persisted for 3 days. He had been treated with methotrexate and adalimumab (a tumor necrosis factor-alpha [TNF-alpha] inhibitor) for rheumatoid arthritis for 2 years, and he had also been treated with S-1 (tegafur, gimeracil, and oteracil potassium) for pancreatic metastasis of gastric cancer for 2 months. Regardless of the underlying pathologies, his general condition was good and he had worked as an electrician until 2 days before admission. However, his appetite had suddenly decreased from the day before admission, and high fever and hypoxia were also evident upon admission. A chest X-ray and computed tomography scan revealed left pleural effusion and consolidation in both lungs. The pneumonia severity index score was 165 and the risk class was V. Accordingly, we started to treat the pneumonia with a combination of levofloxacin and meropenem. Thereafter, we received positive urinary antigen test findings for Legionella pneumophila. After hospitalization, hypoxia was progressed and hypotension was emerged. Despite the application of appropriate antibiotics, vasopressors, and oxygenation, the patient died 8 h after admission. Even after his death, blood cultures were continued to consider the possibility of bacterial co-infection. Although no bacteria were detected from blood cultures, Gimenez staining revealed pink bacteria in blood culture fluids. Subsequent blood fluid culture in selective medium revealed L. pneumophila serogroup 1. Recently, TNF-alpha inhibitors have been described as a risk factor for Legionnaires' disease. In consideration of the increased frequency of TNF-alpha inhibitors, we may need to recognize anew that L. pneumophila might be a pathogen of severe community-acquired pneumonia.
C1 [Kaku, Norihito; Sato, Tsuyoshi; Nakashima, Munetoshi; Nagashima, Seiji; Fukuda, Minoru; Hashiguchi, Kohji] Japanese Red Cross Nagasaki Genbaku Hosp, Dept Internal Med, Nagasaki, Japan.
   [Kaku, Norihito; Yanagihara, Katsunori; Morinaga, Yoshitomo] Nagasaki Univ, Dept Internal Med 2, Grad Sch Biomed Sci, Nagasaki 8528501, Japan.
   [Yanagihara, Katsunori; Morinaga, Yoshitomo; Kohno, Shigeru] Nagasaki Univ, Dept Lab Med, Grad Sch Biomed Sci, Nagasaki 8528501, Japan.
   [Sakai, Takahiro; Tominaga, Hiroo; Wakigawa, Fumiko] Japanese Red Cross Nagasaki Genbaku Hosp, Dept Clin Lab, Nagasaki, Japan.
C3 Nagasaki University; Nagasaki University
RP Yanagihara, K (corresponding author), Nagasaki Univ, Dept Lab Med, Grad Sch Biomed Sci, 1-7-1 Sakamoto, Nagasaki 8528501, Japan.
EM kyana-ngs@umin.ac.jp
RI Kaku, Norihito/HJY-8750-2023; Kaku, Norihito/N-4488-2015
OI Kaku, Norihito/0000-0002-4086-4853
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NR 38
TC 10
Z9 11
U1 0
U2 12
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
   JAPAN
SN 1341-321X
EI 1437-7780
J9 J INFECT CHEMOTHER
JI J. Infect. Chemother.
PD FEB
PY 2013
VL 19
IS 1
BP 166
EP 170
DI 10.1007/s10156-012-0459-7
PG 5
WC Infectious Diseases; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases; Pharmacology & Pharmacy
GA 091JJ
UT WOS:000315045300025
PM 22911089
OA Green Submitted
DA 2025-06-01
ER

PT J
AU Massironi, S
   Zilli, A
   Fanetti, I
   Ciafardini, C
   Conte, D
   Peracchi, M
AF Massironi, Sara
   Zilli, Alessandra
   Fanetti, Ilaria
   Ciafardini, Clorinda
   Conte, Dario
   Peracchi, Maddalena
TI Intermittent treatment of recurrent type-1 gastric carcinoids with
   somatostatin analogues in patients with chronic autoimmune atrophic
   gastritis
SO DIGESTIVE AND LIVER DISEASE
LA English
DT Article
DE Lanreotide; Neuroendocrine tumours; Octreotide
ID ENDOSCOPIC SUBMUCOSAL DISSECTION; TERM-FOLLOW-UP; NEUROENDOCRINE TUMORS;
   RECEPTOR ANTAGONIST; ENDOCRINE TUMORS; CELL CARCINOIDS; MANAGEMENT;
   HYPERGASTRINEMIA; CLASSIFICATION; ANTRECTOMY
AB Background: Optimal management and treatment of type-1 gastric carcinoids is under debate.
   Aims: This prospective study evaluates the outcome of patients with recurrent type-1 gastric carcinoids treated with somatostatin analogues.
   Methods: From 2000 to 2013, among a population of 107 chronic atrophic gastritis patients, 25(20% males, median age 62 years) developed type-1 gastric carcinoids and underwent regular clinical and endoscopic follow-up (median 77 months, range 6-165) after the initial treatment. Those patients showing recurrent disease were treated with somatostatin analogues until carcinoid disappearance.
   Results: 12125 patients (33% males, median age 65 years) showed recurrent gastric carcinoids and were treated with somatostatin analogues for a median duration of 12 months. Median gastrin and chromogranin A levels, which were 802 pg/mL and 33 U/L, respectively, decreased to 299 pg/mL (p = 0.002) and 15.6 U/L (p = 0.001) at the end of the treatment. Gastric carcinoids disappeared after a median length of treatment of 12 months. After a median time of 19.5 months from somatostatin analogues discontinuation, 4112 patients (25% males, median age 56 years) showed a further recurrence. A new cycle of treatment was performed successfully.
   Conclusions: This study confirms that type-1 gastric carcinoids are a recurring disease and somatostatin analogues, administered on 12-month cycles, represent an effective treatment. (C) 2015 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
C1 [Massironi, Sara; Zilli, Alessandra; Fanetti, Ilaria; Ciafardini, Clorinda; Conte, Dario; Peracchi, Maddalena] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, I-20122 Milan, Italy.
   [Zilli, Alessandra; Fanetti, Ilaria; Ciafardini, Clorinda; Conte, Dario; Peracchi, Maddalena] Univ Milan, Dept Pathophysiol & Transplantat, Postgrad Sch Gastroenterol, Milan, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Milan
RP Massironi, S (corresponding author), Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, Via F Sforza 35, I-20122 Milan, Italy.
EM sara.massironi@policlinico.mi.it
RI Massironi, Sara/X-4138-2019
OI Fanetti, Ilaria/0000-0002-8295-0098; Massironi, Sara/0000-0003-3214-8192
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NR 56
TC 31
Z9 35
U1 0
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1590-8658
EI 1878-3562
J9 DIGEST LIVER DIS
JI Dig. Liver Dis.
PD NOV
PY 2015
VL 47
IS 11
BP 978
EP 983
DI 10.1016/j.dld.2015.07.155
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CU4HV
UT WOS:000363489400015
PM 26321479
DA 2025-06-01
ER

PT J
AU Haghbin, H
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   Zakirkhodjaev, N
   Lee-Smith, W
   Aziz, M
AF Haghbin, Hossein
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   Fatima, Rawish
   Zakirkhodjaev, Nuruddinkhodja
   Lee-Smith, Wade
   Aziz, Muhammad
TI Correlation of Autoimmune Pancreatitis and Malignancy: Systematic Review
   and Meta-Analysis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Autoimmune pancreatitis; Immunoglobulin G4-related disease;
   Inflammation; Malignancy; Metabolic syndrome
ID IGG4-RELATED DISEASE; DIAGNOSTIC-CRITERIA; STEROID-THERAPY; GUT
   MICROBIOTA; CANCER; RISK; INFLAMMATION; ASSOCIATION; EXPERIENCE;
   OUTCOMES
AB Background There is conflicting evidence regarding autoimmune pancreatitis (AIP) association with pancreatic and non-pancreatic cancers. Literature lacks data on overall prevalence of malignancies in autoimmune pancreatitis. Aim Given the lack of definite evidence, we aimed to pool and summarize data from available literature regarding prevalence of different malignancies in AIP. Methods We conducted a systematic search of MEDLINE, EMBASE, Cochrane Register of Controlled Trials, and Web of Science through February 16, 2021, to include observational studies assessing the incidence of cancer in AIP. We used the DerSimonian-Laird method with random effects for meta-analysis. Pooled prevalence, 95% confidence interval (CI), and I-2 statistic are reported. Results A total of 17 studies with 2746 patients were included assessing the prevalence of cancer in AIP. The overall prevalence of cancer in AIP was 9.6% [95% confidence interval (CI), 5.7-13.5%]. The cancers with the highest prevalence in AIP population were gastric and colorectal cancer, with prevalence of 1.3% (95% CI, 0.5-2.1%) and 1.2% (95% CI, 0.6-1.8%), respectively. Conclusion We demonstrate the prevalence of different cancers in AIP. Inflammatory surge in AIP and subsequent carcinogenesis is one explanation for this association. Moreover, AIP can be a paraneoplastic syndrome manifestation of malignancies.
C1 [Haghbin, Hossein; Chuang, Justin; Fatima, Rawish] Univ Toledo, Dept Internal Med, 2801 W Bancroft St, Toledo, OH 43606 USA.
   [Zakirkhodjaev, Nuruddinkhodja] Stony Brook Med, Dept Surg, Stony Brook, NY USA.
   [Lee-Smith, Wade] Univ Toledo, Univ Toledo Lib, 2801 W Bancroft St, Toledo, OH 43606 USA.
   [Aziz, Muhammad] Univ Toledo, Div Gastroenterol & Hepatol, 2801 W Bancroft St, Toledo, OH 43606 USA.
C3 University System of Ohio; University of Toledo; State University of New
   York (SUNY) System; Stony Brook University; Stony Brook University
   Hospital; University System of Ohio; University of Toledo; University
   System of Ohio; University of Toledo
RP Haghbin, H (corresponding author), Univ Toledo, Dept Internal Med, 2801 W Bancroft St, Toledo, OH 43606 USA.
EM hoshaq@yahoo.com
RI ; Lee-Smith, Wade/D-3361-2009
OI Haghbin, Hossein/0000-0001-8947-287X; Lee-Smith,
   Wade/0000-0003-1744-8525
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NR 63
TC 9
Z9 10
U1 1
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD JUL
PY 2022
VL 67
IS 7
BP 3252
EP 3264
DI 10.1007/s10620-021-07179-9
EA JUL 2021
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 2M1EH
UT WOS:000676052700002
PM 34297267
DA 2025-06-01
ER

PT J
AU D'Elios, MM
   Amedei, A
   Benagiano, M
   Azzurri, A
   Del Prete, G
AF D'Elios, MM
   Amedei, A
   Benagiano, M
   Azzurri, A
   Del Prete, G
TI Helicobacter pylori, T cells and cytokines:: the "dangerous
   liaisons"
SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
LA English
DT Article; Proceedings Paper
CT 6th International Workshop on Pathogenesis and Host Responses in
   Helicobacter Infections
CY JUN 23-26, 2004
CL Helsingor, DENMARK
SP European Study Grp Pathogenesis & Immunol Helicobacter Infect
DE mucosal immunity; Th1-Th2 response; cytokines; Helicobacter pylori;
   chronic gastritis; peptic ulcer; gastric cancer; gastric lymphoma;
   autoimmunity
ID HUMAN GASTRIC-MUCOSA; PATHOGENICITY ISLAND; IMMUNE-RESPONSES; INFECTION;
   HELPER; LYMPHOCYTES; EXPRESSION; ANTRUM; GROWTH; INFLAMMATION
AB Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop chronic and life threatening diseases, as peptic ulcer, gastric cancer, B-cell lymphoma, or autoimmune gastritis. The type of host immune response against H. pylori is crucial for the outcome of the infection. A predominant H. pylori-specific Th1 response, characterized by high IFN-gamma, TNF-alpha, and IL-12 production associates with peptic ulcer, whereas combined secretion of both Th1 and Th2 cytokines are present in uncomplicated gastritis. Gastric T cells from MALT lymphoma exhibit abnormal help for autologous B-cell proliferation and reduced perforin- and Fas-Fas ligand-mediated killing of B cells. In H. pylori-infected patients with autoimmune gastritis cytolytic T cells infiltrating the gastric mucosa cross-recognize different epitopes of H. pylori proteins and H+K+ ATPase autoantigen. These data suggest that peptic ulcer can be regarded as a Th1-driven immunopathological response to some H. pylori antigens, whereas deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support the onset of low-grade B-cell lymphoma. Alternatively, If. pylori infection may lead in some individuals to gastric autoimmunity via molecular mimicry. (c) 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.
C1 Univ Florence, Dept Internal Med, I-50134 Florence, Italy.
C3 University of Florence
RP Univ Florence, Dept Internal Med, Viale Morgagni 85, I-50134 Florence, Italy.
EM delios@unifi.it
RI Benagiano, Marisa/AAD-6443-2019; Amedei, Amedeo/G-5378-2011; D'Elios,
   Mario Milco/Y-9573-2019
OI D'Elios, Mario Milco/0000-0001-9160-0930
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NR 48
TC 74
Z9 85
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0928-8244
EI 1574-695X
J9 FEMS IMMUNOL MED MIC
JI FEMS Immunol. Med. Microbiol.
PD MAY 1
PY 2005
VL 44
IS 2
BP 113
EP 119
DI 10.1016/j.femsim.2004.10.013
PG 7
WC Immunology; Infectious Diseases; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology; Infectious Diseases; Microbiology
GA 928GP
UT WOS:000229259700002
PM 15866204
DA 2025-06-01
ER

PT J
AU Cui, XB
   Xu, W
   Zhang, YC
   Wang, F
   Guo, P
   Gong, W
AF Cui, Xiaobing
   Xu, Wen
   Zhang, Yingchun
   Wang, Fang
   Guo, Pei
   Gong, Wei
TI Autoimmune pancreatitis with pancreatic calculi and pseudocyst: a case
   report
SO JOURNAL OF INTERNATIONAL MEDICAL RESEARCH
LA English
DT Article
DE Autoimmune pancreatitis; case report; endoscopic ultrasonography;
   pancreatic calculus; pancreatic pseudocyst; immunoglobulin G4
ID DIAGNOSTIC-CRITERIA
AB Autoimmune pancreatitis (AIP) is a unique form of pancreatitis often associated with infiltration of immunoglobulin G4-positive cells, a swollen pancreas, and diffuse narrowing of the pancreatic ducts. Unlike acute pancreatitis, AIP is rarely complicated with pseudocysts. Pancreatic calculi, a feature of ordinary chronic pancreatitis, are unusual during short-term follow-up in patients with AIP. We herein describe a 46-year-old man who initially presented with a submucosal tumor of the stomach. The patient was finally diagnosed with AIP accompanied by a pancreatic tail pseudocyst located in the gastric wall and pancreatic calculi by endoscopic ultrasonography-guided fine-needle aspiration. He underwent endoscopic retrograde cholangiopancreatography, pancreatic duct stent placement, and steroid treatment and achieved good clinical and laboratory responses. Although AIP is a common autoimmune disease that responds well to steroids, pseudocysts and pancreatic calculi are rare manifestations of AIP and should be given special attention, especially in patients with disease relapse.
C1 [Cui, Xiaobing; Xu, Wen; Zhang, Yingchun; Wang, Fang; Gong, Wei] Southern Med Univ, Shenzhen Hosp, Dept Digest Med, 1333 Xinhu Rd, Shenzhen 518000, Guangdong, Peoples R China.
   [Guo, Pei] Southern Med Univ, Shenzhen Hosp, Dept Pathol, Shenzhen, Guangdong, Peoples R China.
C3 Southern Medical University - China; Southern Medical University - China
RP Gong, W (corresponding author), Southern Med Univ, Shenzhen Hosp, Dept Digest Med, 1333 Xinhu Rd, Shenzhen 518000, Guangdong, Peoples R China.
EM drgwei@foxmail.com
RI Guo, Peixuan/AAE-2573-2022; Xu, Wenqi/NAZ-7068-2025; Cui,
   XiaoBing/K-8159-2012
OI Cui, XiaoBing/0000-0002-5460-0357
FU Medical Scientific Research Foundation of Guangdong Province of China
   [A2019564]; Research Foundation of Shenzhen Hospital of Southern Medical
   University [PT2018KY01]
FX This work was supported by the Medical Scientific Research Foundation of
   Guangdong Province of China (A2019564) and by the Research Foundation of
   Shenzhen Hospital of Southern Medical University (PT2018KY01).
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NR 10
TC 3
Z9 3
U1 0
U2 11
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0300-0605
EI 1473-2300
J9 J INT MED RES
JI J. Int. Med. Res.
PD MAY
PY 2021
VL 49
IS 5
AR 03000605211014798
DI 10.1177/03000605211014798
PG 7
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA UW3NR
UT WOS:000700067500001
PM 34034562
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Fisher, SG
   Fisher, RI
AF Fisher, SG
   Fisher, RI
TI The epidemiology of non-Hodgkin's lymphoma
SO ONCOGENE
LA English
DT Review
DE non-Hodgkin's lymphoma; epidemiology; etiology
ID CARDIAC-TRANSPLANT RECIPIENTS; EPSTEIN-BARR-VIRUS; UNITED-STATES;
   HELICOBACTER-PYLORI; LYMPHOPROLIFERATIVE DISORDERS; GASTRIC LYMPHOMA;
   TIME TRENDS; RHEUMATOID-ARTHRITIS; BLOOD-TRANSFUSION; CELL LYMPHOMAS
AB The incidence of non-Hodgkin's lymphoma (NHL) has doubled over the past two decades in the US and most other westernized countries. While improved cancer reporting, changes in lymphoma classification, and increases in AIDS-associated lymphomas have contributed to the startling escalation of disease incidence, these factors are estimated to account for only about 50% of the increase in observed incidence. The elucidation of etiologic factors and their mechanistic role in the pathogenesis of this malignancy are critical to advancements in disease prevention and treatment. Current evidence suggests that factors/conditions that precipitate either chronic antigenic stimulation or immunosuppression may provide a preferential milieu for development of NHL. High rates of lymphoma have been observed among individuals with autoimmune disease, organ transplants, and primary or acquired immunodeficiencies. Ultraviolet radiation, previously demonstrated to have an immunosuppressive effect, has also been suggested as a possible risk factor for NHL. Several pathogens have been linked to the risk of lymphoma, including Epstein-Barr virus, human immunodeficiency virus, human T-cell lymphotropic virus-1, Helicobacter pylori, hepatitis C, and simian virus 40. Whether these microbes are responsible for specific genetic mutations that initiate tumor growth, antigenic stimulation leading to B-cell proliferation, and increased potential of random cell replication errors, or immunosuppression, which thereby promotes tumor growth, has not been clearly delineated. Other exogenous factors which have been implicated in lymphomagenesis are chemicals and agricultural exposures, hair dyes, and blood transfusions. We must build on our current knowledge regarding the etiology of NHL in order that prevention, treatment, and ultimately, cure of this malignancy becomes a reality.
C1 Univ Rochester, Sch Med & Dent, Dept Community & Prevent Med, Div Epidemiol, Rochester, NY 14642 USA.
   Univ Rochester, Sch Med & Dent, James P Wilmot Canc Ctr, Rochester, NY 14642 USA.
C3 University of Rochester; University of Rochester
RP Univ Rochester, Sch Med & Dent, Dept Community & Prevent Med, Div Epidemiol, 601 Elmwood Ave,Box 644, Rochester, NY 14642 USA.
EM susan_fisher@urmc.rochester.edu
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NR 110
TC 306
Z9 350
U1 0
U2 28
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
EI 1476-5594
J9 ONCOGENE
JI Oncogene
PD AUG 23
PY 2004
VL 23
IS 38
BP 6524
EP 6534
DI 10.1038/sj.onc.1207843
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
   Heredity
GA 848LJ
UT WOS:000223468800016
PM 15322522
DA 2025-06-01
ER

PT J
AU Zingone, F
   Pilotto, V
   Cardin, R
   Maddalo, G
   Orlando, C
   Fassan, M
   Marsilio, I
   Collesei, E
   Pelizzaro, F
   Farinati, F
AF Zingone, Fabiana
   Pilotto, Valentina
   Cardin, Romilda
   Maddalo, Gemma
   Orlando, Costanza
   Fassan, Matteo
   Marsilio, Ilaria
   Collesei, Eugenio
   Pelizzaro, Filippo
   Farinati, Fabio
TI Autoimmune Atrophic Gastritis: The Role of miRNA in Relation to
   Helicobacter Pylori Infection
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE miRNA; autoimmune gastritis; gastric cancer; Helicobacter pylori;
   biomarkers
ID BIOMARKERS; CLASSIFICATION; MICRORNAS
AB IntroductionMicroRNAs (miRNAs) have been proposed as diagnostic markers, biomarkers of neoplastic progression, and possible therapeutic targets in several immune-mediated diseases. We aimed to analyze the expression profile of selected miRNAs (miR21, miR142, miR223, miR155) in patients with autoimmune atrophic gastritis (AAG), patients with non-autoimmune multifocal atrophic gastritis (MAG), and healthy control subjects (HC). Materials and methodsA total of 103 patients with AAG were consecutively recruited for this study among those attending our gastroenterology outpatient clinic. Participating patients were divided into two groups: primary, not Helicobacter pylori (HP)-associated related AAG (n=57, P-AAG) and HP-associated AAG (n=46, HP-AAG); this subgroup included HP-positive patients, patients with previously reported HP infection, and patients harboring antral atrophy, considered as a stigma of HP infection. We also included 20 sex-age-matched MAG patients and 10 HC. Upper endoscopy with gastric biopsies were performed on each AAG and MAG patient. Circulating levels of miR21-5p, miR142-3p, miR223-3p, and miR155-5p were measured by RT-PCR in all groups. ResultsMiR-21 was over-expressed in P-AAG (p=0.02), HP-AAG (p = 0.04), and MAG (p=0.03) compared with HC. By contrast, miR-142 was more expressed in HC than in HP-AAG (p=0.04) and MAG (p=0.03). MiR-155 showed no significant differences among the four subgroups, while, unexpectedly, miR-223 was overexpressed in HC compared to P-AAG (p=0.01), HP-AAG (p=0.003), and MAG (p<0.001), and was higher in P-AAG than in MAG (p=0.05). ConclusionsMiR-21 was over-expressed in patients with gastric precancerous conditions irrespective of etiology, while in the same subgroups miR-142 and miR-223 were under-expressed compared to healthy controls. Controlling miRNAs up- or downregulation could lead to a breakthrough in treating chronic autoimmune diseases and potentially interfere with the progression to cancer.
C1 [Zingone, Fabiana; Pilotto, Valentina; Cardin, Romilda; Maddalo, Gemma; Orlando, Costanza; Marsilio, Ilaria; Collesei, Eugenio; Pelizzaro, Filippo; Farinati, Fabio] Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.
   [Zingone, Fabiana; Pilotto, Valentina; Maddalo, Gemma; Orlando, Costanza; Pelizzaro, Filippo; Farinati, Fabio] Azienda Osped Univ Padova, Gastroenterol Unit, Padua, Italy.
   [Fassan, Matteo] Univ Padua, Dept Med, Surg Pathol Unit, Padua, Italy.
   [Fassan, Matteo] Veneto Inst Oncol, Ist Ricovero & Cura Carattere Sci IRCCS, Padua, Italy.
C3 University of Padua; University of Padua; Azienda Ospedaliera -
   Universita di Padova; University of Padua; IRCCS Istituto Oncologico
   Veneto (IOV)
RP Farinati, F (corresponding author), Univ Padua, Dept Surg Oncol & Gastroenterol, Padua, Italy.; Farinati, F (corresponding author), Azienda Osped Univ Padova, Gastroenterol Unit, Padua, Italy.
EM fabio.farinati@unipd.it
RI Zingone, Fabiana/AGP-7008-2022; Farinati, Fabio/A-8267-2012; Fassan,
   Matteo/F-5152-2012; Zingone, Fabiana/O-5361-2018
OI FARINATI, FABIO/0000-0002-2944-1374; Fassan, Matteo/0000-0001-6515-5482;
   Zingone, Fabiana/0000-0003-1133-1502
FU Italian Health Ministry/Veneto region research program
   [NET-2016-02363853]; AIRC [22759]; Department of Surgery, Oncology and
   Gastroenterology, University of Padua
FX MF is supported by grants from the Italian Health Ministry/Veneto region
   research program NET-2016-02363853 and AIRC 5 per mille 2019 (ID. 22759
   program). This research was in part supported by the Department of
   Surgery, Oncology and Gastroenterology, University of Padua with the
   project titled: "The role of immune-inflammatory mechanisms, miRNA and
   gastric microbiome in the development of autoimmune atrophy neoplastic
   complications" (BIRD Budget 2021).
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NR 38
TC 6
Z9 7
U1 2
U2 8
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUL 22
PY 2022
VL 13
AR 930989
DI 10.3389/fimmu.2022.930989
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 3P0RX
UT WOS:000837246700001
PM 35941891
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Marshall, ACJ
   Toh, BH
   Alderuccio, F
AF Marshall, ACJ
   Toh, BH
   Alderuccio, F
TI Tumor necrosis factor alpha is not implicated in the genesis of
   experimental autoimmune gastritis
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE autoimmunity; apoptosis; stomach; TNF
ID COLLAGEN-INDUCED ARTHRITIS; NONOBESE DIABETIC MICE;
   RHEUMATOID-ARTHRITIS; CROHNS-DISEASE; TNF-ALPHA; T-CELLS;
   PERNICIOUS-ANEMIA; TRANSGENIC EXPRESSION; MOLECULAR TARGETS; LOCAL
   EXPRESSION
AB Experimental autoimmune gastritis (EAG) characterised by mononuclear cell infiltrate, parietal and zymogenic cell destruction and circulating autoantibodies to gastric H+/K+ ATPase is an animal model for human autoimmune gastritis, that leads to pernicious anaemia. We have previously shown that Fas has a role in initiating damage to target cells in EAG. Here we used three strategies to examine the role of TNFalpha in this disease. We administered neutralising anti-TNFalpha antibody either as a single injection or as twice weekly injections for 8 weeks to mice subjected to neonatal thymectomy-induced EAG. To address the role of apoptotic signals through TNFR1, TNFR1 deficient mice were either neonatally thymectomised or crossed to PC-GMCSF transgenic mice that spontaneously develop EAG. Neonatally thymectomised mice treated with anti-TNFalpha antibody developed destructive gastritis and autoantibodies to gastric H+/K+ ATPase similar to control mice. Following either neonatal thymectomy or crossing to PC-GMCSF transgenic mice, TNFR1 deficient mice developed autoantibody-positive destructive gastritis at similar frequency compared with wild type and heterozygous littermates. Our observations that neutralisation of TNFalpha and absence of TNFR1 has no discernible effect on development of EAG suggest that TNFalpha is not required for mucosal cell damage or development of autoimmune gastritis. While blocking TNFalpha activity has therapeutic benefit in certain autoimmune diseases, this is not the case for EAG. (C) 2003 Elsevier Ltd. All rights reserved.
C1 Monash Univ, Dept Pathol & Immunol, Cent & Eastern Clin Sch, AMREP, Prahran, Vic 3181, Australia.
C3 Monash University
RP Monash Univ, Dept Pathol & Immunol, Cent & Eastern Clin Sch, AMREP, Commercial Rd, Prahran, Vic 3181, Australia.
EM frank.alderuccio@med.monash.edu.au
RI Alderuccio, Frank/D-5808-2011
OI Alderuccio, Frank/0000-0003-4853-3394
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NR 52
TC 10
Z9 10
U1 2
U2 2
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD FEB
PY 2004
VL 22
IS 1
BP 1
EP 11
DI 10.1016/j.jaut.2003.09.003
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 766HV
UT WOS:000188371700001
PM 14709408
DA 2025-06-01
ER

PT J
AU Wang, Y
   Sun, ZC
   Wang, X
   Liu, FN
   Wu, Y
   Wei, QC
   Duan, SJ
AF Wang, Yu
   Sun, Zhichang
   Wang, Xue
   Liu, Funan
   Wu, Ying
   Wei, Qiaochu
   Duan, Shijie
TI Myasthenia gravis and myocarditis induced by chemoimmunotherapy in
   locally advanced gastric cancer: A case report
SO EXPERIMENTAL AND THERAPEUTIC MEDICINE
LA English
DT Article
DE gastric cancer; myasthenia gravis; immune checkpoint inhibitors;
   immuno-related adverse events; chemoimmunotherapy; case report
ID MANAGEMENT; MYOSITIS
AB The treatment strategy of patients with locally advanced gastric cancer has undergone notable changes since immune checkpoint inhibitors (ICIs) were developed. Although ICIs are generally well-tolerated, they can also cause serious adverse events, such as autoimmune diseases. In patients with gastric cancer and without a history of immune disease, the incidence of myasthenia gravis combined with myocarditis caused by ICI treatment is rare. Furthermore, cases of gastric cancer with ocular myasthenia gravis, without limb weakness or severe dyspnea, although with urination difficulties and symptoms of third-degree atrioventricular block have not been previously reported, to the best of our knowledge. The present study describes the case of a 72-year-old male patient with locally advanced gastric cancer that was treated with chemoimmunotherapy with oxaliplatin + tigio + sintilimab. At 19 days following only one cycle of therapy, the patient developed a left eyelid weakness and difficulty in urinating, as well as diplopia. At 5 days after the symptom of eyelid weakness, a third-degree atrioventricular block occurred. Hormone therapy, a temporary pacemaker and gamma-globulin therapy were administered, and the patient was discharged 1 month later with the resolution of myasthenia gravis and the atrioventricular block. At the final follow-up (1 month after discharge), the patient had a full recovery from myasthenia gravis and arrhythmias. Although some similar cases have been previously reported, the majority of patients with limb weakness and have eventually succumbed; moreover, clinical symptoms were identified at a late stage, and the disease evolution records were not detailed. Therefore, the present study describes the case of the patient and treatment strategy, also providing detailed laboratory indicators and clinical symptom evolution. This was performed with the aim to aid future research and the treatment of immune-related diseases.
C1 [Wang, Yu; Sun, Zhichang; Wang, Xue] Panjin Cent Hosp, Dept Oncol, 23 Liaohe Middle Rd, Panjin 124000, Liaoning, Peoples R China.
   [Liu, Funan; Wu, Ying; Wei, Qiaochu; Duan, Shijie] China Med Univ, Hosp 1, Dept Oncol, Shenyang 124000, Liaoning, Peoples R China.
C3 China Medical University
RP Wang, Y (corresponding author), Panjin Cent Hosp, Dept Oncol, 23 Liaohe Middle Rd, Panjin 124000, Liaoning, Peoples R China.
EM 942578767@qq.com
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NR 29
TC 0
Z9 0
U1 0
U2 2
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-0981
EI 1792-1015
J9 EXP THER MED
JI Exp. Ther. Med.
PD NOV
PY 2024
VL 28
IS 5
AR 426
DI 10.3892/etm.2024.12715
PG 8
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA G3Z2X
UT WOS:001316054200001
PM 39301255
OA gold
DA 2025-06-01
ER

PT J
AU Papamichael, K
   Papaioannou, G
   Cheifetz, MA
   Cheifetz, AS
AF Papamichael, Konstantinos
   Papaioannou, Garyfallia
   Cheifetz, Marcy A.
   Cheifetz, Adam S.
TI Bone of Contention: Helicobacter pylori and Osteoporosis-Is There
   an Association?
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE Helicobacter pylori; Osteoporosis; Endocrine; Fracture; Bone
ID LIFE-STYLE FACTORS; MINERAL DENSITY; INFECTION; EPIDEMIOLOGY; GASTRITIS;
   DECREASE; WOMEN; MEN
AB Helicobacter pylori (H. pylori) infection is a common disease that can cause chronic gastritis, peptic ulcers, and gastric cancer. Nevertheless, due to its ability to elicit a systemic inflammatory response, it has also been related to several extra-gastric manifestations including endocrine disorders, such as autoimmune thyroid diseases, diabetes mellitus, dyslipidemia, and obesity. H. pylori infection has also been linked to osteoporosis, although currently available data are equivocal. This brief review will focus on the possible association between H. pylori infection and osteoporosis, a silent disease characterized by decreased bone mass that can increase the occurrence of fractures, disability, and mortality.
C1 [Papamichael, Konstantinos; Cheifetz, Adam S.] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Ctr Inflammatory Bowel Dis, Div Gastroenterol & Hepatol, 330 Brookline Ave, Boston, MA 02215 USA.
   [Papaioannou, Garyfallia] Univ Cent Florida, Coll Med, Internal Med Residency Program, North Florida Reg Med Ctr, Gainesville, FL USA.
   [Cheifetz, Marcy A.] Harvard Vanguard Med Associates Atrius Hlth, Dept Endocrinol, Chestnut Hill, MA USA.
C3 Harvard University; Harvard University Medical Affiliates; Beth Israel
   Deaconess Medical Center; Harvard Medical School; State University
   System of Florida; University of Central Florida; Harvard Vanguard
   Medical Associates
RP Papamichael, K (corresponding author), Harvard Med Sch, Beth Israel Deaconess Med Ctr, Ctr Inflammatory Bowel Dis, Div Gastroenterol & Hepatol, 330 Brookline Ave, Boston, MA 02215 USA.
EM kpapamic@bidmc.harvard.edu
RI Papaioannou, Garyfallia/LCE-0610-2024
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NR 32
TC 6
Z9 9
U1 1
U2 10
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD OCT
PY 2019
VL 64
IS 10
BP 2736
EP 2739
DI 10.1007/s10620-019-05775-4
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IX8PT
UT WOS:000485950500010
PM 31407131
DA 2025-06-01
ER

PT J
AU Hirano, K
   Tada, M
   Sasahira, N
   Isayama, H
   Mizuno, S
   Takagi, K
   Watanabe, T
   Saito, T
   Kawahata, S
   Uchino, R
   Hamada, T
   Miyabayashi, K
   Mohri, D
   Sasaki, T
   Kogure, H
   Yamamoto, N
   Nakai, Y
   Yoshida, H
   Ito, Y
   Akiyama, D
   Toda, N
   Arizumi, T
   Yagioka, H
   Takahara, N
   Matsubara, S
   Yashima, Y
   Koike, K
AF Hirano, Kenji
   Tada, Minoru
   Sasahira, Naoki
   Isayama, Hiroyuki
   Mizuno, Suguru
   Takagi, Kaoru
   Watanabe, Takeo
   Saito, Tomotaka
   Kawahata, Shuhei
   Uchino, Rie
   Hamada, Tsuyoshi
   Miyabayashi, Koji
   Mohri, Dai
   Sasaki, Takashi
   Kogure, Hirofumi
   Yamamoto, Natsuyo
   Nakai, Yousuke
   Yoshida, Haruhiko
   Ito, Yukiko
   Akiyama, Dai
   Toda, Nobuo
   Arizumi, Toshihiko
   Yagioka, Hiroshi
   Takahara, Naminatsu
   Matsubara, Saburo
   Yashima, Yoko
   Koike, Kazuhiko
TI Incidence of Malignancies in Patients with IgG4-related Disease
SO INTERNAL MEDICINE
LA English
DT Article
DE IgG4-related disease; autoimmune pancreatitis; malignancy; diabetes
   mellitus
ID LONG-TERM PROGNOSIS; AUTOIMMUNE PANCREATITIS; DIAGNOSTIC-CRITERIA;
   ASSOCIATION; CANCER; RISK; POPULATION; CONSENSUS; PROPOSAL; JAPAN
AB Objective It has been discussed whether IgG4-related disease (IgG4-RD), including autoimmune pancreatitis (AIP), is associated with malignancy; however, the issue has not been clarified.
   Methods We analyzed 113 patients with IgG4-RD in whom malignancy was not diagnosed at the time of IgG4-RD onset and the follow-up period was longer than six months. A total of 95 patients had AIP. The mean follow-up period was 73 months. The incidence of the observed malignancies was compared with the expected incidence in an age-and sex-matched general Japanese population based on the Vital Statistics of Japan.
   Results There were 15 malignancies (lung cancer in five patients, pancreatic cancer in two patients, gastric cancer in two patients, bile duct cancer in one patient, renal cancer in one patient, breast cancer in one patient, tongue cancer in one patient, malignant melanoma in one patient and acute myeloid leukemia in one patient) in 14 patients during the follow-up period. The calculated standardized incidence rate of the total malignancies was not significant, that is, 1.04 (95% CI 0.57-1.75).
   Conclusion The incidence of total malignancies in IgG4-RD patients is similar to that observed in the general population. At present, it is reasonable to conclude that IgG4-RD is not associated with an increased incidence of total malignancies.
C1 [Hirano, Kenji; Tada, Minoru; Sasahira, Naoki; Isayama, Hiroyuki; Mizuno, Suguru; Takagi, Kaoru; Watanabe, Takeo; Saito, Tomotaka; Kawahata, Shuhei; Uchino, Rie; Hamada, Tsuyoshi; Miyabayashi, Koji; Mohri, Dai; Sasaki, Takashi; Kogure, Hirofumi; Yamamoto, Natsuyo; Nakai, Yousuke; Yoshida, Haruhiko; Koike, Kazuhiko] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138654, Japan.
   [Ito, Yukiko; Akiyama, Dai] Japanese Red Cross Med Ctr, Dept Gastroenterol, Tokyo, Japan.
   [Toda, Nobuo; Arizumi, Toshihiko] Mitsui Mem Hosp, Dept Gastroenterol, Tokyo, Japan.
   [Yagioka, Hiroshi] JR Tokyo Gen Hosp, Dept Gastroenterol, Tokyo, Japan.
   [Takahara, Naminatsu] Mutual Aid Assoc Publ Sch Teachers, Kanto Cent Hosp, Dept Gastroenterol, Tokyo, Japan.
   [Matsubara, Saburo] Tokyo Metropolitan Police Hosp, Dept Gastroenterol, Tokyo, Japan.
   [Yashima, Yoko] Kyoundo Hosp, Dept Hepatol, Tokyo, Japan.
C3 University of Tokyo; University of Tokyo; Japanese Red Cross Medical
   Center; Mitsui Memorial Hospital
RP Hirano, K (corresponding author), Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138654, Japan.
EM khirano-tky@umin.ac.jp
RI Isayama, Hiroyuki/AER-9916-2022; Nakai, Yousuke/H-2964-2019; Takahara,
   Naminatsu/K-8497-2019; Sasahira, Naoki/JNT-5053-2023; Sasaki,
   Takashi/AEF-5796-2022; Tada, Minoru/AHB-5933-2022; Mizuno,
   Suguru/AAF-8867-2019
OI Watanabe, Takeo/0000-0003-4097-3758
FU Research Program on Intractable Disease (Research on IgG4-related
   Disease)
FX This work was partially supported by the Research Program on Intractable
   Disease (Research on IgG4-related Disease) provided by the Ministry of
   Health, Labour and Welfare of Japan.
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NR 22
TC 133
Z9 139
U1 0
U2 8
PU JAPAN SOC INTERNAL MEDICINE
PI TOKYO
PA 34-3 3-CHOME HONGO BUNKYO-KU, TOKYO, 113, JAPAN
SN 0918-2918
EI 1349-7235
J9 INTERNAL MED
JI Intern. Med.
PY 2014
VL 53
IS 3
BP 171
EP 176
DI 10.2169/internalmedicine.53.1342
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 302UU
UT WOS:000330631200002
PM 24492683
OA hybrid
DA 2025-06-01
ER

PT J
AU Thompson, MA
   Ohnuma, K
   Abe, M
   Morimoto, C
   Dang, NH
AF Thompson, Michael A.
   Ohnuma, Kei
   Abe, Masako
   Morimoto, Chikao
   Dang, Nam H.
TI CD26/dipeptidyl peptidase IV as a novel therapeutic target for cancer
   and immune disorders
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE CD26; dipeptidyl peptidase IV (DPPIV, DPP4); adenosine deaminase (ADA);
   autoimmune; T-cell
ID T-CELL-ACTIVATION; DIPEPTIDYL AMINOPEPTIDASE-IV;
   ADENOSINE-DEAMINASE-BINDING; HUMAN-IMMUNODEFICIENCY-VIRUS; IMPROVED
   GLUCOSE-TOLERANCE; GASTRIC-INHIBITORY POLYPEPTIDE; AMINO-TERMINAL
   TRUNCATION; TOPOISOMERASE-II-ALPHA; NON-HODGKINS-LYMPHOMAS; ANAPLASTIC
   LARGE-CELL
AB CD26 is a 110 kDa surface glycoprotein with intrinsic dipeptidyl peptidase IV (DPPIV) activity that is expressed on numerous cell types and has a multitude of biological functions. An important aspect of CD26 biology is its peptidase activity and its functional and physical association with molecules with key roles in various cellular pathways and biological programs. CD26 role in immune regulation has been extensively characterized, with recent findings elucidating its linkage with signaling pathways and structures involved in T-lymphocyte activation as well as antigen presenting cell-T-cell interaction. Recent work also suggests that CD26 has a significant role in tumor biology, being both a marker of disease behavior clinically as well as playing an important role in tumor pathogenesis and development. In this paper, we will review emerging data that suggest CD26 may be an appropriate therapeutic target for the treatment of selected neoplasms and immune disorders. Through the use of various experimental approaches and agents to influence CD26/DPPIV expression and activity, such as anti-CD26 antibodies, CD26/DPPIV chemical inhibitors, siRNAs to inhibit CD26 expression, overexpressing CD26 transfectants and soluble CD26 molecules, our group has shown that CD26 interacts with structures with essential cellular functions. Its association with such key molecules as topoisomerase II alpha, p38 MAPK, and integrin PI, has important clinical implications, including its potential ability to regulate tumor sensitivity to selected chemotherapies and to influence tumor migration/metastases and tumorigenesis. Importantly, our recent in vitro and in vivo data support the hypothesis that CD26 may indeed be an appropriate target for therapy for selected cancers and immune disorders.
C1 Nevada Canc Inst, Dept Hematol Malignencies, Las Vegas, NV 89135 USA.
   Univ Texas, MD Anderson Canc Ctr, Div Canc Med, Houston, TX 77030 USA.
   Univ Tokyo, Inst Med Sci, Adv Clin Res Ctr, Div Clin Immunol, Tokyo, Japan.
C3 University of California System; University of California San Diego;
   Nevada Cancer Institute; University of Texas System; UTMD Anderson
   Cancer Center; University of Tokyo
RP Dang, NH (corresponding author), Nevada Canc Inst, Dept Hematol Malignencies, 10441 W Twain Ave, Las Vegas, NV 89135 USA.
EM ndang@nvcancer.org
RI Thompson, Michael/B-8953-2013
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SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PD MAR
PY 2007
VL 7
IS 3
BP 253
EP 273
DI 10.2174/138955707780059853
PG 21
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 135MR
UT WOS:000244158200005
PM 17346218
DA 2025-06-01
ER

PT J
AU Ko, GH
   Park, HB
   Shin, MK
   Park, CK
   Lee, JH
   Youn, HS
   Cho, MJ
   Lee, WK
   Rhee, KH
AF Ko, GH
   Park, HB
   Shin, MK
   Park, CK
   Lee, JH
   Youn, HS
   Cho, MJ
   Lee, WK
   Rhee, KH
TI Monoclonal antibodies against Helicobacter pylori cross-react with human
   tissue
SO HELICOBACTER
LA English
DT Article
ID HUMAN GASTRIC-MUCOSA; DAMAGE; ASSOCIATION; GLUTATHIONE; INFECTION;
   CANCER; ULCER
AB Background. H. pylori is a causative agent of chronic gastritis. However, the pathogenic mechanism by which H. pylori induces chronic inflammation and epithelial injuries in the gastric and duodenal mucosa is not well known. Investigators have recently reported that some monoclonal antibodies against H. pylori cross-react with the gastric epithelial cells. So, there exists the possibility that the autoimmune mechanism may be involved in the pathogenesis of chronic gastritis caused by H. pylori. The purpose of his study is to investigate whether the antibodies against H. pylori react with human tissues or not, using a large panel of monoclonal antibodies.
   Materials and Methods. Two hundred and fourteen monoclonal antibodies against H. pylori were produced. An immunohistochemical staining of human tissues, including H. pylori infected gastric mucosa, was performed using the antibodies.
   Results. Of 214 monoclonal antibodies, 71 antibodies reacted with H. pylori in the gastric mucosa. Of 71 antibodies, 25 antibodies also reacted with gastric epithelial cells, 11 antibodies reacted with ductal cells of the salivary gland, 11 antibodies reacted with renal tubular cells, and 8 antibodies reacted with duodenal epithelial cells. The antibodies which showed cross-reactivity with gastric epithelial cells included those against urease, flagella, lipopolysaccharide, and heat shock protein of H. pylori.
   Conclusions. It is believed that the autoimmune reaction might be involved in the pathogenesis of chronic gastritis due to H. pylori Infection, and that the autoimmune reaction induced by H. pylori infection might also be involved in the pathogenesis of various diseases in other organs.
C1 GYEONGSANG NATL UNIV, COLL MED, DEPT PEDIAT, KYUNG NAM 660280, SOUTH KOREA.
   GYEONGSANG NATL UNIV, COLL MED, DEPT MICROBIOL, KYUNG NAM 660280, SOUTH KOREA.
   SAMSUNG SEOUL HOSP, DEPT DIAGNOST PATHOL, SEOUL, SOUTH KOREA.
C3 Gyeongsang National University; Gyeongsang National University;
   Sungkyunkwan University (SKKU); Samsung Medical Center
RP GYEONGSANG NATL UNIV, COLL MED, DEPT PATHOL, 92 CHILAM DONG, KYUNG NAM 660280, SOUTH KOREA.
OI Youn, Hee-Shang/0000-0002-5498-838X
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NR 29
TC 54
Z9 59
U1 0
U2 6
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1083-4389
EI 1523-5378
J9 HELICOBACTER
JI Helicobacter
PY 1997
VL 2
IS 4
BP 210
EP 215
DI 10.1111/j.1523-5378.1997.tb00090.x
PG 6
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Microbiology
GA YJ336
UT WOS:A1997YJ33600010
PM 9421126
DA 2025-06-01
ER

PT J
AU Kavanagh, DO
   O'Riain, C
   Ridgway, PF
   Neary, P
   Crotty, TC
   Geoghegan, JG
   Traynor, O
AF Kavanagh, D. O.
   O'Riain, C.
   Ridgway, P. F.
   Neary, P.
   Crotty, T. C.
   Geoghegan, J. G.
   Traynor, O.
TI Radical Pancreaticoduodenectomy for Benign Disease
SO THESCIENTIFICWORLDJOURNAL
LA English
DT Article
DE pancreaticoduodenectomy; endoscopic ultrasound; chronic pancreatitis;
   choledochal cyst; Whipple's
ID FINE-NEEDLE-ASPIRATION; PANCREATIC-CANCER; DIFFERENTIAL-DIAGNOSIS;
   PERITONEAL CYTOLOGY; AUTOIMMUNE PANCREATITIS; COMPUTED-TOMOGRAPHY; FOCAL
   PANCREATITIS; SURGICAL-TREATMENT; BRUSH CYTOLOGY; ADENOCARCINOMA
AB Whipple's procedure is the treatment of choice for pancreatic and periampullary malignancies. Preoperative histological confirmation of malignancy is frequently unavailable and some patients will subsequently be found to have benign disease. Here, we review our experience with Whipple's procedure for patients ultimately proven to have benign disease. The medical records of all patients who underwent Whipple's procedure during a 15-year period (1987-2002) were reviewed; 112 patients underwent the procedure for suspected malignancy. In eight cases, the final histology was benign (7.1%). One additional patient was known to have benign disease at resection. The mean age was 50 years (range: 30-75). The major presenting features included jaundice (five), pain (two), gastric outlet obstruction (one), and recurrent gastrointestinal haemorrhage (one). Investigations included ultrasound (eight), computerised tomography (eight), endoscopic retrograde cholangiopancreatography (seven; of these, four patients had a stent inserted and three patients had sampling for cytology), and endoscopic ultrasound (two). The pathological diagnosis included benign biliary stricture (two), chronic pancreatitis (two), choledochal cyst (one), inflammatory pseudotumour (one), cystic duodenal wall dysplasia (one), duodenal angiodysplasia (one), and granular cell neoplasm (one). There was no operative mortality. Morbidity included intra-abdominal collection (one), anastomotic leak (one), liver abscess (one), and myocardial infarction (one). All patients remain alive and well at mean follow-up of 41 months. Despite recent advances in diagnostic imaging, 8% of the patients undergoing Whipple's procedure had benign disease. A range of unusual pathological entities can mimic malignancy. Accurate preoperative histological diagnosis may have allowed a less radical operation to be performed. Endoscopic ultrasound-guided fine needle aspirate (EUS-FNA) may reduce the need for Whipple's operation in benign pancreaticobiliary disease in the future.
C1 [Kavanagh, D. O.; Ridgway, P. F.; Neary, P.; Geoghegan, J. G.; Traynor, O.] St Vincents Univ Hosp, Liver Unit, Dublin, Ireland.
   [O'Riain, C.; Crotty, T. C.] St Vincents Univ Hosp, Dept Pathol, Dublin, Ireland.
C3 University College Dublin; Saint Vincent's University Hospital;
   University College Dublin; Saint Vincent's University Hospital
RP Kavanagh, DO (corresponding author), St Vincents Univ Hosp, Liver Unit, Dublin, Ireland.
EM dara_kav@hotmail.com
RI Alemanno, Giovanni/AAC-1759-2022
OI Ridgway, Paul/0000-0002-8500-8532
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NR 55
TC 12
Z9 12
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1537-744X
J9 THESCIENTIFICWORLDJO
JI TheScientificWorldJOURNAL
PY 2008
VL 8
BP 1156
EP 1167
DI 10.1100/tsw.2008.147
PG 12
WC Environmental Sciences; Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Environmental Sciences & Ecology; Science & Technology - Other Topics
GA 380QE
UT WOS:000261479500051
PM 19030761
OA Green Submitted, Green Published, gold
DA 2025-06-01
ER

PT J
AU Li, DY
   Xiong, XZ
AF Li, Dan-Yang
   Xiong, Xian-Zhi
TI ICOS<SUP>+</SUP>Tregs: A Functional Subset of Tregs in Immune Diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE ICOS; Treg cells; autoimmune disease; neoplasm; immunotherapy
ID REGULATORY T-CELLS; PLASMACYTOID DENDRITIC CELLS; INDUCIBLE
   COSTIMULATOR; ICOS-LIGAND; SUPPRESSIVE FUNCTION; IL-10 PRODUCTION;
   DOWN-REGULATION; GASTRIC-CANCER; CUTTING EDGE; B-CELLS
AB Recent studies have reported the pathological effect of ICOS+T cells, but ICOS signals also widely participate in anti-inflammatory responses, particularly ICOS(+)regulatory T (Treg) cells. The ICOS signaling pathway endows Tregs with increased generation, proliferation, and survival abilities. Furthermore, there is enough evidence to suggest a superior capacity of ICOS(+)Tregs, which is partly attributable to IL-10 induced by ICOS, yet the associated mechanism needs further investigation. In this review, we discuss the complicated role of ICOS(+)Tregs in several classical autoimmune diseases, allergic diseases, and cancers and investigate the related therapeutic applications in these diseases. Moreover, we identify ICOS as a potential biomarker for disease treatment and prognostic prediction. In addition, we believe that anti-ICOS/ICOSL monoclonal antibodies exhibit excellent clinical application potential. A thorough understanding of the effect of ICOS(+)Tregs and the holistic role of ICOS toward the immune system will help to improve the therapeutic schedule of diseases.
C1 [Li, Dan-Yang; Xiong, Xian-Zhi] Natl Minist Hlth Peoples Republ China, Natl Clin Res Ctr Resp Dis, Key Lab Resp Dis, Wuhan, Peoples R China.
   [Li, Dan-Yang; Xiong, Xian-Zhi] Huazhong Univ Sci & Technol, Dept Resp & Crit Care Med, Union Hosp, Tongji Med Coll, Wuhan, Peoples R China.
C3 Huazhong University of Science & Technology
RP Xiong, XZ (corresponding author), Natl Minist Hlth Peoples Republ China, Natl Clin Res Ctr Resp Dis, Key Lab Resp Dis, Wuhan, Peoples R China.; Xiong, XZ (corresponding author), Huazhong Univ Sci & Technol, Dept Resp & Crit Care Med, Union Hosp, Tongji Med Coll, Wuhan, Peoples R China.
EM xxz0508@hust.edu.cn
RI danyang, li/GLT-1067-2022
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NR 150
TC 98
Z9 107
U1 0
U2 11
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD AUG 28
PY 2020
VL 11
AR 2104
DI 10.3389/fimmu.2020.02104
PG 17
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA NQ0BZ
UT WOS:000570535300001
PM 32983168
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Kao, PF
   Lin, JD
   Chiu, CT
   Hsu, HT
   See, LC
   Tzen, KY
AF Kao, PF
   Lin, JD
   Chiu, CT
   Hsu, HT
   See, LC
   Tzen, KY
TI Gastric emptying function changes in patients with thyroid cancer after
   withdrawal of thyroid hormone therapy
SO JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE gastric emptying; hypothyroidism; scintigraphy
ID HYPOTHYROIDISM; DISEASE; DISORDERS; SECRETION
AB Background: Hypothyroidism is commonly thought to cause decreased gastric emptying but is mostly associated with autoimmune disease. In the present study the gastric emptying function of thyroid cancer patients with severe hypothyroidism of short duration was evaluated with a radionuclide solid meal gastric emptying study.
   Methods: Twenty-two patients who had undergone surgical operation and I-131 ablation for thyroid cancer participated in solid meal gastric emptying studies before the withdrawal of thyroxine and then again 4 weeks after the withdrawal of thyroxine. Eleven patients had an additional gastric emptying study at 6 weeks after withdrawal of thyroxine. Gastric emptying curves and emptying parameters were calculated. Student's paired t-test was used for statistical analysis of data for all cases between the baseline and at 4 weeks after withdrawal. An additional repeated measure ANOVA with multiple comparisons was performed on data between baseline, 4 weeks and 6 weeks after withdrawal for the other 11 patients. All P values presented are two-tailed and the significance level is 0.05.
   Results: Hypothyroidism status was confirmed by the marked change of the serum thyroxine and thyroid-stimulating hormone 4 weeks and 6 weeks after withdrawal of the thyroxine replacement (P < 0.001). The gastric half-emptying time and emptying rate changed significantly after short-term severe thyroid hormone deficiency (P < 0.005). However, the length of the lag phase did not have a statistically significant change at 4 weeks or 6 weeks after withdrawal of the thyroxin replacement (P = 0.219 and 0.142).
   Conclusions: Hypothyroidism following the withdrawal of the thyroxine replacement in thyroid cancer patients preparing for I-131 cancer work-up can significantly prolong gastric half-emptying time and emptying rate. (C) 2004 Blackwell Publishing Asia Pty Ltd.
C1 Chang Gung Mem Hosp, Dept Nucl Med, Taipei 105, Taiwan.
   Chang Gung Mem Hosp, Dept Endocrinol, Taipei 105, Taiwan.
   Chang Gung Mem Hosp, Dept Gastroenterol, Taipei 105, Taiwan.
   Chang Gung Mem Hosp, Biostat Consulting Ctr, Taipei 105, Taiwan.
   Chang Gung Univ, Taoyuan, Taiwan.
C3 Chang Gung Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung
   Memorial Hospital; Chang Gung Memorial Hospital; Chang Gung University
RP Kao, PF (corresponding author), Chang Gung Mem Hosp, Dept Nucl Med, 199 Tung Hwa North Rd, Taipei 105, Taiwan.
EM kao-panfu@umail.hinet.net
RI Lin, Jiadong/KUC-9725-2024
OI See, Lai-Chu/0000-0002-1379-8969; TZEN, KAI-YUAN/0000-0002-5657-8579
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NR 19
TC 5
Z9 5
U1 0
U2 3
PU BLACKWELL PUBLISHING ASIA
PI CARLTON
PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA
SN 0815-9319
J9 J GASTROEN HEPATOL
JI J. Gastroenterol. Hepatol.
PD JUN
PY 2004
VL 19
IS 6
BP 655
EP 660
DI 10.1111/j.1440-1746.2003.03326.x
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 822BB
UT WOS:000221508200009
PM 15151620
DA 2025-06-01
ER

PT J
AU Cabañero-Navalon, MD
   Garcia-Bustos, V
   Balastegui-Martin, H
   Bracke, C
   Mateu, L
   Solanich, X
   Carrillo-Linares, JL
   Robles-Marhuenda, A
   Puchades, F
   Ballesta, AP
   Lopez-Osle, N
   Torralba-Cabeza, MA
   Masdeu, AMB
   Niño, JG
   Gaya, NT
   Castellanos, GP
   Sánchez-Martínez, R
   Barragán-Casas, JM
   González-García, A
   de la Peña, JLP
   López-Wolf, D
   Rufete, AM
   Mora, AC
   Moral, PM
AF Cabanero-Navalon, Marta Dafne
   Garcia-Bustos, Victor
   Balastegui-Martin, Hector
   Bracke, Carmen
   Mateu, Lourdes
   Solanich, Xavier
   Carrillo-Linares, Juan Luis
   Robles-Marhuenda, Angel
   Puchades, Francesc
   Pelaez Ballesta, Ana
   Lopez-Osle, Nuria
   Torralba-Cabeza, Miguel angel
   Bielsa Masdeu, Ana Maria
   Nino, Jorge Gil
   Tornador Gaya, Nuria
   Castellanos, Guillem Pascual
   Sanchez-Martinez, Rosario
   Barragan-Casas, Jose Manuel
   Gonzalez-Garcia, Andres
   de la Pena, Jose Luis Patier
   Lopez-Wolf, Daniel
   Rufete, Antonia Mora
   Canovas Mora, Alba
   Moral Moral, Pedro
TI The impact of immune dysregulation on the risk of malignancy in common
   variable immunodeficiency: insights from a multicenter study
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE common variable immunodeficiency; immune dysregulation; malignancy;
   cancer risk; immunosuppressants
ID DEFICIENCY; PHENOTYPE; CANCER
AB Background: Common Variable Immunodeficiency (CVID) represents a heterogenic group of primary immunodeficiencies (PID) characterized by impaired antibody production and susceptibility to infections. Non-infectious complications, such as autoimmune diseases, lymphoproliferative disorders, and malignancies, now significantly impact prognosis. Moreover, both hematologic and solid organ malignancies are more frequently observed in CVID patients compared to other PIDs. The risk factors for carcinogenesis in CVID remain largely unknown. Objective: This multicenter study aims to characterize the clinical profile of cancer in CVID patients in Spain and to identify independent risk factors associated with malignancy development, focusing on the role of immune dysregulation. Methods: A nationwide, cross-sectional study was conducted from November 2019 to May 2022, involving 17 hospitals treating PID patients in Spain. Data were collected systematically on demographics, infectious and non-infectious comorbidities, immunological parameters, and treatment. Statistical analysis, including multivariate logistic regression, was performed to identify risk factors associated to malignancy. Results: Of 250 CVID patients, 38 (15.26%) were diagnosed with cancer, predominantly non-Hodgkin lymphoma, gastric cancer, and lung adenocarcinoma. Cancer patients were significantly older (mean age 60.70 vs. 49.36 years, p<0.001) and had higher rates of immune dysregulation (81.58% vs. 59.7%, p=0.01). Immune dysregulation was an independent risk factor for cancer (OR 2.19, p=0.04), alongside previous immunosuppressant therapy (OR 2, p=0.031), higher IgM levels (OR 1.008 per SD, p=0.012), older age (OR 1.04, p<0.001), and lower CD4 cell counts at diagnosis (OR 0.997, p<0.001). Conclusions: This study highlights the increased cancer risk in CVID patients, with immune dysregulation, prior immunosuppressant use, elevated IgM levels, and lower CD4 cell counts as conjointly associated. These findings underscore the need for vigilant cancer screening and tailored management strategies in CVID patients to improve outcomes. Future research should focus on elucidating the molecular mechanisms linking immune dysregulation and malignancy in CVID.
C1 [Cabanero-Navalon, Marta Dafne; Garcia-Bustos, Victor; Balastegui-Martin, Hector; Moral Moral, Pedro] Univ & Polytech Hosp La Fe, Dept Internal Med, Primary Immunodeficiencies Unit, Valencia, Spain.
   [Cabanero-Navalon, Marta Dafne; Balastegui-Martin, Hector; Moral Moral, Pedro] Hlth Res Inst La Fe, Res Grp Chron Dis & HIV Infect, Valencia, Spain.
   [Garcia-Bustos, Victor] Hlth Res Inst La Fe, Severe Infect Res Grp, Valencia, Spain.
   [Bracke, Carmen; Mateu, Lourdes] Germans Trias & Pujol Hosp, Infect Dis Serv, Badalona, Spain.
   [Bracke, Carmen; Mateu, Lourdes] Germans Trias & Pujol Hosp, Fight Infect Fdn, Badalona, Spain.
   [Solanich, Xavier] Hosp Univ Bellvitge, Internal Med Dept, Lhospitalet De Llobregat, Barcelona, Spain.
   [Solanich, Xavier] Inst Invest Biomed Bellvitge IDIBELL, Translat Med Area, Barcelona, Spain.
   [Solanich, Xavier] Univ Barcelona, Fac Med & Hlth Sci, Dept Clin Sci, Barcelona, Spain.
   [Carrillo-Linares, Juan Luis] Virgen Victoria Univ Hosp, Dept Internal Med, Malaga, Spain.
   [Robles-Marhuenda, Angel] La Paz Univ Hosp, Dept Internal Med, Madrid, Spain.
   [Puchades, Francesc] Univ Gen Hosp Valencia, Dept Internal Med, Valencia, Spain.
   [Pelaez Ballesta, Ana] Rafael Mendez Univ Hosp, Dept Internal Med, Murcia, Spain.
   [Lopez-Osle, Nuria] Cruces Univ Hosp, Dept Immunol, Bilbao, Bizkaia, Spain.
   [Torralba-Cabeza, Miguel angel] Hosp Clin Univ Lozano Blesa, Serv Urgencias, Dept Internal Med, Zaragoza, Spain.
   [Bielsa Masdeu, Ana Maria] Miguel Servet Univ Hosp, Dept Internal Med, Zaragoza, Spain.
   [Nino, Jorge Gil] 12 Octubre Hosp, Internal Med Dept, Immunodeficiencies Clin, Madrid, Spain.
   [Tornador Gaya, Nuria; Castellanos, Guillem Pascual] Univ Gen Hosp Castellon, Dept Internal Med, Castellon de La Plana, Castellon, Spain.
   [Sanchez-Martinez, Rosario] Dr Balmis Gen Univ Hosp, Inst Invest Sanitaria & Biomed Alicante ISABIAL, Internal Med Dept, Alicante, Spain.
   [Barragan-Casas, Jose Manuel] Complejo Asistencial Avila, Dept Internal Med, Avila, Spain.
   [Gonzalez-Garcia, Andres; de la Pena, Jose Luis Patier] Ramon & Cajal Hosp, Inst Ramon & Cajal Invest Sanitaria IRYCIS, Internal Med Serv, Syst Autoimmune Dis Unit, Madrid 28034, Spain.
   [Lopez-Wolf, Daniel] Univ Hosp Alcorcon Fdn, Dept Internal Med, Madrid, Spain.
   [Rufete, Antonia Mora; Canovas Mora, Alba] Gen Univ, Hosp Elche, Alicante, Spain.
C3 Hospital Universitari i Politecnic La Fe; Instituto de Investigacion
   Sanitaria La Fe (IIS La Fe); Hospital Universitari i Politecnic La Fe;
   Instituto de Investigacion Sanitaria La Fe (IIS La Fe); Institut
   d'Investigacio Biomedica de Bellvitge (IDIBELL); Bellvitge University
   Hospital; Institut d'Investigacio Biomedica de Bellvitge (IDIBELL);
   University of Barcelona; Hospital Universitario La Paz; Hospital
   Universitario Cruces; Lozano Blesa University Clinical Hospital; Miguel
   Servet University Hospital; Hospital Universitario 12 de Octubre;
   General University Hospital of Alicante; Universidad Miguel Hernandez de
   Elche; Universitat d'Alacant; Instituto de Investigacion Sanitaria y
   Biomedica de Alicante (ISABIAL); Hospital Universitario Ramon y Cajal;
   Alcorcon Foundation University Hospital
RP Garcia-Bustos, V (corresponding author), Univ & Polytech Hosp La Fe, Dept Internal Med, Primary Immunodeficiencies Unit, Valencia, Spain.; Garcia-Bustos, V (corresponding author), Hlth Res Inst La Fe, Severe Infect Res Grp, Valencia, Spain.
EM victorgarciabustos@gmail.com
RI Garcia-Bustos, Victor/ABA-7652-2020; BARRAGAN CASAS, JOSE/HNP-5076-2023;
   Mateu, Lourdes/MIO-4147-2025
OI Garcia-Bustos, Victor/0000-0002-1785-258X; Hector, Balastegui
   Martin/0000-0002-4651-6841; Mateu, Lourdes/0000-0001-7223-7611; Lopez
   Wolf, Daniel/0000-0003-2480-9907
FU CSL Behring
FX We would like to thank the Working Group of Rare Diseases of the Spanish
   Society of Internal Medicine (GTEM), the Spanish Society of Internal
   Medicine (SEMI), and the Valencian Community Society of Internal
   Medicine (SMICV) for their support. We also acknowledge the European
   Society for Immunodeficiencies (ESID) for their financial support to the
   first author. Additionally, we thank the Service of Data Science,
   Biostatistics, and Bioinformatics of the Health Research Institute La Fe
   for their assistance with the statistical analysis.
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NR 31
TC 0
Z9 0
U1 2
U2 4
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD OCT 16
PY 2024
VL 15
AR 1465159
DI 10.3389/fimmu.2024.1465159
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA K7L7E
UT WOS:001345657800001
PM 39478863
OA gold
DA 2025-06-01
ER

PT J
AU Rougemont, AL
   Fournet, JC
   Martin, SR
   de Saint-Basile, G
   Latour, S
   Primeau, MN
   Rubbia-Brandt, L
   Haddad, E
   Le Deist, F
AF Rougemont, Anne-Laure
   Fournet, Jean-Christophe
   Martin, Steven R.
   de Saint-Basile, Genevieve
   Latour, Sylvain
   Primeau, Marie-Noel
   Rubbia-Brandt, Laura
   Haddad, Elie
   Le Deist, Francoise
TI Chronic active gastritis in X-linked lymphoproliferative disease
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE dysimmune atrophic chronic gastritis; intestinal metaplasia; immune
   deficiency; XLP; pediatric
ID COMMON VARIABLE IMMUNODEFICIENCY; BARR-VIRUS INFECTION; GENE; SAP;
   HYPOGAMMAGLOBULINEMIA; AGAMMAGLOBULINEMIA; ADENOCARCINOMA; DEFICIENCY;
   RESPONSES; PRODUCT
AB Gastric lesions in primary constitutive immune deficiencies include multifocal atrophic gastritis, erosive pangastritis, and a pattern of gastric lesions reminiscent of graft-versus-host disease. We describe the genetic anomalies in 2 monozygotic twins with an X-linked lymphoproliferative disease (XLP; MIM 308240), a rare familial setting of high susceptibility to Epstein-Barr virus (EBV). Since early childhood, both twin brothers exhibited a severe chronic active atrophic pangastritis. A germline screening of the SH2D1A (MIM 300490) and BIRC4 (MIM 300079) genes was performed, and also a high-resolution whole-genome SNP profiling (Infinium Sentrix Human-1 Genotyping BeadChip, Illumina). A 3 Megabase deletion in the Xq25 region, encompassing the SH2D1A gene, was defined by SNP array genotyping. Histologic analysis of yearly or twice yearly gastric biopsies in both children showed a Helicobacter pylori-negative, Epstein-Barr virus-negative chronic active atrophic pangastritis, with superficial ulcer formation, foveolar hyperplasia, glandular dilatation and ultimately pseudopyloric and intestinal metaplasia. No such chronic active inflammatory gastric lesions have been reported to date in XLP. The similarities between XLP and common variable immunodeficiency (MIM 240500) underscore the need for early recognition and close monitoring of these gastric lesions, with special regard to their neoplastic potential. No infectious cause was determined. We favor a dysimmune mechanism in the development of this chronic atrophic gastritis, presenting a striking similarity to the recently described atrophic autoimmune pangastritis.
C1 [Rougemont, Anne-Laure; Fournet, Jean-Christophe] CHU St Justine, Dept Pathol, Montreal, PQ H3T 1C5, Canada.
   [Martin, Steven R.] CHU St Justine, Unit Gastroentrerol Hepatol & Nutr, Dept Pediat, Montreal, PQ H3T 1C5, Canada.
   [Rougemont, Anne-Laure; Fournet, Jean-Christophe] Univ Montreal, Dept Pathol & Cell Biol, Montreal, PQ H3C 3J7, Canada.
   [Primeau, Marie-Noel; Haddad, Elie] Univ Montreal, Immunol Allergol Rhematol Unit, Dept Pediat, Quebec City, PQ, Canada.
   [Le Deist, Francoise] Univ Montreal, CHU St Justine, Dept Microbiol & Immunol, Quebec City, PQ, Canada.
   [de Saint-Basile, Genevieve] Hop Necker Enfants Malad, APHP, INSERM, U768, Paris, France.
   [Rubbia-Brandt, Laura] Hop Cantonal Univ Geneva, Gastrointestinal & Liver Pathol Unit, Div Clin Pathol, Geneva, Switzerland.
C3 Universite de Montreal; Centre Hospitalier Universitaire Sainte-Justine;
   Universite de Montreal; Centre Hospitalier Universitaire Sainte-Justine;
   Universite de Montreal; Universite de Montreal; Universite de Montreal;
   Centre Hospitalier Universitaire Sainte-Justine; Laval University;
   University of Quebec; Assistance Publique Hopitaux Paris (APHP);
   Universite Paris Cite; Hopital Universitaire Necker-Enfants Malades -
   APHP; Hopital Universitaire Ambroise-Pare - APHP; Institut National de
   la Sante et de la Recherche Medicale (Inserm); Hopital Universitaire
   Hotel-Dieu - APHP; University of Geneva
RP Fournet, JC (corresponding author), CHU St Justine, Dept Pathol, 3175 Cote St Catherine, Montreal, PQ H3T 1C5, Canada.
EM jean-christophe_fournet@ssss.gouv.qc.ca
RI Haddad, Elie/AAQ-4971-2020; Rougemont, Anne-Laure/C-5612-2015; Latour,
   Sylvain/H-3652-2017; de Saint Basile, Genevieve/G-9731-2017
OI Latour, Sylvain/0000-0001-8238-4391; de Saint Basile,
   Genevieve/0000-0002-1913-5269; Rougemont,
   Anne-Laure/0000-0002-1785-792X; Haddad, Elie/0000-0003-2446-6879
CR Bachmeyer C, 2000, EUR J GASTROEN HEPAT, V12, P1033, DOI 10.1097/00042737-200012090-00013
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NR 20
TC 10
Z9 11
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD FEB
PY 2008
VL 32
IS 2
BP 323
EP 328
DI 10.1097/PAS.0b013e318141fca1
PG 6
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA 256WF
UT WOS:000252759900018
PM 18223336
DA 2025-06-01
ER

PT J
AU Sayi, A
   Kohler, E
   Toller, IM
   Flavell, RA
   Müller, W
   Roers, A
   Müller, A
AF Sayi, Ayca
   Kohler, Esther
   Toller, Isabella M.
   Flavell, Richard A.
   Mueller, Werner
   Roers, Axel
   Mueller, Anne
TI TLR-2-Activated B Cells Suppress Helicobacter-Induced
   Preneoplastic Gastric Immunopathology by Inducing T Regulatory-1 Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; PYLORI INFECTION; AFRICAN
   ENIGMA; CANCER; RISK; MICE; RESPONSES; INTERLEUKIN-10; IL-10;
   INFLAMMATION
AB B cells regulate autoimmune pathologies and chronic inflammatory conditions such as autoimmune encephalomyelitis and inflammatory bowel disease. The potential counterregulatory role of B cells in balancing pathogen-specific immune responses and the associated immunopathology is less well understood owing to the lack of appropriate persistent infection models. In this paper, we show that B cells have the ability to negatively regulate adaptive immune responses to bacterial pathogens. Using mouse models of infection with Helicobacter felis, a close relative of the human gastrointestinal pathogen H. pylori, we found that B cells activated by Helicobacter TLR-2 ligands induce IL-10-producing CD4(+)CD25(+) T regulatory-1 (Tr-1)-like cells in vitro and in vivo. Tr-1 conversion depends on TCR signaling and a direct T-/B-interaction through CD40/CD40L and CD80/CD28. B cell-induced Tr-1 cells acquire suppressive activity in vitro and suppress excessive gastric Helicobacter-associated immunopathology in vivo. Adoptive cotransfer of MyD88-proficient B cells and Tr-1 cells restores a normal gastric mucosal architecture in MyD88(-/-) and IL-10(-/-) mice in a manner that depends on T cellular, but not B cellular, IL-10 production. Our findings describe a novel mechanism of B cell-dependent Tr-1 cell generation and function in a clinically relevant disease model. In conclusion, we demonstrate that the B cell/Tr-1 cell axis is essential for balancing the control of Helicobacter infection with the prevention of excessive Th1-driven gastric immunopathology, promoting gastric mucosal homeostasis on the one hand and facilitating Helicobacter persistence on the other. The Journal of Immunology, 2011, 186: 878-890.
C1 [Sayi, Ayca; Kohler, Esther; Toller, Isabella M.; Mueller, Anne] Univ Zurich, Inst Mol Canc Res, CH-8057 Zurich, Switzerland.
   [Flavell, Richard A.] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT 06519 USA.
   [Mueller, Werner] Univ Manchester, Fac Life Sci, Manchester M13 9PL, Lancs, England.
   [Roers, Axel] Tech Univ Dresden, Inst Immunol, D-01307 Dresden, Germany.
C3 University of Zurich; Yale University; University of Manchester;
   Technische Universitat Dresden
RP Müller, A (corresponding author), Univ Zurich, Inst Mol Canc Res, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
EM mueller@imcr.uzh.ch
RI Flavell, Richard/ACH-3245-2022; Sayi Yazgan, Ayca/C-4733-2016; Muller,
   Werner/B-9044-2008
OI Sayi Yazgan, Ayca/0000-0002-9015-8244; Muller, Anne/0000-0002-1368-8276;
   Muller, Werner/0000-0002-1297-9725
FU Swiss National Science Foundation; UBS Foundation; Swiss Cancer League;
   University Research Priority Program in Systems Biology/Functional
   Genomics
FX This work was supported by grants from the Swiss National Science
   Foundation, the UBS Foundation, and the Swiss Cancer League (to A. M.)
   and by additional funding from the University Research Priority Program
   in Systems Biology/Functional Genomics.
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NR 39
TC 102
Z9 115
U1 0
U2 8
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD JAN 15
PY 2011
VL 186
IS 2
BP 878
EP 890
DI 10.4049/jimmunol.1002269
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 702TB
UT WOS:000285917700027
PM 21149607
OA Bronze
DA 2025-06-01
ER

PT J
AU Klöppel, G
   Anlauf, M
   Perren, A
AF Kloeppel, Guenter
   Anlauf, Martin
   Perren, Aurel
TI Endocrine precursor lesions of gastroenteropancreatic neuroendocrine
   tumors
SO ENDOCRINE PATHOLOGY
LA English
DT Article
DE stomach; ECL cell hyperplasia; duodenum; MEN1; gastrin cell hyperplasia;
   colon; endocrine cell hyperplasia
ID ZOLLINGER-ELLISON SYNDROME; ULCERATIVE-COLITIS; CELL TUMORS; MULTIPLE
   MICROCARCINOIDS; NEOPLASIA TYPE-1; CARCINOID-TUMOR; RET ALLELE;
   GASTRINOMAS; PANCREAS; PATIENT
AB This review focuses on precursor lesions of gastrointestinal and pancreatic neuroendocrine tumors (GEP-NETs). There are three conditions that are associated with hyperplastic changes in endocrine cells preceding GEP-NETs: autoimmune chronic atrophic gastritis or multiple endocrine neoplasia type 1 (MEN1) with gastric enterochromaffin-like (ECL) cell hyperplasia; MEN1 with gastrin and somatostatin cell hyperplasia in the duodenum and glucagon cell hyperplasia in the islets of the pancreas; and inflammatory bowel disease with endocrine cell hyperplasia in the colon. In gastric ECL cell hyperplasia, it is assumed that hypergastrinemia promotes the growth of the ECL cells of the corpus mucosa and leads to hyperplasia and neoplasia. In the duodenum and the pancreas, the MEN1-associated germline mutation of the menin gene obviously causes hyperplasia of the gastrin and somatostatin cells (duodenum) and the glucagon cells (pancreas), resulting in multifocal development of tumors. These tumors show allelic deletion of the MEN1 gene, whereas the precursor lesions retain their heterozygosity. The endocrine cell hyperplasia in the colon described in inflammatory bowel disease has neither a genetic nor a definite hormonal background.
C1 [Kloeppel, Guenter; Anlauf, Martin] Univ Kiel, Dept Pathol, D-24105 Kiel, Germany.
   [Perren, Aurel] Univ Zurich Hosp, Dept Pathol, CH-8091 Zurich, Switzerland.
   [Perren, Aurel] Tech Univ Munich, Dept Pathol, Munich, Germany.
C3 University of Kiel; University of Zurich; University Zurich Hospital;
   Technical University of Munich
RP Klöppel, G (corresponding author), Univ Kiel, Dept Pathol, Michaelisstr 11, D-24105 Kiel, Germany.
EM guenterkloeppel@path.uni-kiel.de
RI Perren, Aurel/A-9383-2018
OI Perren, Aurel/0000-0002-6819-6092
CR Anlauf M, 2005, GASTROENTEROLOGY, V128, P1187, DOI 10.1053/j.gastro.2005.01.058
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NR 32
TC 44
Z9 46
U1 0
U2 4
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1046-3976
EI 1559-0097
J9 ENDOCR PATHOL
JI Endocr. Pathol.
PD FAL
PY 2007
VL 18
IS 3
BP 150
EP 155
DI 10.1007/s12022-007-0025-5
PG 6
WC Endocrinology & Metabolism; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Pathology
GA 245DJ
UT WOS:000251914700004
PM 18058264
DA 2025-06-01
ER

PT J
AU Pokupec, JSG
   Lukenda, DB
AF Pokupec, Josipa Sanja Gruden
   Lukenda, Dolores Biocina
TI Comorbidity of Recurrent Aphthous Stomatitis and Polyps Ventriculi
SO COLLEGIUM ANTROPOLOGICUM
LA English
DT Article
DE recurrent aphthae; polyp
AB As it is known, many diseases of gastric system cause changes in the oral cavity, with either pathological findings or subjective impressions. When these changes are of pathological nature, the most common finding is recurrent aphthous stomatitis on the tongue, which emerges as a consequence of gastric diseases. Recurrent aphthous stomatitis is a disorder characterised by recurrent ulcerations limited to the oral mucosa, without any other signs of diseases. According to their clinical form, they may be big, small and hyperform. Etiology of recurrent aphthae is genetic predisposition, systemic diseases (virus, certain vitamin deficiency, gastric disorders), and autoimmune disorder and psychogenesis. The symptoms include a prodromal burning sensation and ulceration emerging within 24-48 hours as round symmetrical lesions inflicting the entire oral cavity except for palate and gingiva. Polyps ventriculi are tumours on the gastric mucosa. They can lie on a broad background or hang on the stem, and may be both individual and clustered at the same time. They are more common with elderly male population. They may have a malignant alteration. According to WHO, they have been classified as hyperplastic and neoplastic polyps. Etiology of polyps is atrophic gastritis or H. Pylori.
C1 [Pokupec, Josipa Sanja Gruden; Lukenda, Dolores Biocina] Univ Split, Sch Med, Dept Stomatol, Split, Croatia.
   [Pokupec, Josipa Sanja Gruden] Stomatol Polyclin, Zagreb, Croatia.
C3 University of Split
RP Pokupec, JSG (corresponding author), Dedici 76, Zagreb 10000, Croatia.
EM jspokupec@net.hr
CR BACCGLINI L, 2012, J ORAL PATHOL MED, DOI [10.1111/jop.12015, DOI 10.1111/J0P.12015]
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   STIPETIC-MRAVAK M, 2006, BURKETOVA ORALNA MED
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   ZIVKOVIC R, 2001, INTERNA MED
NR 5
TC 2
Z9 2
U1 0
U2 2
PU COLLEGIUM ANTROPOLOGICUM
PI ZAGREB
PA INST ANTHROPOLOGICAL RESEARCH, GAJEVA 32, PO BOX 290, HR-10000 ZAGREB,
   CROATIA
SN 0350-6134
J9 COLLEGIUM ANTROPOL
JI Coll. Anthropol.
PD MAR
PY 2013
VL 37
IS 1
BP 297
EP 299
PG 3
WC Anthropology
WE Social Science Citation Index (SSCI)
SC Anthropology
GA 134HI
UT WOS:000318200600046
PM 23697288
DA 2025-06-01
ER

PT J
AU Orning, P
   Lien, E
   Fitzgerald, KA
AF Orning, Pontus
   Lien, Egil
   Fitzgerald, Katherine A.
TI Gasdermins and their role in immunity and inflammation
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Review
ID CAMPAIGN INTERNATIONAL GUIDELINES; GASTRIC-CANCER; PORE FORMATION;
   SEPTIC SHOCK; CELL-DEATH; PYROPTOSIS; GSDMD; ACTIVATION; CASPASE-11;
   MEMBRANE
AB The gasdermins are a family of pore-forming proteins recently implicated in the immune response. One of these proteins, gasdermin D (GSDMD), has been identified as the executioner of pyroptosis, an inflammatory form of lytic cell death that is induced upon formation of caspase-1-activating inflammasomes. The related proteins GSDME and GSDMA have also been implicated in autoimmune diseases and certain cancers. Most gasdermin proteins are believed to have pore-forming capabilities. The best-studied member, GSDMD, controls the release of the proinflammatory cytokines IL-1 beta and IL-18 and pyroptotic cell death. Because of its potential as a driver of inflammation in septic shock and autoimmune diseases, GSDMD represents an attractive drug target. In this review, we discuss the gasdermin proteins with particular emphasis on GSDMD and its mechanism of action and biological significance.
C1 [Orning, Pontus; Lien, Egil; Fitzgerald, Katherine A.] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol,Program Innate Immun, Worcester, MA 01655 USA.
   [Orning, Pontus; Lien, Egil; Fitzgerald, Katherine A.] Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, Ctr Mol Inflammat Res, Trondheim, Norway.
C3 University of Massachusetts System; University of Massachusetts
   Worcester; Norwegian University of Science & Technology (NTNU)
RP Fitzgerald, KA (corresponding author), Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol,Program Innate Immun, Worcester, MA 01655 USA.; Fitzgerald, KA (corresponding author), Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, Ctr Mol Inflammat Res, Trondheim, Norway.
EM kate.fitzgerald@umassmed.edu
RI Fitzgerald, Katherine/ABE-6317-2020
OI Lien, Egil/0000-0002-8536-2419; Fitzgerald, Kate/0000-0003-3175-609X;
   Orning, Pontus/0000-0002-6177-6916
FU National Institutes of Health [AI146855, AI128547, AI067497]; Norwegian
   Cancer Society [B05035/001]; Research Council of Norway (Center of
   Excellence Funding Scheme) [223255/F50]
FX K.A. Fitzgerald is a consultant for Quench Bio, a biotech company
   focused on the treatment of inflammatory disease. The authors are
   supported by grants from the National Institutes of Health (AI146855 and
   AI128547 to E. Lien and AI067497 to K.A. Fitzgerald), the Norwegian
   Cancer Society (B05035/001 to E. Lien), the Research Council of Norway
   (Center of Excellence Funding Scheme 223255/F50 to P. Orning, E. Lien,
   and K.A. Fitzgerald).
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NR 114
TC 211
Z9 234
U1 1
U2 34
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD NOV
PY 2019
VL 216
IS 11
BP 2453
EP 2465
DI 10.1084/jem.20190545
PG 13
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA JL2IX
UT WOS:000495355800003
PM 31548300
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Li, JY
   Fong, DYT
   Lok, KYW
   Wong, JYH
   Ho, MM
   Choi, EPH
   Pandian, V
   Davidson, PM
   Duan, WJ
   Tarrant, M
   Lee, JJ
   Lin, CC
   Akingbade, O
   Alabdulwahhab, KM
   Ahmad, MS
   Alboraie, M
   Alzahrani, MA
   Bilimale, AS
   Boonpatcharanon, S
   Byiringiro, S
   Hasan, MKC
   Schettini, LC
   Corzo, W
   De Leon, JM
   De Leon, AS
   Deek, H
   Efficace, F
   El Nayal, MA
   El-Raey, F
   Ensaldo-Carrasco, E
   Escotorin, P
   Fadodun, OA
   Fawole, IO
   Goh, YSS
   Irawan, D
   Khan, NE
   Koirala, B
   Krishna, A
   Kwok, C
   Le, TT
   Leal, DG
   Lezana-Fernández, MA
   Manirambona, E
   Mantoani, LC
   Meneses-González, F
   Mohamed, IE
   Mukeshimana, M
   Nguyen, CTM
   Nguyen, HTT
   Nguyen, KT
   Nguyen, ST
   Nurumal, MS
   Nzabonimana, A
   Omer, NAMA
   Ogungbe, O
   Poon, ACY
   Reséndiz-Rodríguez, A
   Puang-Ngern, B
   Sagun, CG
   Shaik, RA
   Shankar, NG
   Sommer, K
   Toro, E
   Tran, HTH
   Urgel, EL
   Uwiringiyimana, E
   Vanichbuncha, T
   Youssef, N
AF Li, Jiaying
   Fong, Daniel Yee Tak
   Lok, Kris Yuet Wan
   Wong, Janet Yuen Ha
   Ho, Mandy Man
   Choi, Edmond Pui Hang
   Pandian, Vinciya
   Davidson, Patricia M.
   Duan, Wenjie
   Tarrant, Marie
   Lee, Jung Jae
   Lin, Chia-Chin
   Akingbade, Oluwadamilare
   Alabdulwahhab, Khalid M.
   Ahmad, Mohammad Shakil
   Alboraie, Mohamed
   Alzahrani, Meshari A.
   Bilimale, Anil S.
   Boonpatcharanon, Sawitree
   Byiringiro, Samuel
   Hasan, Muhammad Kamil Che
   Schettini, Luisa Clausi
   Corzo, Walter
   De Leon, Josephine M.
   De Leon, Anjanette S.
   Deek, Hiba
   Efficace, Fabio
   El Nayal, Mayssah A.
   El-Raey, Fathiya
   Ensaldo-Carrasco, Eduardo
   Escotorin, Pilar
   Fadodun, Oluwadamilola Agnes
   Fawole, Israel Opeyemi
   Goh, Yong-Shian Shawn
   Irawan, Devi
   Khan, Naimah Ebrahim
   Koirala, Binu
   Krishna, Ashish
   Kwok, Cannas
   Le, Tung Thanh
   Leal, Daniela Giambruno
   Lezana-Fernandez, Miguel Angel
   Manirambona, Emery
   Mantoani, Leandro Cruz
   Meneses-Gonzalez, Fernando
   Mohamed, Iman Elmahdi
   Mukeshimana, Madeleine
   Nguyen Chinh Thi Minh
   Nguyen Huong Thi Thanh
   Nguyen Khanh Thi
   Nguyen Son Truong
   Nurumal, Mohd Said
   Nzabonimana, Aimable
   Omer, Nagla Abdelrahim Mohamed Ahmed
   Ogungbe, Oluwabunmi
   Poon, Angela Chiu Yin
   Resendiz-Rodriguez, Areli
   Puang-Ngern, Busayasachee
   Sagun, Ceryl G.
   Shaik, Riyaz Ahmed
   Shankar, Nikhil Gauri
   Sommer, Kathrin
   Toro, Edgardo
   Tran Hanh Thi Hong
   Urgel, Elvira L.
   Uwiringiyimana, Emmanuel
   Vanichbuncha, Tita
   Youssef, Naglaa
TI Key lifestyles and health outcomes across 16 prevalent chronic diseases:
   A network analysis of an international observational study
SO JOURNAL OF GLOBAL HEALTH
LA English
DT Article
ID SUGAR-SWEETENED BEVERAGES; SEDENTARY BEHAVIOR; PHYSICAL-ACTIVITY; US
   ADULTS; EXERCISE; IMPACT; RISK
AB Background Central and bridge nodes can drive significant overall improvements within their respective networks. We aimed to identify them in 16 prevalent chronic diseases during the coronavirus disease 2019 (COVID-19) pandemic to guide effective intervention strategies and appropriate resource allocation for most significant holistic lifestyle and health improvements. Methods We surveyed 16 512 adults from July 2020 to August 2021 in 30 territories. Participants self-reported their medical histories and the perceived impact of COVID-19 on 18 lifestyle factors and 13 health outcomes. For each disease subgroup, we generated lifestyle, health outcome, and bridge networks. Variables with the highest centrality indices in each were identified central or bridge. We validated these networks using nonparametric and case-dropping subset bootstrapping and confirmed central and bridge variables' significantly higher indices through a centrality difference test. Findings Among the 48 networks, 44 were validated (all correlation -stability coefficients >0.25). Six central lifestyle factors were identified: less consumption of snacks (for the chronic disease: anxiety), less sugary drinks (cancer, gastric ulcer, hypertension, insomnia, and pre -diabetes), less smoking tobacco (chronic obstructive pulmonary disease), frequency of exercise (depression and fatty liver disease), duration of exercise (irritable bowel syndrome), and overall amount of exercise (autoimmune disease, diabetes, eczema, heart attack, and high cholesterol). Two central health outcomes emerged: less emotional distress (chronic obstructive pulmonary disease, eczema, fatty liver disease, gastric ulcer, heart attack, high cholesterol, hypertension, insomnia, and pre -diabetes) and quality of life (anxiety, autoimmune disease, cancer, depression, diabetes, and irritable bowel syndrome). Four bridge lifestyles were identified: consumption of fruits and vegetables (diabetes, high cholesterol, hypertension, and insomnia), less duration of sitting (eczema, fatty liver disease, and heart attack), frequency of exercise (autoimmune disease, depression, and heart attack), and overall amount of exercise (anxiety, gastric ulcer, and insomnia). The centrality difference test showed the central and bridge variables had significantly higher centrality indices than others in their networks (P < 0.05). Conclusion To effectively manage chronic diseases during the COVID-19 pandemic, enhanced interventions and optimised resource allocation toward central lifestyle factors, health outcomes, and bridge lifestyles are paramount. The key variables shared across chronic diseases emphasise the importance of coordinated intervention strategies.
C1 [Li, Jiaying; Fong, Daniel Yee Tak; Lok, Kris Yuet Wan; Ho, Mandy Man; Choi, Edmond Pui Hang; Lee, Jung Jae; Lin, Chia-Chin] Univ Hong Kong, Li Ka Shing Fac Med, Sch Nursing, Pokfulam, 5-F Acad Bldg,3 Sassoon Rd, Hong Kong, Peoples R China.
   [Wong, Janet Yuen Ha] Hong Kong Metropolitan Univ, Sch Nursing & Hlth Studies, Hong Kong, Peoples R China.
   [Pandian, Vinciya; Byiringiro, Samuel; Koirala, Binu; Ogungbe, Oluwabunmi] Johns Hopkins Univ, Sch Nursing, Baltimore, MD USA.
   [Davidson, Patricia M.] Univ Wollongong, Wollongong, NSW, Australia.
   [Duan, Wenjie] East China Univ Sci & Technol, Dept Social Work, Shanghai, Peoples R China.
   [Tarrant, Marie] Univ British Columbia, Sch Nursing, Kelowna, BC, Canada.
   [Akingbade, Oluwadamilare] Chinese Univ Hong Kong, Nethersole Sch Nursing, Hong Kong, Peoples R China.
   [Akingbade, Oluwadamilare] Inst Nursing Res, Osogbo, Osun, Nigeria.
   [Alabdulwahhab, Khalid M.] Majmaah Univ, Coll Med, Al Majmaah, Saudi Arabia.
   [Ahmad, Mohammad Shakil; Shaik, Riyaz Ahmed] Majmaah Univ, Coll Med, Dept Family & Community Med, Al Majmaah, Saudi Arabia.
   [Alboraie, Mohamed] Al Azhar Univ, Dept Internal Med, Cairo, Egypt.
   [Alzahrani, Meshari A.] Majmaah Univ, Coll Med, Dept Urol, Al Majmaah, Saudi Arabia.
   [Bilimale, Anil S.] JSS AHER, Sch Publ Hlth, JSS Med Coll, Mysuru, India.
   [Boonpatcharanon, Sawitree; Puang-Ngern, Busayasachee; Vanichbuncha, Tita] Chulalongkorn Business Sch, Dept Stat, Bangkok, Thailand.
   [Hasan, Muhammad Kamil Che; Nurumal, Mohd Said] Int Islamic Univ Malaysia, Kulliyyah Nursing, Kuantan, Malaysia.
   [Schettini, Luisa Clausi] Italian Assoc Leukaemia Lymphoma & Myeloma AIL, Rome, Italy.
   [Corzo, Walter] Dialogos Guatemala, Guatemala City, Guatemala.
   [De Leon, Josephine M.; De Leon, Anjanette S.; Sagun, Ceryl G.; Urgel, Elvira L.] Ctr Escolar Univ, Sch Nursing, Manila, Philippines.
   [Deek, Hiba] Beirut Arab Univ, Fac Hlth Sci, Nursing Dept, Beirut, Lebanon.
   [Efficace, Fabio] Italian Grp Adult Hematol Dis GIMEMA, Data Ctr & Hlth Outcomes Res Unit, Rome, Italy.
   [El Nayal, Mayssah A.; Sommer, Kathrin] Beirut Arab Univ, Dept Psychol, Beirut, Lebanon.
   [El-Raey, Fathiya] Al Azhar Univ, Damietta Fac Med, Dept Hepatogastroenterol & Infect Dis, Cairo, Egypt.
   [Ensaldo-Carrasco, Eduardo] Univ Guadalajara, Ergon Res Ctr ECR, Guadalajara, Jalisco, Mexico.
   [Escotorin, Pilar] Autonomous Univ Barcelona, Dept Basic Dev & Educ Psychol, Lab Appl Prosocial Res, Barcelona, Spain.
   [Fadodun, Oluwadamilola Agnes] Univ Lethbridge, Fac Hlth Sci, Lethbridge, AB, Canada.
   [Fawole, Israel Opeyemi] Ladoke Akintola Univ Technol, Fac Nursing, Ogbomosho, Nigeria.
   [Goh, Yong-Shian Shawn] Natl Univ Singapore, Alice Lee Ctr Nursing Studies, Singapore, Singapore.
   [Irawan, Devi] Wijaya Husada Hlth Inst, Sch Nursing, Bogor, Indonesia.
   [Khan, Naimah Ebrahim] Univ KwaZulu Natal, Dept Optometry, Durban, South Africa.
   [Krishna, Ashish] Ecove, Ghaziabad, India.
   [Kwok, Cannas] Charles Sturt Univ, Sch Nursing Paramed & Hlth Care Sci, Sydney, NSW, Australia.
   [Le, Tung Thanh; Nguyen Chinh Thi Minh; Nguyen Huong Thi Thanh; Nguyen Khanh Thi; Nguyen Son Truong; Tran Hanh Thi Hong] Nam Dinh Univ Nursing, Nam Dinh, Vietnam.
   [Leal, Daniela Giambruno; Toro, Edgardo] Pontificia Univ Catolica Valparaiso, Sch Social Work, Valparaiso, Chile.
   [Lezana-Fernandez, Miguel Angel; Meneses-Gonzalez, Fernando] Natl Commiss Med Arbitrat, Res Dept, Mexico City, Mexico.
   [Manirambona, Emery; Uwiringiyimana, Emmanuel] Univ Rwanda, Coll Med & Hlth Sci, Kigali, Rwanda.
   [Mantoani, Leandro Cruz] Sao Paulo State Univ UNESP, Dept Physiotherapy, Fac Sci & Technol, Presidente Prudente, Brazil.
   [Mohamed, Iman Elmahdi] Benghazi Univ, Fac Pharm, Pharmacol & Toxicol Dept, Benghazi, Libya.
   [Mukeshimana, Madeleine] Univ Rwanda, Coll Med & Hlth Sci, Sch Nursing & Midwifery, Kigali, Rwanda.
   [Nzabonimana, Aimable] Univ Rwanda, Coll Arts & Social Sci, Ctr Language Enhancement, Huye, Rwanda.
   [Omer, Nagla Abdelrahim Mohamed Ahmed] Alzaiem Alazhari Univ, Fac Med, Khartoum, Sudan.
   [Poon, Angela Chiu Yin] Macao Polytech Univ, Fac Hlth Sci & Sports, Taipa, Macao, Peoples R China.
   [Resendiz-Rodriguez, Areli] Univ Nacl Autonoma Mexico, Mexico City, Mexico.
   [Shankar, Nikhil Gauri] Wrexham Maelor Hosp, Mental Hlth & Learning Div, Wrexham, Wales.
   [Youssef, Naglaa] Cairo Univ, Fac Nursing, Med Surg Nursing Dept, Cairo, Egypt.
C3 University of Hong Kong; Hong Kong Metropolitan University; Johns
   Hopkins University; University of Wollongong; East China University of
   Science & Technology; University of British Columbia; Chinese University
   of Hong Kong; Majmaah University; Majmaah University; Egyptian Knowledge
   Bank (EKB); Al Azhar University; Majmaah University; JSS Academy of
   Higher Education & Research; JSS Medical College, Mysuru; Chulalongkorn
   University; International Islamic University Malaysia; Centro Escolar
   University; Beirut Arab University; Fondazione GIMEMA; American
   University of Beirut; Beirut Arab University; Egyptian Knowledge Bank
   (EKB); Al Azhar University; Universidad de Guadalajara; Autonomous
   University of Barcelona; University of Lethbridge; National University
   of Singapore; University of Kwazulu Natal; Charles Sturt University;
   Pontificia Universidad Catolica de Valparaiso; University of Rwanda;
   Universidade Estadual Paulista; University of Benghazi; University of
   Rwanda; University of Rwanda; Macao Polytechnic University; Universidad
   Nacional Autonoma de Mexico; Egyptian Knowledge Bank (EKB); Cairo
   University
RP Fong, DYT (corresponding author), Univ Hong Kong, Li Ka Shing Fac Med, Sch Nursing, Pokfulam, 5-F Acad Bldg,3 Sassoon Rd, Hong Kong, Peoples R China.
EM dytfong@hku.hk
RI Irawan, Devi/LCE-2896-2024; Goh, Shawn Yong-Shian/I-1489-2019; Youssef,
   Naglaa/GQP-7870-2022; Ho, Mandy/P-8821-2019; EL-Raey,
   Fathiya/AAU-6534-2020; Alboraie, Mohamed/F-5688-2011; Kwok,
   Cannas/AGZ-4949-2022; Le, Tung/AAD-7494-2020; Mukeshimana,
   Madeleine/C-1547-2018; Wong, Janet/F-4433-2011; Ogungbe,
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   Mohammad/GSN-3192-2022; Pandian, Vinciya/AAM-1218-2020; Lin,
   Cheng-Hui/AAV-7085-2021; Nguyen, Son/AAG-4274-2020; Duan,
   Wenjie/C-8722-2016; Ahamed, Riyaz/GRF-4695-2022; Choi,
   Edmond/H-4187-2019; Byiringiro, Samuel/ABF-6161-2021; Akingbade,
   Oluwadamilare/ACH-6708-2022; Deek, Hiba/Y-9356-2019; Mantoani,
   Leandro/AAW-4370-2021; Alzahrani, Meshari/AAW-3948-2020; EbrahimKhan,
   Naimah/KIG-2113-2024; Fong, Daniel/C-4269-2009; Ensaldo-Carrasco,
   Eduardo/C-4774-2018; Lok, Kris Yuet Wan/P-8814-2019; Bilimale,
   Anil/X-5476-2018; Manirambona, Emery/ADF-0353-2022
OI Fong, Daniel/0000-0001-7365-9146; Ensaldo-Carrasco,
   Eduardo/0000-0002-5474-7500; Lok, Kris Yuet Wan/0000-0002-3227-0799;
   Lee, Jay Jung Jae/0000-0001-9704-2116; Youssef,
   Naglaa/0000-0002-0368-1759; Davidson, Patricia M./0000-0003-2050-1534;
   Goh, Yong Shian/0000-0002-9610-5397; Li, Jiaying/0000-0002-5473-4320;
   Bilimale, Anil/0000-0002-3601-2930; Krishna, Ashish/0000-0003-2325-6183;
   Uwiringiyimana, Emmanuel/0000-0001-5092-6109; Manirambona,
   Emery/0000-0002-0579-3607; , cannas/0000-0002-6296-1144
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NR 42
TC 7
Z9 7
U1 6
U2 17
PU INT SOC GLOBAL HEALTH
PI EDINBURGH
PA CALEDONIAN EXCHANGE, 19A CANNING ST, EDINBURGH, Lothian, ENGLAND
SN 2047-2978
EI 2047-2986
J9 J GLOB HEALTH
JI J. Glob. Health
PY 2024
VL 14
AR 04068
DI 10.7189/jogh.14.04068
PG 15
WC Public, Environmental & Occupational Health
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Public, Environmental & Occupational Health
GA OR3Z8
UT WOS:001208974600001
PM 38606605
DA 2025-06-01
ER

PT J
AU Koc, DO
   Bektas, S
AF Koc, Deniz Ogutmen
   Bektas, Sibel
TI Serum pepsinogen levels and OLGA/OLGIM staging in the assessment of
   atrophic gastritis types
SO POSTGRADUATE MEDICAL JOURNAL
LA English
DT Article
DE gastroduodenal disease; endoscopy; pathology
ID HELICOBACTER-PYLORI; AUTOIMMUNE GASTRITIS; CLASSIFICATION; OLGA;
   METAPLASIA; GASTRIN-17; DISTINCT; CANCER
AB Background We assessed the validity of using serum pepsinogen tests (sPGTs) to differentiate autoimmune atrophic gastritis (AAG) from environmental atrophic gastritis (EAG). We also investigated the correlation and prognostic value between disease stage, according to Operative Link for Gastritis Assessment (OLGA)/Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM), and sPGT results in patients with gastric atrophy. Methods We enroled 115 patients in this prospective study: 95 with atrophic gastritis (16 with AAG and 79 with EAG) and 20 non-atrophic gastritis. These patients, along with 32 control patients, underwent esophagogastroduodenoscopy. Atrophy and intestinal metaplasia of the gastric biopsy specimens were staged according to the OLGA/OLGIM staging systems. Results The median (IQR) age of the patients (83 females (56.5%)) was 58 (46-67) years. Patients in the AAG group represented histologically advanced stages. The AAG group had lower pepsinogen (PG) I and II levels, as well as a lower PGI/PGII ratio, compared with the EAG group (p<0.01, p<0.05 and p<0.01, respectively). The optimal PGI/PGII ratio for predicting AAG was <= 1.9 (100% sensitivity and 100% specificity), and that for predicting EAG was <= 9.2 (47.5% sensitivity and 90.6% specificity). The OLGA/OLGIM stage was negatively correlated with the PGI level and PGI/PGII ratio. In the AAG group, four of five patients with low-grade dysplasia had OLGA/OLGIM stage III-IV disease. Conclusions sPGT may provide valuable information for differentiating advanced-stage AAG from EAG, and in patients with atrophic gastritis, use of sPGTs and OLGA/OLGIM staging together may predict gastric cancer risk.
C1 [Koc, Deniz Ogutmen; Bektas, Sibel] Univ Hlth Sci, Gaziosmanpasa Training & Res Hosp, Dept Pathol, Istanbul, Turkey.
C3 University of Health Sciences Turkey
RP Koc, DO (corresponding author), Univ Hlth Sci, Dept Gastroenterol, Gaziosmanpasa Training & Res Hosp, Istanbul, Turkey.
EM drdenizkoc@gmail.com
OI OGUTMEN KOC, DENIZ/0000-0003-2738-625X
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NR 29
TC 16
Z9 16
U1 0
U2 6
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0032-5473
EI 1469-0756
J9 POSTGRAD MED J
JI Postgrad. Med. J.
PD JUN
PY 2022
VL 98
IS 1160
BP 441
EP 445
DI 10.1136/postgradmedj-2020-139183
PG 5
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 1M8AC
UT WOS:000800187300009
PM 33380437
DA 2025-06-01
ER

PT J
AU Wotherspoon, AC
   Diss, TC
   Pan, L
   Singh, N
   Whelan, J
   Isaacson, PG
AF Wotherspoon, AC
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   Singh, N
   Whelan, J
   Isaacson, PG
TI Low grade gastric B-cell lymphoma of mucosa associated lymphoid tissue
   in immunocompromised patients
SO HISTOPATHOLOGY
LA English
DT Article
DE malignant lymphoma; MALT lymphoma; HIV infection; AIDS; post-transplant
   lymphoproliferative disorder; stomach
ID EPSTEIN-BARR-VIRUS; POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS;
   ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PYLORI-ASSOCIATED GASTRITIS;
   POLYMERASE CHAIN-REACTION; NON-HODGKINS LYMPHOMA; MALIGNANT-LYMPHOMA;
   SAN-FRANCISCO; DISEASE; TRANSPLANTATION
AB An increased incidence of non-Hodgkin's lymphoma is seen in patients with immunodeficiency from any cause. The majority of these are high grade B-cell lymphoma and most are associated with the Epstein-Barr virus (EBV). In post-transplant lymphoma/lymphoproliferative disorders the tumour may regress following reduction of immunosuppression but in AIDS the lymphomas show a characteristic aggressive course and poor prognosis. We describe low grade B-cell gastric lymphoma of mucosa associated lymphoid tissue (MALT) in three immunocompromised patients (two post-transplant, one HIV positive). In each case, the tumour showed classical morphological features of gastric MALT lymphoma and was not associated with EBV. Helicobacter pylori was identified in each case. Clinical follow-up suggests that the behaviour in these tumours is similar to that seen in MALT lymphomas in immunocompetent patients and not typical of the lymphomas usually associated with immunosuppression. Although the finding of MALT lymphoma in immunosuppressed patients might be coincidental, the association of some MALT lymphomas with autoimmune disease suggests that dysregulation of the immune system might play a role in the pathogenesis of these tumours.
C1 UCL, SCH MED, DEPT HISTOPATHOL, LONDON W1N 8AA, ENGLAND.
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C3 University of London; University College London; UCL Medical School;
   University of London; University College London
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NR 49
TC 46
Z9 46
U1 0
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0309-0167
EI 1365-2559
J9 HISTOPATHOLOGY
JI Histopathology
PD FEB
PY 1996
VL 28
IS 2
BP 129
EP 134
DI 10.1046/j.1365-2559.1996.292338.x
PG 6
WC Cell Biology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Pathology
GA TU408
UT WOS:A1996TU40800004
PM 8834520
DA 2025-06-01
ER

PT J
AU Grozinsky-Glasberg, S
   Thomas, D
   Strosberg, JR
   Pape, UF
   Felder, S
   Tsolakis, AV
   Alexandraki, KI
   Fraenkel, M
   Saiegh, L
   Reissman, P
   Kaltsas, G
   Gross, DJ
AF Grozinsky-Glasberg, Simona
   Thomas, Dimitrios
   Strosberg, Jonathan R.
   Pape, Ulrich-Frank
   Felder, Stephan
   Tsolakis, Apostolos V.
   Alexandraki, Krystallenia I.
   Fraenkel, Merav
   Saiegh, Leonard
   Reissman, Petachia
   Kaltsas, Gregory
   Gross, David J.
TI Metastatic type 1 gastric carcinoid: A real threat or just a myth?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Metastatic gastric carcinoids; Gastrin; Chromogranin A; Somatostatin
   analogues; Stomach neuroendocrine tumor
ID DIGESTIVE NEUROENDOCRINE TUMORS; ACTING SOMATOSTATIN ANALOGS; ENETS
   CONSENSUS GUIDELINES; ECL CELL; I INTERFERONS; MANAGEMENT; GROWTH;
   OCTREOTIDE; HYPERGASTRINEMIA; EPIDEMIOLOGY
AB AIM: To describe disease characteristics and treatment modalities in a group of rare patients with metastatic gastric carcinoid type 1 (GCA1).
   METHODS: Information on clinical, biochemical, radiological, histopathological findings, the extent of the disease, as well as the use of different therapeutic modalities and the long-term outcome were recorded. Patients' data were assessed at presentation, and thereafter at 6 to 12 monthly intervals both clinically and biochemically, but also endoscopically and histopathologically. Patients were evaluated for the presence of specific symptoms; the presence of autoimmune disorders and the presence of other gastrointestinal malignancies in other family members were also recorded. The evaluation of response to treatment was defined using established WHO criteria.
   RESULTS: We studied twenty consecutive patients with a mean age of 55.1 years. The mean follow-up period was 83 mo. Twelve patients had regional lymph node metastases and 8 patients had liver metastases. The primary tumor mean diameter was 20.13 +/- 10.83 mm (mean +/- SD). The mean Ki-67 index was 6.8% +/- 11.2%. All but one patient underwent endoscopic or surgical excision of the tumor. The disease was stable in all but 3 patients who had progressive liver disease. All patients remained alive during the follow-up period.
   CONCLUSION: Metastatic GCA1 carries a good overall prognosis, being related to a tumor size of >= 1 cm, an elevated Ki-67 index and high serum gastrin levels. (C) 2013 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Grozinsky-Glasberg, Simona; Gross, David J.] Hadassah Hebrew Univ Med Ctr, Dept Med, Endocrinol & Metab Serv, Neuroendocrine Tumor Unit, IL-91120 Jerusalem, Israel.
   [Thomas, Dimitrios; Alexandraki, Krystallenia I.; Kaltsas, Gregory] Natl Univ Athens, Dept Pathophysiol, Endocrine Unit, Athens 11527, Greece.
   [Strosberg, Jonathan R.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
   [Pape, Ulrich-Frank; Felder, Stephan] Charite, Dept Internal Med, Div Hepatol Gastroenterol Endocrinol & Metab, DE-13353 Berlin, Germany.
   [Tsolakis, Apostolos V.] Uppsala Univ, Dept Med Sci, Sect Endocrine Oncol, S-75185 Uppsala, Sweden.
   [Fraenkel, Merav] Soroka Ben Gurion Univ Hosp, Inst Endocrinol, IL-84965 Beer Sheva, Israel.
   [Saiegh, Leonard] Bnei Zion Hosp, Inst Endocrinol, IL-33394 Haifa, Israel.
   [Reissman, Petachia] Hebrew Univ Jerusalem, Sch Med, Shaare Zedek Med Ctr, Dept Surg, IL-93722 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Hospital; National &
   Kapodistrian University of Athens; H Lee Moffitt Cancer Center &
   Research Institute; Berlin Institute of Health; Free University of
   Berlin; Humboldt University of Berlin; Charite Universitatsmedizin
   Berlin; Uppsala University; Ben-Gurion University of the Negev; Bnai
   Zion Medical Center; Hebrew University of Jerusalem; Shaare Zedek
   Medical Center
RP Grozinsky-Glasberg, S (corresponding author), Hadassah Hebrew Univ Med Ctr, Dept Med, Endocrinol & Metab Serv, Neuroendocrine Tumor Unit, POB 12000, IL-91120 Jerusalem, Israel.
EM simonag@hadassah.org.il
RI Tsolakis, Apostolos/AAK-3974-2020; Fraenkel, Mearv/A-5120-2016; Kaltsas,
   Gregory/AAD-7193-2019; Alexandraki, Krystallenia/S-4058-2019
OI Kaltsas, Gregory/0000-0002-5876-7883; Alexandraki,
   Krystallenia/0000-0003-2398-6768
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NR 36
TC 65
Z9 73
U1 0
U2 6
PU BAISHIDENG PUBL GRP CO LTD
PI WANCHAI
PA ROOM 1701, 17-F, HENAN BUILDING, NO. 90, JAFFE RD, WANCHAI, HONG KONG
   100025, PEOPLES R CHINA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD DEC 14
PY 2013
VL 19
IS 46
BP 8687
EP 8695
DI 10.3748/wjg.v19.i46.8687
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 281VN
UT WOS:000329129200025
PM 24379587
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Gonzalez-Gronow, M
   Pizzo, SV
AF Gonzalez-Gronow, Mario
   Pizzo, Salvatore Vincent
TI Physiological Roles of the Autoantibodies to the 78-Kilodalton
   Glucose-Regulated Protein (GRP78) in Cancer and Autoimmune Diseases
SO BIOMEDICINES
LA English
DT Review
DE cancer; autoimmune diseases; ER dysfunctions; GRP78 autoantigenicity;
   GRP78 cell surface compartments; GRP78 citrullination; GRP78
   N-glycosylation
ID ENDOPLASMIC-RETICULUM STRESS; CELL-SURFACE GRP78; EXPRESSED
   CITRULLINATED GRP78; LINKED OLIGOSACCHARIDE CHAINS; SERUM
   IMMUNOGLOBULIN-G; RHEUMATOID-ARTHRITIS; NEUROMYELITIS-OPTICA;
   ANTIBODIES; IGG; INDUCTION
AB The 78 kDa glucose-regulated protein (GRP78), a member of the 70 kDa heat-shock family of molecular chaperones (HSP70), is essential for the regulation of the unfolded protein response (UPR) resulting from cellular endoplasmic reticulum (ER) stress. During ER stress, GRP78 evades retention mechanisms and is translocated to the cell surface (csGRP78) where it functions as an autoantigen. Autoantibodies to GRP78 appear in prostate, ovarian, gastric, malignant melanoma, and colorectal cancers. They are also found in autoimmune pathologies such as rheumatoid arthritis (RA), neuromyelitis optica (NMO), anti-myelin oligodendrocyte glycoprotein antibody-associated disorder (AMOGAD), Lambert-Eaton myasthenic syndrome (LEMS), multiple sclerosis (MS), neuropsychiatric systemic lupus erythematosus (NPSLE) and type 1 diabetes (T1D). In NMO, MS, and NPSLE these autoantibodies disrupt and move across the blood-brain barrier (BBB), facilitating their entry and that of other pathogenic antibodies to the brain. Although csGRP78 is common in both cancer and autoimmune diseases, there are major differences in the specificity of its autoantibodies. Here, we discuss how ER mechanisms modulate csGRP78 antigenicity and the production of autoantibodies, permitting this chaperone to function as a dual compartmentalized receptor with independent signaling pathways that promote either pro-proliferative or apoptotic signaling, depending on whether the autoantibodies bind csGRP78 N- or C-terminal regions.
C1 [Gonzalez-Gronow, Mario; Pizzo, Salvatore Vincent] Duke Univ, Dept Pathol, Med Ctr, Durham, NC 27710 USA.
C3 Duke University
RP Gonzalez-Gronow, M (corresponding author), Duke Univ, Dept Pathol, Med Ctr, Durham, NC 27710 USA.
EM gonza002@mc.duke.edu; salvatore.pizzo@duke.edu
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NR 87
TC 14
Z9 18
U1 1
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD JUN
PY 2022
VL 10
IS 6
AR 1222
DI 10.3390/biomedicines10061222
PG 13
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA 2M2ST
UT WOS:000817556600001
PM 35740249
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bilinska, ZT
   Grzybowski, J
   Szajewski, T
   Stepinska, J
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   Walczak, E
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   Ruzyllo, W
AF Bilinska, ZT
   Grzybowski, J
   Szajewski, T
   Stepinska, J
   Michalak, E
   Walczak, E
   Wagner, T
   Kwiatkowska, B
   Ruzyllo, W
TI Active lymphocytic myocarditis treated with murine OKT3 monoclonal
   antibody in a patient presenting with intractable ventricular
   tachycardia
SO TEXAS HEART INSTITUTE JOURNAL
LA English
DT Article
DE antibodies, monoclonal/therapeutic use; autoimmune
   diseases/complications; case report; female; heart failure,
   congestive/etiology; immunosuppression; Muromonab-CD3; Helicobacter
   pylori/immunology; myocarditis/etiology; myocarditis/drug therapy;
   myocardium/immunology; tachycardia, ventricular/therapy
ID GIANT-CELL MYOCARDITIS; HELICOBACTER-PYLORI; TRANSPLANTATION; INDUCTION;
   RECOVERY; DISEASE; BRIDGE; DEVICE
AB This report describes the case of a 33-year-old woman with biopsy-proven, active lymphocytic myocarditis manifested by intractable ventricular tachycardia, nonspecific intraventricular block, and myocardial dysfunction, We treated her successfully with OKT3 monoclonal antibody and antiarrhythmic agents. Immunosuppression is not recommended in patients with infectious or postinfectious myocarditis. However it may have an important role in autoimmune myocarditis. In the few reports in the medical literature that we were able to find, OKT3 monoclonal antibody was administered early, in the setting of acute, fulminant autoimmune myocarditis. Our patient received OKT3 therapy in a later phase of the disease, when inflammatory infiltrates were accompanied by extensive fibrosis and severe damage of cardiomyocytes.
   Our patient had concomitant Helicobacter pylori infection and a strong positive family history of gastric cancer a disease often associated with H. pylori. We discuss the possibility of a causal relationship between H. pylori infection and autoimmune myocarditis.
C1 Inst Cardiol, Dept Gen Cardiol, PL-04628 Warsaw, Poland.
C3 Institute of Cardiology - Poland
RP Ruzyllo, W (corresponding author), Inst Cardiol, Dept Gen Cardiol, Alpejska 42, PL-04628 Warsaw, Poland.
RI Michalak, Ewa/AAA-5741-2021
OI Bilinska, Zofia/0000-0003-1451-2069
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NR 19
TC 5
Z9 6
U1 0
U2 2
PU TEXAS HEART INST
PI HOUSTON
PA PO BOX 20345, HOUSTON, TX 77225-0345 USA
SN 0730-2347
J9 TEX HEART I J
JI Tex. Heart Inst. J.
PY 2002
VL 29
IS 2
BP 113
EP 117
PG 5
WC Cardiac & Cardiovascular Systems
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology
GA 561RN
UT WOS:000176156600007
PM 12075867
DA 2025-06-01
ER

PT J
AU Zhang, C
   Ding, Z
   Lv, GQ
   Li, JP
   Zhang, JF
   Zhou, P
AF Zhang, Chun
   Ding, Zhi
   Lv, Guoqiang
   Li, Jianping
   Zhang, Jun Feng
   Zhou, Ping
TI CD226 rs727088A&gt;G polymorphism increases the susceptibility to
   gastric cancer in Chinese populations
SO GENE
LA English
DT Article
DE CD226; Gastric cancer; Polymorphisms
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; MULTIPLE AUTOIMMUNE-DISEASES;
   SQUAMOUS-CELL CARCINOMA; RISK-FACTORS; EFFECTOR FUNCTIONS;
   T-LYMPHOCYTES; PVR CD155; TH1 CELLS; DNAM-1; ASSOCIATION
AB Gastric cancer (GC) is one of the most common cancers worldwide, especially in Asia The development of GC is a multifactorial process and numerous studies have linked genetic variation to GC risk. In this study, we evaluated the effects of single nucleotide polymorphisms (SNPs) of CD226 on GC susceptibility in Chinese populations including 687 cancer patients and 936 control subjects. We found that the G allele of the rs727088A>G polymorphism in the 3'-untranslated region of CD226 was significantly associated with risk of GC using logistic regression (P < 10(-3)). GC patients who harbored the rs727088G allele had significantly increased cancer risk (odds ratio = 1.43, 95% confidence interval = 1.23-1.67) compared with those patients harboring the rs727088A allele. Moreover, functional relevance was further performed that individuals carrying the rs727088G allele were correlated with lower expression level of CD226 than individuals carrying the rs727088AA homozygous genotype. These findings indicated that functional polymorphism rs727088A>G in CD226 might modify the susceptibility for the development of GC. (C) 2014 Published by Elsevier B.V.
C1 [Zhang, Chun; Ding, Zhi; Zhang, Jun Feng] Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210093, Jiangsu, Peoples R China.
   [Zhang, Chun; Lv, Guoqiang; Li, Jianping; Zhou, Ping] Nantong Univ, Affiliated Hosp 3, Dept Gen Surg, Wuxi 214041, Peoples R China.
C3 Nanjing University; Nantong University
RP Zhang, JF (corresponding author), Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Nanjing 210093, Jiangsu, Peoples R China.
EM jfzhang@nju.edu.cn; zhoupingwuxi@126.com
RI zhang, junfeng/JHT-7871-2023
FU Jiangsu Provincial Natural Science Foundation [BK2011176]
FX This study was supported by Jiangsu Provincial Natural Science
   Foundation (BK2011176).
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NR 29
TC 1
Z9 1
U1 0
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
EI 1879-0038
J9 GENE
JI Gene
PD FEB 15
PY 2015
VL 557
IS 1
BP 92
EP 97
DI 10.1016/j.gene.2014.12.022
PG 6
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA CA4PC
UT WOS:000348885900012
PM 25510399
DA 2025-06-01
ER

PT J
AU Sipponen, P
AF Sipponen, P
TI Helicobacter pylori gastritis - Epidemiology
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE chronic gastritis; peptic ulcer; gastric cancer; Helicobacter pylori
ID CAMPYLOBACTER-PYLORI; SYDNEY SYSTEM; ULCER DISEASE; INFECTION;
   PREVALENCE; STOMACH; BIOPSY; COHORT; CANCER
AB The acquisition of Helicobacter pylori is the main cause of chronic gastritis in humans. In Europe, a small proportion (less than 1%) of gastritis cases are caused by H. Heilmannii, and somewhat more (5%) are autoimmune in origin, in which condition H. pylori may not probably play a role. Recent findings on chronic gastritis and H. pylori acquisition in developed countries can be summarized as: (1) H. pylori gastritis is acquired in childhood and adolescence (age less than 20) in more than 50% of cases; (2) the risk and rate of acquisition is highest in early childhood, after which the rate exponentially declines; (3) new infections occur in adulthood but are quite rare (annual incidence 0.4%, on average, in Finland); (4) H. pylori gastritis is a birth cohort-related phenomenon; i.e., different cohorts show a rate and prevalence of H. pylori gastritis that varies between cohorts; (5) the rate and risk of H. pylori infection is high in cohorts born in the beginning of the century, but is much lower in those born later; (6) this decline is due to a decrease in the rate and risk of H. pylori acquisition in childhood in particular. H. pylori gastritis-related complications, such as peptic ulcer diseases and gastric cancer, show epidemiological features similar to H. pylori gastritis. Both peptic ulcer and gastric cancer have declined in incidence over time. Gastric cancer is a birth-cohort phenomenon in the same way as is H. pylori gastritis, and the incidence of gastric cancer shows a positive but exponential relationship with the "birth-cohort-specific" prevalence of gastritis in the general population.
RP JORVI HOSP, DEPT PATHOL, SF-02740 ESPOO, FINLAND.
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NR 31
TC 47
Z9 52
U1 0
U2 2
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD APR
PY 1997
VL 32
IS 2
BP 273
EP 277
DI 10.1007/BF02936382
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA WN384
UT WOS:A1997WN38400024
PM 9085182
DA 2025-06-01
ER

PT J
AU Lee, J
   Choi, J
   Kang, MS
   Yu, SY
   Kim, K
AF Lee, Junwoo
   Choi, Jaehwan
   Kang, Min Seok
   Yu, Seung-Young
   Kim, Kiyoung
TI Bilateral optic neuropathy in Krukenberg tumor treated with FOLFOX plus
   nivolumab: a case report
SO BMC OPHTHALMOLOGY
LA English
DT Article
DE FOLFOX; Nivolumab; Immune checkpoint inhibitor; Optic neuropathy;
   Krukenberg tumor; Immune-related adverse events
AB BackgroundA combination of FOLFOX and nivolumab is a first-line treatment for HER2-negative advanced gastric cancer, significantly improving survival. However, this regimen is associated with potential neurotoxicity. 5-Fluorouracil and oxaliplatin in FOLFOX have been linked to optic neuropathy, whereas nivolumab, an immune checkpoint inhibitor, may cause immune-related optic neuropathy. Although FOLFOX plus nivolumab provides considerable survival benefits, careful monitoring for ocular complications is essential. We report a case of bilateral optic neuropathy in a patient who received FOLFOX plus nivolumab. Despite discontinuation of chemotherapy and treated with high-dose corticosteroid pulse therapy, the patient's symptoms did not improve.Case presentationA 48-year-old woman with a Krukenberg tumor developed progressive bilateral visual impairment during treatment with FOLFOX plus nivolumab. Her ophthalmologic history included branch retinal vein occlusion in the right eye but no systemic diseases. She presented with bilateral central scotomas and visual field defects. On examination, best-corrected visual acuity (BCVA) was 20/40 in the right eye and 20/25 in the left eye, with bilateral optic disc swelling and hemorrhage. Fluorescein angiography confirmed optic disc leakage, and a visual evoked potential (VEP) test indicated axonal loss. Brain magnetic resonance imaging (MRI) and positron emission tomography-computed tomography (PET-CT) ruled out metastatic disease, and autoimmune markers were negative. High-dose intravenous methylprednisolone was administered, and chemotherapy was discontinued. Despite initial stabilization, vision deteriorated, ultimately progressing to light perception in both eyes. Repeated steroid pulse therapy failed to improve outcomes.ConclusionsThis case highlights the potential for severe bilateral optic neuropathy associated with FOLFOX plus nivolumab, leading to irreversible vision loss. These findings suggest that close ophthalmologic monitoring is warranted in patients receiving FOLFOX plus nivolumab for early recognition of bilateral visual impairment. Further research is needed to elucidate the mechanisms and identify agents responsible for the development of optic neuropathy.
C1 [Lee, Junwoo] Gachon Univ, Dept Ophthalmol, Gil Med Ctr, Incheon, South Korea.
   [Choi, Jaehwan; Kang, Min Seok; Yu, Seung-Young; Kim, Kiyoung] Kyung Hee Univ, Kyung Hee Univ Hosp, Dept Ophthalmol, 23,Kyungheedae ro, Seoul 02447, South Korea.
C3 Gachon University; Kyung Hee University; Kyung Hee University Hospital
RP Kim, K (corresponding author), Kyung Hee Univ, Kyung Hee Univ Hosp, Dept Ophthalmol, 23,Kyungheedae ro, Seoul 02447, South Korea.
EM pourma@khu.ac.kr
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NR 23
TC 0
Z9 0
U1 0
U2 0
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2415
J9 BMC OPHTHALMOL
JI BMC Ophthalmol.
PD APR 30
PY 2025
VL 25
IS 1
AR 262
DI 10.1186/s12886-025-04102-y
PG 8
WC Ophthalmology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Ophthalmology
GA 2CY6Y
UT WOS:001479693900002
PM 40307761
DA 2025-06-01
ER

PT J
AU Kariya, S
   Okano, M
   Nishizaki, K
AF Kariya, Shin
   Okano, Mitsuhiro
   Nishizaki, Kazunori
TI An association between Helicobacter pylori and upper respiratory
   tract disease: Fact or fiction?
SO WORLD JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Paranasal sinus; Ear; Adenoid; Oral cavity; Pharynx; Larynx; Upper
   respiratory tract; Cancer
ID RECURRENT APHTHOUS STOMATITIS; GASTROESOPHAGEAL-REFLUX DISEASE; CHRONIC
   OTITIS-MEDIA; CHRONIC NONSPECIFIC PHARYNGITIS;
   POLYMERASE-CHAIN-REACTION; SQUAMOUS-CELL CARCINOMA; GASTRIC BIOPSY
   SAMPLES; OF-THE-LITERATURE; POSITIVE DYSPEPTIC PATIENTS; ORAL
   LICHEN-PLANUS
AB Helicobacter pylori (H. pylori) is a major cause of chronic gastritis and gastric ulcers and considerable evidence supports the notion that infection with this bacterium is also associated with gastric malignancy in addition to various other conditions including pulmonary, vascular and autoimmune disorders. Gastric juice infected with H. pylori might play an important role in upper respiratory tract infection. Although direct and/or indirect mechanisms might be involved in the association between H. pylori and upper respiratory tract diseases, the etiological role of H. pylori in upper respiratory tract disorders has not yet been fully elucidated. Although various studies over the past two decades have suggested a relationship between H. pylori and upper respiratory tract diseases, the findings are inconsistent. The present overview describes the outcomes of recent investigations into the impact of H. pylori on upper respiratory tract and adjacent lesions. (C) 2014 Baishideng Publishing Group Co., Limited. All rights reserved.
C1 [Kariya, Shin; Okano, Mitsuhiro; Nishizaki, Kazunori] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg, Okayama 7008558, Japan.
C3 Okayama University
RP Kariya, S (corresponding author), Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Otolaryngol Head & Neck Surg, Kita Ku, 2-5-1 Shikata Cho, Okayama 7008558, Japan.
EM skariya@cc.okayama-u.ac.jp
FU JSPS KAKENHI [23791900, 25462642]; Grants-in-Aid for Scientific Research
   [25462642, 23791900] Funding Source: KAKEN
FX Supported by JSPS KAKENHI (Grants-in-Aid for Scientific Research), No.
   23791900 and No. 25462642
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NR 251
TC 29
Z9 31
U1 3
U2 29
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 8226 REGENCY DR, PLEASANTON, CA 94588 USA
SN 1007-9327
EI 2219-2840
J9 WORLD J GASTROENTERO
JI World J. Gastroenterol.
PD FEB 14
PY 2014
VL 20
IS 6
BP 1470
EP 1484
DI 10.3748/wjg.v20.i6.1470
PG 15
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AB2HH
UT WOS:000331613300006
PM 24587622
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Zhang, Y
   Wu, J
   Zhang, HB
   Wu, C
AF Zhang, Ying
   Wu, Jun
   Zhang, Haibo
   Wu, Chen
TI The Regulation between CD4<SUP>+</SUP>CXCR5<SUP>+</SUP> Follicular
   Helper T (Tfh) Cells and
   CD19<SUP>+</SUP>CD24<SUP>hi</SUP>CD38<SUP>hi</SUP> Regulatory B (Breg)
   Cells in Gastric Cancer
SO JOURNAL OF IMMUNOLOGY RESEARCH
LA English
DT Article
ID CLINICAL-SIGNIFICANCE; DIFFERENTIATION; LANDSCAPE; ROLES
AB Purpose. T follicular helper (Tfh) cells and regulatory B (Breg) cells are reported to play essential roles in humoral immunity, especially in inflammation, autoimmune diseases, and cancer. Hence, we sought to investigate the involvement of CXCR5(+)CD4(+) Tfh cells and CD19(+)CD24(hi)CD38(hi) Breg cells in gastric cancer. Methods. The blood samples were obtained from 36 gastric cancer patients and 18 healthy individuals. The percentage of Tfh cells (Tfh%) and Breg cells (Breg%) was detected via flow cytometry, while IL-21, IL-10, and CXCL13 levels were examined with ELISA. The association between them and clinical parameters of patients was also assessed. The in vitro Tfh-B cell coculture experiments were performed for six days, and then, Tfh%, Breg%, and cytokines were valued by flow cytometry and ELISA, respectively. Results. Tfh%, Breg%, and CXCL13 level were significantly increased among gastric cancer patients. Moreover, higher Tfh% was associated with lymphatic metastasis, patients' worse outcomes and Breg%. Tfh differentiation and CXCL13 were upregulated by cocultured B cells in vitro, while Tfh cells seem to not participate in Breg cell differentiation from B cells. Conclusion. Altogether, increased Tfh and Breg cells could be involved in immune suppression in gastric cancer. Moreover, B cell may be a potential regulator for Tfh differentiation, while Tfh cells had no significant effects on the regulation of Breg cells.
C1 [Zhang, Ying; Wu, Jun; Wu, Chen] Soochow Univ, Affiliated Hosp 3, Dept Oncol, Changzhou 213003, Jiangsu, Peoples R China.
   [Zhang, Ying] Jiangnan Univ, Affiliated Hosp, Dept Oncol, Wuxi 214000, Jiangsu, Peoples R China.
   [Zhang, Haibo] Peoples Hosp Ziyang, Dept Ophthalmol, Ankang 725399, Shanxi, Peoples R China.
   [Wu, Chen] Peoples Hosp Ziyang, Dept Gen Internal Med, Ankang 725399, Shanxi, Peoples R China.
C3 Soochow University - China; Jiangnan University
RP Wu, C (corresponding author), Soochow Univ, Affiliated Hosp 3, Dept Oncol, Changzhou 213003, Jiangsu, Peoples R China.; Wu, C (corresponding author), Peoples Hosp Ziyang, Dept Gen Internal Med, Ankang 725399, Shanxi, Peoples R China.
EM zhangyingdyx@163.com; wujun68@sina.com; 345958504@qq.com;
   chenwucz@163.com
RI Zhang, Haibo/HLP-9266-2023; wu, chen/LPQ-7578-2024
OI wu, chen/0000-0002-3410-492X
FU National Natural Science Foundation of China; Maternal and Child Health
   Association Foundation of Jiangsu; Science and Technology Plan of
   Changzhou;  [31700792];  [FYX202017];  [CE20225039]
FX AcknowledgmentsThis study was financially funded by the National Natural
   Science Foundation of China (grant no. 31700792), the Maternal and Child
   Health Association Foundation of Jiangsu (grant no. FYX202017), and the
   Science and Technology Plan of Changzhou (grant no. CE20225039).
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NR 43
TC 13
Z9 12
U1 2
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2314-8861
EI 2314-7156
J9 J IMMUNOL RES
JI J Immunol. Res.
PD OCT 26
PY 2022
VL 2022
AR 9003902
DI 10.1155/2022/9003902
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 6L5HH
UT WOS:000888213900001
PM 36339942
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Li, C
   Ni, YQ
   Xu, H
   Xiang, QY
   Zhao, Y
   Zhan, JK
   He, JY
   Li, S
   Liu, YS
AF Li, Chen
   Ni, Yu-Qing
   Xu, Hui
   Xiang, Qun-Yan
   Zhao, Yan
   Zhan, Jun-Kun
   He, Jie-Yu
   Li, Shuang
   Liu, You-Shuo
TI Roles and mechanisms of exosomal non-coding RNAs in human health and
   diseases
SO SIGNAL TRANSDUCTION AND TARGETED THERAPY
LA English
DT Review
ID MESENCHYMAL STEM-CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ACUTE
   MYOCARDIAL-INFARCTION; GASTRIC-CANCER PROGRESSION; AMYLOID PRECURSOR
   PROTEIN; TYPE-2 DIABETES-MELLITUS; ISLET BETA-CELL;
   HEPATOCELLULAR-CARCINOMA; EXTRACELLULAR VESICLES; BREAST-CANCER
AB Exosomes play a role as mediators of cell-to-cell communication, thus exhibiting pleiotropic activities to homeostasis regulation. Exosomal non-coding RNAs (ncRNAs), mainly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are closely related to a variety of biological and functional aspects of human health. When the exosomal ncRNAs undergo tissue-specific changes due to diverse internal or external disorders, they can cause tissue dysfunction, aging, and diseases. In this review, we comprehensively discuss the underlying regulatory mechanisms of exosomes in human diseases. In addition, we explore the current knowledge on the roles of exosomal miRNAs, lncRNAs, and circRNAs in human health and diseases, including cancers, metabolic diseases, neurodegenerative diseases, cardiovascular diseases, autoimmune diseases, and infectious diseases, to determine their potential implication in biomarker identification and therapeutic exploration.
C1 [Li, Chen; Ni, Yu-Qing; Xu, Hui; Xiang, Qun-Yan; Zhao, Yan; Zhan, Jun-Kun; He, Jie-Yu; Li, Shuang; Liu, You-Shuo] Cent South Univ, Xiangya Hosp 2, Dept Geriatr, Changsha 410011, Hunan, Peoples R China.
   [Li, Chen; Ni, Yu-Qing; Xu, Hui; Xiang, Qun-Yan; Zhao, Yan; Zhan, Jun-Kun; He, Jie-Yu; Li, Shuang; Liu, You-Shuo] Cent South Univ, Inst Aging & Age Related Dis Res, Changsha 410011, Hunan, Peoples R China.
C3 Central South University; Central South University
RP Liu, YS (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Geriatr, Changsha 410011, Hunan, Peoples R China.; Liu, YS (corresponding author), Cent South Univ, Inst Aging & Age Related Dis Res, Changsha 410011, Hunan, Peoples R China.
EM liuyoushuo@csu.edu.cn
OI Liu, Youshuo/0000-0001-9835-4074; Xiang, Qunyan/0009-0009-0315-2740
FU National Natural Science Foundation of China [82071593, 81770833,
   81974223, 82101663]; Fundamental Research Funds For the Central
   Universities of Central South University [2019zzts354]
FX This work was supported by the National Natural Science Foundation of
   China (No. 82071593, 81770833, 81974223, and 82101663); the Fundamental
   Research Funds For the Central Universities of Central South University
   (NO. 2019zzts354).
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NR 575
TC 243
Z9 253
U1 3
U2 89
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 2095-9907
EI 2059-3635
J9 SIGNAL TRANSDUCT TAR
JI Signal Transduct. Target. Ther.
PD NOV 10
PY 2021
VL 6
IS 1
AR 383
DI 10.1038/s41392-021-00779-x
PG 31
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA WU3FJ
UT WOS:000716433900001
PM 34753929
OA Green Published, gold
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Kalkan, EA
   Kalkan, C
   Gumussoy, M
   Gucbey, O
   Soykan, I
AF Kalkan, Emra Asfuroglu
   Kalkan, Cagdas
   Gumussoy, Mesut
   Gucbey, Ozge
   Soykan, Irfan
TI Prevalence and predictors of colonoscopic findings in patients with
   autoimmune gastritis
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Article
DE colonoscopy; autoimmune diseases; colorectal neoplasms
ID COLORECTAL-CANCER RISK; ATROPHIC GASTRITIS; HELICOBACTER-PYLORI;
   CELL-PROLIFERATION; PERNICIOUS-ANEMIA; INVITRO GROWTH; VITAMIN-B-12;
   PENTAGASTRIN
AB The clinical spectrum of autoimmune gastritis is silent in the early stages of the disease and no specific symptom is related to this entity. Although gastroscopic findings of this entity are well defined, data regarding colonoscopic findings are limited. The aims of this study were to determine the prevalence of colonoscopic findings and to explore factors that might affect these findings. This is a retrospective chart review of patients with autoimmune gastritis (n=240). Data regarding colonoscopic findings, serum gastrin and chromogranin A (CgA) levels and gastric histopathological results were extracted and compared with 550 patients positive for Helicobacter pylori and gastric atrophy. Control subjects had colonoscopy and gastroscopy with biopsies. Colorectal lesions were observed in 64 (26.6%) of patients with autoimmune gastritis and 36 (6.6%) patients had colorectal lesions in the control group (p<0.001). Serum gastrin (OR: 8.59, 95% CI 1.72 to 25.07, p<0.001) and CgA levels (OR: 6.79, 95% CI 0.41 to 27.26, p<0.001) were found as factors affecting the presence of colorectal carcinoma. Serum gastrin and CgA levels were also found as predictors for the presence of colorectal adenomas. There is a higher prevalence of colorectal neoplastic lesions in patients with autoimmune gastritis. Serum gastrin and CgA levels were found to be determinants of colorectal neoplastic lesions observed in patients. In the workup of these patients, serum gastrin and CgA levels may guide physicians for the demonstration of colorectal neoplastic lesions.
C1 [Kalkan, Emra Asfuroglu; Gucbey, Ozge] Ankara City Hosp, Dept Internal Med, Minist Hlth, Ankara, Turkey.
   [Kalkan, Cagdas] Ankara City Hosp, Gastroenterol, Ankara, Turkey.
   [Gumussoy, Mesut; Soykan, Irfan] Ankara Univ, Ibni Sina Hosp, Div Gastroenterol, Fac Med, TR-06100 Ankara, Turkey.
C3 Ministry of Health - Turkey; City Hospital Ankara; City Hospital Ankara;
   Ankara University
RP Soykan, I (corresponding author), Ankara Univ, Ibni Sina Hosp, Div Gastroenterol, Fac Med, TR-06100 Ankara, Turkey.
EM isoykan@medicine.ankara.edu.tr
RI Gümüşsoy, Mesut/IUP-2029-2023; soykan, irfan/KMD-7090-2024; Kalkan,
   Cagdas/AAD-7481-2020
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NR 34
TC 0
Z9 0
U1 0
U2 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1081-5589
EI 1708-8267
J9 J INVEST MED
JI J. Investigative Med.
PD JAN
PY 2022
VL 70
IS 1
BP 73
EP 78
DI 10.1136/jim-2021-001911
EA AUG 2021
PG 6
WC Medicine, General & Internal; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine; Research & Experimental Medicine
GA XY9PH
UT WOS:000725054000001
PM 34341100
DA 2025-06-01
ER

PT J
AU Wakiguchi, H
AF Wakiguchi, H
TI Overview of Epstein-Barr virus-associated diseases in Japan
SO CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY
LA English
DT Review
DE EBV-associated diseases; SCAEBV; PTLD; VAHS; GLPD; mosquito allergy;
   ALPS; gastric cancer; HCC
ID LINKED LYMPHOPROLIFERATIVE-DISEASE; PYOTHORAX-ASSOCIATED LYMPHOMA;
   POLYMERASE-CHAIN-REACTION; REED-STERNBERG CELLS; ACTIVE EBV INFECTION;
   HEMOPHAGOCYTIC SYNDROME; VIRAL-DNA; CLONAL LYMPHOPROLIFERATION;
   GASTRIC-CARCINOMA; MOSQUITO BITES
AB Epstein-Barr virus (EBV) associated diseases and studies performed in Japan are reviewed. Infectious mononucleosis is a common disease in Japanese infants. Chronic and severe EBV-infections include severe chronic active EBV-infection (SCAEBV), EBV-associated hemophagocytic syndrome, and mosquito allergy with granular lymphocyte proliferative disorder (GLPD). Autoimmune lymphoproliferative syndrome (ALPS), a disease caused by a defect in the Fas-Fas ligand pathway of cell-death, may develop into lymphoproliferative disease after early exposure to EBV. More than ten cases of X-linked lymphoproliferative syndrome (XLP) were discovered in Japanese children, and the frequency of post-transplant lymphoproliferative disorder (PTLD) increased after the number of patients receiving organ transplantation increased. Recently, an association of EBV with gastric carcinoma and hepatocellular carcinoma has been suggested. EBV-infected cells, such as B-cells, T-cells, NK-cells, and epithelial cells in EBV-associated diseases have also been clarified. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
C1 Kochi Med Sch, Dept Pediat, Nankoku, Kochi 7838505, Japan.
C3 Kochi University
RP Kochi Med Sch, Dept Pediat, Oko Cho, Nankoku, Kochi 7838505, Japan.
EM wakiguti/KMS@kochi-ms.ac.jp
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NR 72
TC 26
Z9 32
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1040-8428
EI 1879-0461
J9 CRIT REV ONCOL HEMAT
JI Crit. Rev. Oncol./Hematol.
PD DEC
PY 2002
VL 44
IS 3
BP 193
EP 202
AR PII S1040-8428(02)00111-7
DI 10.1016/S1040-8428(02)00111-7
PG 10
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 625CE
UT WOS:000179798700002
PM 12467960
DA 2025-06-01
ER

PT J
AU Go, MF
AF Go, MF
TI What are the host factors that place an individual at risk for
   Helicobacter pylori-associated disease?
SO GASTROENTEROLOGY
LA English
DT Article
ID BLOOD-GROUP ANTIGENS; GASTRIC EPITHELIUM; DUODENAL-ULCER; UNITED-STATES;
   SOCIOECONOMIC-STATUS; LYMPHOID-TISSUE; LEWIS-X; INFECTION; POPULATION;
   STRAINS
AB Helicobacter pylori infection is associated with duodenal and gastric ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma. Although more than half the world's population harbors H. pylori, only a proportion will develop clinically significant disease. The specific clinical outcome of an individual can be examined as the modulation of host factors by H. pylori infection. Host acid-secretory status and sensitivity to gastrin can be modulated by H. pylori infection. Once H. pylori has established itself in the stomach, virtually everyone develops gastritis, and variations in gastritis patterns have been associated with different gastric acid responses to H. pylori infection. The patterns of gastritis are important because they seem to determine disease outcome. Blood group antigens have been implicated in studies of ulcer disease. Receptors to Lewis antigens in gastric mucosa indicate that host mucosal factors influence H. pylori attachment. Conversely, H. pylori strains express Lewis antigen-like molecules, suggesting an autoimmune component for some H. pylori-associated diseases. HLA genotypes may influence the host response to H. pylori infection, and those of H. pylori-infected individuals have been correlated with histological features. The clinical outcome of H. pylori infection is most likely a result of complex interactions among host, bacterial, and environmental factors. The mechanisms by which these diverse factors influence the pathogenesis of different clinical outcomes remain under investigation.
RP Go, MF (corresponding author), VET AFFAIRS MED CTR,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA.
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NR 45
TC 73
Z9 78
U1 0
U2 1
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD DEC
PY 1997
VL 113
IS 6
SU S
BP S15
EP S20
DI 10.1016/S0016-5085(97)80005-4
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA YJ608
UT WOS:A1997YJ60800005
PM 9394754
DA 2025-06-01
ER

PT J
AU Taniuchi, K
   Takata, M
   Matsui, C
   Fushida, Y
   Uchiyama, K
   Mori, T
   Kawara, S
   Yancey, KB
   Takehara, K
AF Taniuchi, K
   Takata, M
   Matsui, C
   Fushida, Y
   Uchiyama, K
   Mori, T
   Kawara, S
   Yancey, KB
   Takehara, K
TI Antiepiligrin (laminin 5) cicatricial pemphigoid associated with an
   underlying gastric carcinoma producing laminin 5
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Article
DE antibasement membrane zone antibodies; epiligrin; gastric carcinoma;
   laminin 5 cicatricial pemphigoid
ID EPIDERMAL BASEMENT-MEMBRANE; ANCHORING FILAMENTS; AUTOANTIBODIES;
   EPILIGRIN; DISEASE; IMMUNOFLUORESCENT; SUBUNITS; TARGET; CELLS
AB Although bullous pemphigoid and cicatricial pemphigoid are sometimes associated with malignancy, it remains uncertain whether such an association is pathogenetically related or just a coincidence attributable to the advanced age of the patients, We report a 61-year-old patient with antiepiligrin (laminin 5) cicatricial pemphigoid (AeCP) associated with an advanced gastric carcinoma. The gastric carcinoma cells in this patient were shown to produce laminin 5 by immunofluorescence microscopy, and the patient's serum contained autoantibodies directed against laminin 5 on immunoprecipitation. Furthermore, the blistering symptoms and the titre of antibasement membrane zone antibodies coordinately changed with the resection and subsequent relapse of the gastric cancer. These observations suggest that the gastric carcinoma producing laminin 5 may have induced the production of autoantibodies to this laminin, which were pathogenic to the skin and mucous membranes in this patient. This report demonstrates a link between this autoimmune subepithelial blistering disease and malignancy. It is of interest and potential great importance to examine other cases of AeCP for such a potential association.
C1 Kanazawa Univ, Sch Med, Dept Dermatol, Kanazawa, Ishikawa 9208641, Japan.
   Kanazawa Univ, Sch Med, Dept Surg 2, Kanazawa, Ishikawa 9208641, Japan.
   Kanazawa Univ, Sch Med, Dept Ophthalmol, Kanazawa, Ishikawa 9208641, Japan.
   Toyama Med & Pharmaceut Univ, Fac Med, Dept Dermatol, Toyama 93001, Japan.
   NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
C3 Kanazawa University; Kanazawa University; Kanazawa University;
   University of Toyama; National Institutes of Health (NIH) - USA; NIH
   National Cancer Institute (NCI)
RP Taniuchi, K (corresponding author), Kanazawa Univ, Sch Med, Dept Dermatol, 13-1 Takara Machi, Kanazawa, Ishikawa 9208641, Japan.
RI Takata, Minoru/K-3772-2019; Yancey, Kim/AIC-0005-2022
OI Yancey, Kim/0000-0001-6101-4690
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NR 21
TC 35
Z9 36
U1 0
U2 1
PU BLACKWELL SCIENCE LTD
PI OXFORD
PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND
SN 0007-0963
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD APR
PY 1999
VL 140
IS 4
BP 696
EP 700
PG 5
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA 189VD
UT WOS:000079926100021
PM 10233324
DA 2025-06-01
ER

PT J
AU Arnold, R
AF Arnold, Rudolf
TI Diagnosis and differential diagnosis of hypergastrinemia
SO WIENER KLINISCHE WOCHENSCHRIFT
LA English
DT Article
DE hypergastrinemia; Zollinger-Ellison syndrome; chronic atrophic
   gastritis; type A gastritis
ID ZOLLINGER-ELLISON-SYNDROME; SERUM GASTRIN-LEVELS; HELICOBACTER-PYLORI;
   CELL HYPERPLASIA; SOMATOSTATIN; SECRETION; OMEPRAZOLE; ENDOCRINE;
   EFFICACY; DISEASE
AB The most frequent conditions of hypergastrinemia in man are the Zollinger-Ellison syndrome with autonomous gastrin hypersecretion by the tumour cell and reactive hypergastrinemia in type A autoimmune chronic atrophic gastritis with achlorhydria causing unrestrained gastrin release from the gastrin-producing antral G-cells. Both entities differ with respect to the pH in the gastric fluid, which is < 2 in patients with Zollinger-Ellison syndrome and neutral in type A gastritis. Other conditions with moderate hypergastrinemia as treatment with proton pump inhibitors, gastric outlet obstruction, previous vagotomy, chronic renal failure or short bowel syndrome are of minor clinical importance.
C1 Univ Marburg, Klin Innere Med Schwerpunkt Gastroenterol & Endok, Klinikum Giessen Marburg Standort Marburg, Marburg, Germany.
C3 Philipps University Marburg
RP Arnold, R (corresponding author), Wittelsbacherstr 6, D-80469 Munich, Germany.
EM arnoldr@mailer.uni-marburg.de
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NR 18
TC 26
Z9 26
U1 0
U2 1
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0043-5325
J9 WIEN KLIN WOCHENSCHR
JI Wien. Klin. Wochen.
PD NOV
PY 2007
VL 119
IS 19-20
BP 564
EP 569
DI 10.1007/s00508-007-0878-0
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 228II
UT WOS:000250723200002
PM 17985088
DA 2025-06-01
ER

PT J
AU Mitsinikos, T
   Shillingford, N
   Cynamon, H
   Bhardwaj, V
AF Mitsinikos, Tania
   Shillingford, Nick
   Cynamon, Harry
   Bhardwaj, Vrinda
TI Autoimmune Gastritis in Pediatrics: A Review of 3 Cases
SO JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION
LA English
DT Review
DE autoimmune gastritis; diabetes mellitus; gastrin; iron-deficiency anemia
ID ATROPHIC GASTRITIS; PARIETAL-CELL; THYROIDITIS; ANEMIA
AB Objectives: To bring heightened awareness to a condition, autoimmune gastritis (AIG), which is a well-established entity in adults; however, rarely described in pediatrics. Currently, the literature describes AIG in pediatric patients who also suffer from other autoimmune disorders, which precedes the diagnosis of AIG, and often presents with unexplained anemia. Additionally, there have been case reports describing patients with immunodeficiencies and AIG, which progress to gastric adenocarcinoma. AIG is a histopathologic diagnosis, demonstrating chronic inflammatory process with loss of parietal cells with or without intestinal metaplasia and enterochromaffin-like cell hyperplasia. Management of these patients includes nutritional replacement as well as routine surveillance endoscopy with biopsy in search of metaplastic and dysplastic changes. Methods: We queried the pathology database at Children's Hospital Los Angeles (CHLA) for cases with a final diagnosis of AIG and for those with a differential diagnosis that includes AIG in the diagnostic comment. All cases that were identified were selected as long as they did not only meet the histopathologic criteria, but also the biochemical criteria for this condition. Results: Of the 3 patients, 2 were referred to gastroenterology for the evaluation of iron-deficiency anemia in the context of diabetes mellitus and Addison's disease; and diabetes mellitus and Hashimoto's thyroiditis. AIG was confirmed on the biopsies, which showed a reduction in parietal cell mass, pseudopyloric metaplasia and enterochromafin-like cell hyperplasia. Both patients were treated with iron replacement therapy. The third patient presented with symptomatic anemia and diagnosed with pernicious anemia without other autoimmune disorders. She was successfully treated with oral vitamin supplementation. In this case, serial gastric biopsies demonstrated stable intestinal metaplasia without evidence of dysplasia. Conclusion: Although AIG is rare in children, pediatric gastroenterologists and pathologists should have a heightened suspicion for this entity in those patients with a history of autoimmune disorders and/or pernicious anemia.
C1 [Mitsinikos, Tania; Cynamon, Harry; Bhardwaj, Vrinda] Childrens Hosp Los Angeles, Div Gastroenterol Hepatol & Nutr, Keck Sch Med USC, Los Angeles, CA 90027 USA.
   [Shillingford, Nick] Childrens Hosp Los Angeles, Keck Sch Med USC, Dept Pathol & Lab Med, Los Angeles, CA 90027 USA.
C3 Children's Hospital Los Angeles; Children's Hospital Los Angeles
RP Mitsinikos, T (corresponding author), Childrens Hosp Los Angeles, Div Pediat Gastroenterol Hepatol & Nutr, 4650W Sunset Blvd,Mailstop 78, Los Angeles, CA 90027 USA.
EM fmitsinikos@chla.usc.edu
RI Bhardwaj, Vrinda/GLR-1727-2022
FU Alexion Pharmaceuticals, Inc.
FX T.M. has been provided with research support in the way of research
   coordinator and statistical analysis support through Alexion
   Pharmaceuticals, Inc. No direct financial support was provided. The
   remainder of the authors have no other potential conflicts of interest
   to report.
CR Cavalcoli F, 2017, WORLD J GASTROENTERO, V23, P563, DOI 10.3748/wjg.v23.i4.563
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NR 22
TC 5
Z9 5
U1 1
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0277-2116
EI 1536-4801
J9 J PEDIATR GASTR NUTR
JI J. Pediatr. Gastroenterol. Nutr.
PD FEB
PY 2020
VL 70
IS 2
BP 252
EP 257
DI 10.1097/MPG.0000000000002547
PG 6
WC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Nutrition & Dietetics; Pediatrics
GA NC7BR
UT WOS:000561371200031
PM 31978028
OA Bronze
DA 2025-06-01
ER

PT J
AU Lin, KD
   Chiu, GF
   Waljee, AK
   Owyang, SY
   El-Zaatari, M
   Bishu, S
   Grasberger, H
   Zhang, M
   Wu, DC
   Kao, JY
AF Lin, Kun-Der
   Chiu, Guei-Fen
   Waljee, Akbar K.
   Owyang, Stephanie Y.
   El-Zaatari, Mohamad
   Bishu, Shrinivas
   Grasberger, Helmut
   Zhang, Min
   Wu, Deng-Chyang
   Kao, John Y.
TI Effects of Anti-Helicobacter pylori Therapy on Incidence of
   Autoimmune Diseases, Including Inflammatory Bowel Diseases
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Eradication; Autoimmunity; Immune Response; Bacteria
ID GASTRIC-CANCER; INFECTION; PREVALENCE; RISK; ASSOCIATION; COLONIZATION;
   ERADICATION; COLITIS; ASTHMA; CROHNS
AB BACKGROUND & AIMS: Helicobacter pylori induces immune tolerance and is associated with a lower risk for immune- mediated disorders, such as autoimmune and inflammatory bowel diseases (IBD). We aimed to determine the effects of treatment for H pylori infection on the incidence of autoimmune disease and IBD.
   METHODS: We collected data from the National Health Insurance Research Database in Taiwan on patients younger than 18 years old without a prior diagnosis of autoimmune disease or IBD. Patients with peptic ulcer disease (PUD) with treatment of H pylori infection (PUD + HPRx), PUD without H pylori treatment (PUD-HPRx), a urinary tract infection (UTI) treated with cephalosporin, or without PUD (controls) were matched for age, sex, insurance, and Charlson's comorbidity index score.
   RESULTS: Of the 1 million patients we collected data from in 2005, we included 79,181 patients in the study. We compared the effects of treatment for H pylori infection on the risk of autoimmunity or IBD and found that PUD + HPRx has the highest adjusted hazard risk (aHR) for autoimmunity or IBD (aHR, 2.36), compared to PUD-HPRx (aHR, 1.91) or UTI (aHRs, 1.71) (P < .001). The increased risk of autoimmune disease was not completely accounted for by antibiotic therapy alone, because PUD + HPRx had a higher aHR than UTI (P < .001). A small but significant increase in mortality was observed in the PUD + HPRx cohort (aHR, 1.11; P = .001).
   CONCLUSION: In an analysis of data from the National Health Insurance Research Database in Taiwan, we found that treatment for H pylori infection is associated with a significant increase in the risk for autoimmune disease, including IBD.
C1 [Lin, Kun-Der] Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Kaohsiung Municipal Ta Tung Hosp, Dept Internal Med,Coll Med, Kaohsiung, Taiwan.
   [Chiu, Guei-Fen; Wu, Deng-Chyang] Kaohsiung Municipal Tatung Hosp, Div Gastroenterol, Kaohsiung, Taiwan.
   [Chiu, Guei-Fen; Wu, Deng-Chyang] Kaohsiung Municipal Tatung Hosp, Dept Internal Med, Kaohsiung, Taiwan.
   [Waljee, Akbar K.] Vet Affairs Ctr Clin Management Res, Ann Arbor, MI USA.
   [Waljee, Akbar K.; Owyang, Stephanie Y.; El-Zaatari, Mohamad; Bishu, Shrinivas; Grasberger, Helmut; Zhang, Min; Kao, John Y.] Univ Michigan, Dept Internal Med, Div Gastroenterol, Michigan Med, Ann Arbor, MI 48109 USA.
C3 Kaohsiung Medical University; Kaohsiung Medical University Hospital;
   Kaohsiung Municipal Ta-Tung Hospital; Kaohsiung Medical University;
   Kaohsiung Municipal Ta-Tung Hospital; Kaohsiung Medical University;
   Kaohsiung Municipal Ta-Tung Hospital; University of Michigan System;
   University of Michigan
RP Kao, JY (corresponding author), Univ Michigan Hlth Syst, Dept Internal Med, Div Gastroenterol, 6520A MSRB I,SPC 5682,1150 West Med Ctr Dr, Ann Arbor, MI 48109 USA.; Wu, DC (corresponding author), Kaohsiung Med Univ Hosp, Dept Internal Med, Div Gastroenterol, 100 Zih You 1st Rd, Kaohsiung, Taiwan.
EM dechwu@yahoo.com; johnkao-GI@med.umich.edu
RI Bishu, Shrinivas/S-6084-2019; Grasberger, Helmut/C-4148-2015; Waljee,
   Akbar K./G-2067-2010
OI Owyang, Stephanie/0000-0001-8824-2300; Grasberger,
   Helmut/0000-0002-4065-4418; Waljee, Akbar K./0000-0003-1964-8790; Lin,
   Kun-Der/0000-0003-1148-5915; Bishu, Shrinivas/0000-0003-4823-5805
FU National Institute of Diabetes and Digestive and Kidney Diseases of the
   National Institutes of Health [R01 DK087708-01]
FX This work was supported by the National Institute of Diabetes and
   Digestive and Kidney Diseases of the National Institutes of Health under
   award number R01 DK087708-01 (to John Y. Kao). Its contents are solely
   the responsibility of the authors and do not necessarily represent the
   official views of the National Institutes of Health.
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NR 32
TC 54
Z9 57
U1 0
U2 17
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD SEP
PY 2019
VL 17
IS 10
BP 1991
EP 1999
DI 10.1016/j.cgh.2018.12.014
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IS5UE
UT WOS:000482217300021
PM 30580094
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Yamane, T
   Eto, K
   Morinaga, T
   Matsumura, K
   Yamashita, K
   Tokunaga, R
   Harada, K
   Hiyoshi, Y
   Nagai, Y
   Iwatsuki, M
   Iwagami, S
   Miyamoto, Y
   Yoshida, N
   Baba, H
AF Yamane, Taishi
   Eto, Kojiro
   Morinaga, Takeshi
   Matsumura, Kazuki
   Yamashita, Kohei
   Tokunaga, Ryuma
   Harada, Kazuto
   Hiyoshi, Yukiharu
   Nagai, Yohei
   Iwatsuki, Masaki
   Iwagami, Shiro
   Miyamoto, Yuji
   Yoshida, Naoya
   Baba, Hideo
TI IgG4-related disease presenting as a submucosal tumor of the stomach
   resected with laparoscopic endoscopic cooperative surgery: a case report
SO SURGICAL CASE REPORTS
LA English
DT Article
DE Submucosal tumor of the stomach; IgG4-related disease (IgG4-RD);
   Laparoscopic endoscopic cooperative surgery (LECS)
AB BackgroundIgG4-related disease (IgG4-RD) is an immune-mediated disorder in which abundant IgG4-positive plasma cells infiltrate affected organs. There have been reported four cases of probable IgG4-RD presenting as a submucosal tumor of the stomach. We herein report the first case of definite IgG4-RD presenting as a submucosal tumor of the stomach resected with laparoscopic endoscopic cooperative surgery (LECS).Case presentationA 70-year-old woman with a 6-year history of autoimmune pancreatitis was referred to our department because a 15-mm submucosal tumor in the greater curvature of the lower part of the stomach had been identified via upper gastrointestinal endoscopy. Endoscopic ultrasonography showed a 10-mm low-echoic lesion derived from the submucosal layer of the stomach. A fine-needle aspiration biopsy was attempted, but the tumor was too hard for sampling. F-fluorodeoxyglucose (FDG) positron emission tomography showed an FDG uptake, suggesting a possibility of malignant disease. As the diagnosis could not be confirmed, LECS for both the diagnosis and curative treatment was performed. A histopathological examination showed a tumor with IgG4-positive lymphoplasmacytic infiltration and fibrosis. The ratio of IgG4+/IgG+ lymphoplasmacytic cells was > 80%. A laboratory examination showed elevation of the serum IgG4 levels preoperatively. Thus, the final diagnosis was IgG4-RD of the stomach. No recurrence was observed within 1 year after surgery.ConclusionsWe encountered a case of definite IgG4-RD presenting as a gastric SMT in which a correct diagnosis was achieved by a minimally invasive LECS technique. IgG4-RD may present as a gastric lesion and should be taken into consideration as a differential diagnosis.
C1 [Yamane, Taishi; Eto, Kojiro; Morinaga, Takeshi; Matsumura, Kazuki; Yamashita, Kohei; Tokunaga, Ryuma; Harada, Kazuto; Hiyoshi, Yukiharu; Nagai, Yohei; Iwatsuki, Masaki; Iwagami, Shiro; Miyamoto, Yuji; Yoshida, Naoya; Baba, Hideo] Kumamoto Univ, Grad Sch Life Sci, Dept Gastroenterol Surg, 1-1-1 Honjo, Kumamoto 8608556, Japan.
C3 Kumamoto University
RP Baba, H (corresponding author), Kumamoto Univ, Grad Sch Life Sci, Dept Gastroenterol Surg, 1-1-1 Honjo, Kumamoto 8608556, Japan.
EM hdobaba@kumamoto-u.ac.jp
CR Hanaoka M, 2017, ADV MED SCI-POLAND, V62, P393, DOI 10.1016/j.advms.2017.04.001
   Hiki N, 2015, DIGEST ENDOSC, V27, P197, DOI 10.1111/den.12404
   Lopes J, 2010, J GASTROINTEST SURG, V14, P1031, DOI 10.1007/s11605-010-1172-4
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   Takano K, 2017, AURIS NASUS LARYNX, V44, P7, DOI 10.1016/j.anl.2016.10.011
NR 5
TC 14
Z9 14
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 2198-7793
J9 SURG CASE REP
JI SURG. CASE REP.
PD MAY 7
PY 2020
VL 6
IS 1
DI 10.1186/s40792-020-00851-8
PG 4
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA LP0PV
UT WOS:000534025000001
PM 32382972
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Niess, JH
   Hruz, P
   Kaymak, T
AF Niess, Jan Hendrik
   Hruz, Petr
   Kaymak, Tanay
TI The Interleukin-20 Cytokines in Intestinal Diseases
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE Interleukin-20 family; macrophages; eosinophilic esophagitis; Crohn's
   disease; ulcerative colitis; colorectal cancer
ID INFLAMMATORY-BOWEL-DISEASE; INNATE LYMPHOID-CELLS; GASTRIC-CANCER CELLS;
   HOST-DEFENSE; ULCERATIVE-COLITIS; EPITHELIAL-CELLS; CROHNS-DISEASE;
   CUTTING EDGE; HELICOBACTER-PYLORI; TISSUE HOMEOSTASIS
AB Autoimmune/inflammatory intestinal diseases, such as Crohn's disease and ulcerative colitis, infectious gastrointestinal diseases, and gastrointestinal cancers, such as colorectal cancer, are worldwide a significant health problem. Intercellular communication and direct contact with the environment as the microbiota colonizes the gastrointestinal surface facilitates these diseases. Cytokines mediate the intercellular communication to maintain the equilibrium between host and environment and to regulate immune responses. One cytokine family that exchange information between immune cells and epithelial cells is the IL-20 cytokine family which includes the cytokines IL-19, IL-20, IL-22, IL-24, and IL-26. These cytokines share common receptor subunits and signaling pathways. IL-22 is the most intensively studied cytokine within this family in contexts of gastrointestinal disease, but the importance of other family members is more and more appreciated. In this review, the potential function of IL-20 cytokines concerning gastrointestinal conditions is discussed.
C1 [Niess, Jan Hendrik; Kaymak, Tanay] Univ Basel, Dept Biomed, Basel, Switzerland.
   [Niess, Jan Hendrik; Hruz, Petr] Univ Hosp Basel, Dept Gastroenterol & Hepatol, Basel, Switzerland.
C3 University of Basel; University of Basel
RP Niess, JH (corresponding author), Univ Basel, Dept Biomed, Basel, Switzerland.; Niess, JH (corresponding author), Univ Hosp Basel, Dept Gastroenterol & Hepatol, Basel, Switzerland.
EM janhendrik.niess@usb.ch
RI Hruz, Petr/F-1406-2011; Niess, Jan/E-8361-2017
OI Niess, Jan/0000-0001-6902-5650; Hruz, Petr/0000-0003-2767-0445
FU SNSF [310030_146290]; Swiss National Science Foundation (SNF)
   [310030_146290] Funding Source: Swiss National Science Foundation (SNF)
FX This work is supported by the SNSF grant 310030_146290 to JN.
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NR 86
TC 37
Z9 38
U1 0
U2 10
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUN 18
PY 2018
VL 9
AR 1373
DI 10.3389/fimmu.2018.01373
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GJ6LK
UT WOS:000435495400001
PM 29967613
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Kandulski, A
   Malfertheiner, P
   Wex, T
AF Kandulski, Arne
   Malfertheiner, Peter
   Wex, Thomas
TI Role of Regulatory T-cells in H. pylori-induced Gastritis
   and Gastric Cancer
SO ANTICANCER RESEARCH
LA English
DT Review
DE FOXP3; regulatory T-cells; Treg-cells; gastric cancer; review
ID DUODENAL-ULCER PATIENTS; HELICOBACTER-PYLORI; AUTOIMMUNE-DISEASE; NKT
   CELLS; GENE POLYMORPHISMS; MOLECULAR-BIOLOGY; IMMUNE-RESPONSE;
   HELPER-CELLS; PEPTIC-ULCER; IN-VIVO
AB The current model of gastric carcinogenesis comprises the interaction of multiple risk factors. Besides Helicobacter pylori (H. pylori) infection as the major risk factor for gastric carcinogenesis, environmental factors (e.g. high saline- or nitrosamine-containing food) and genetic susceptibility contribute to the development of gastric cancer (GC). It has been established that the topographical pattern of gastritis and its immune response are the main causes for the persistence of bacteria and the final clinical outcome. Regulatory immune cells, mostly regulatory FOXP3(+)CD4(+)CD25(+high) T-cells (Treg cells), have been identified as the major regulatory component of the adaptive immune response and involved in H. pylori-related inflammation and bacterial persistence. The functional activity of these cells is either mediated by direct cell-cell contact or by the secretion of the immune-modulating cytokines TGF-beta I and IL-10. Based on the differentiation process, Treg cells comprise various lineages that differ in the expression of cell surface marker and pattern of secreted cytokines. Numerous studies have demonstrated important functions of Treg cells for controlling acute and chronic inflammatory processes. This paper reviews the role of Treg for gastric carcinogenesis and precursor lesions related to H. pylori.
C1 [Kandulski, Arne; Malfertheiner, Peter; Wex, Thomas] Otto VonGuericke Univ Magdegurg, Dept Gastroenterol Hepatol & Infect Dis, D-39120 Magdeburg, Germany.
C3 Otto von Guericke University
RP Wex, T (corresponding author), Otto VonGuericke Univ Magdegurg, Dept Gastroenterol Hepatol & Infect Dis, Leipziger Str 44, D-39120 Magdeburg, Germany.
EM thomas.wex@med.ovgu.de
RI Kandulski, Arne/AAV-3681-2020; Malfertheiner, Peter/AEZ-6553-2022
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NR 104
TC 49
Z9 55
U1 0
U2 8
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD APR
PY 2010
VL 30
IS 4
BP 1093
EP 1103
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 609VS
UT WOS:000278686600008
PM 20530414
DA 2025-06-01
ER

PT J
AU Khalaf, K
   Fujiyoshi, Y
   Bechara, R
AF Khalaf, Kareem
   Fujiyoshi, Yusuke
   Bechara, Robert
TI Endoscopic and clinical characteristics of autoimmune atrophic
   gastritis: Retrospective study
SO ENDOSCOPY INTERNATIONAL OPEN
LA English
DT Article
DE Endoscopy Upper GI Tract; Precancerous conditions & cancerous lesions
   (displasia and cancer) stomach; Diagnosis and imaging (inc
   chromoendoscopy, NBI, iSCAN, FICE, CLE)
ID PATHOGENESIS; PATHOLOGY
AB Background and study aims Autoimmune atrophic gastritis (AIG) is a rare chronic autoimmune disease characterized by gastric mucosa inflammation and atrophy. Limited clinical data exist about AIG, especially in western populations. In addition, there are no western series on the magnifying endoscopic features in AIG. This study presents a cohort of 63 patients with AIG, reporting their clinical, laboratory, and endoscopic findings. Patients and methods A retrospective analysis was conducted on patients diagnosed with AIG at Kingston Health Sciences Centre, Canada, between January 2016 and December 2023. Data collected from medical records included age, sex, presenting symptoms, laboratory findings, endoscopic features, histopathology reports, and concomitant autoimmune diseases. Results The study included 63 patients with autoimmune gastritis. Positive anti-parietal cell antibodies were found in the majority of patients (84.13%), whereas positive anti-intrinsic factor antibodies were less prevalent (25.40%). Deficiencies in vitamin B12 (49.21%) and iron (76.19%) were observed, along with a high prevalence of anemia (71.43%) and concomitant autoimmune diseases (58.73%). The dominant magnification pattern of atrophy in the body was oval/slit in 57.14% of patients (n=36), followed by tubular in 30.16% (n=19) and foveolar in 12.70% (n=8). Prevalence of neoplasia in our study was 42.86% (n=27). Conclusion This study offers insights into the clinical, laboratory, and magnifying endoscopic features of patients with AIG. It demonstrates the three main magnifying endoscopic appearances of AIG and highlights the significant prevalence of gastric neoplasia, even in the low-risk Western population. These findings emphasize the importance of the endoscopic exam in identifying AIG and notably present the key magnifying endoscopy findings in a Western setting for the first time.
C1 [Khalaf, Kareem] St Michaels Hosp, Div Gastroenterol, Toronto, ON, Canada.
   [Fujiyoshi, Yusuke] Univ Ottawa, Ottawa Hosp, Ottawa Hosp Fdn, Div Gastroenterol, Ottawa, ON, Canada.
   [Bechara, Robert] Kingston Hlth Sci Ctr, Gastroenterol, Kingston, ON, Canada.
C3 University of Toronto; Saint Michaels Hospital Toronto; University of
   Ottawa; Ottawa Hospital Research Institute
RP Bechara, R (corresponding author), Kingston Hlth Sci Ctr, Gastroenterol, Kingston, ON, Canada.
EM bechara.robert@gmail.com
RI Fujiyoshi, Yusuke/AAK-2630-2021
OI Khalaf, Kareem/0000-0002-5534-7533; Fujiyoshi,
   Yusuke/0000-0002-5893-6552; Bechara, Robert/0000-0002-4543-5580
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NR 33
TC 0
Z9 0
U1 0
U2 0
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA Oswald-Hesse-Strasse 50, D-70469 STUTTGART, GERMANY
SN 2364-3722
EI 2196-9736
J9 ENDOSC INT OPEN
JI Endosc. Int. Open
PD JAN 7
PY 2025
VL 13
AR a24774666
DI 10.1055/a-2477-4666
PG 8
WC Gastroenterology & Hepatology; Surgery
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology; Surgery
GA R9T3Q
UT WOS:001394775000005
PM 40012571
OA gold
DA 2025-06-01
ER

PT J
AU Rau, TT
   Sonst, A
   Rogler, A
   Burnat, G
   Neumann, H
   Oeckl, K
   Neuhuber, W
   Dimmler, A
   Faller, G
   Brzozowski, T
   Hartmann, A
   Konturek, PC
AF Rau, T. T.
   Sonst, A.
   Rogler, A.
   Burnat, G.
   Neumann, H.
   Oeckl, K.
   Neuhuber, W.
   Dimmler, A.
   Faller, G.
   Brzozowski, T.
   Hartmann, A.
   Konturek, P. C.
TI GASTRIN MEDIATED DOWN REGULATION OF GHRELIN AND ITS PATHOPHYSIOLOGICAL
   ROLE IN ATROPHIC GASTRITIS
SO JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
LA English
DT Article
DE ghrelin; gastrin; autoimmune gastritis; gastric cancer; Helicobacter
   pylori; gastrin/cholecystokinin receptor; enterochromaffin-like cells
ID INDUCED GASTROPROTECTION; ACYLATED PEPTIDE; ACID-SECRETION; STOMACH;
   HUMANS; CELLS; ACTIVATION; EXPRESSION; REDUCTION; INTESTINE
AB The gastric hormone ghrelin is known as an important factor for energy homeostasis, appetite regulation and control of body weight. So far, ghrelin has mainly been examined as a serological marker for gastrointestinal diseases, and only a few publications have highlighted its role in local effects like mucus secretion. Ghrelin can be regarded as a gastroprotective factor, but little is known about the distribution and activity of ghrelin cells in pathologically modified tissues. We aimed to examine the morphological changes in ghrelin expression under several inflammatory, metaplastic and carcinogenic conditions of the upper gastrointestinal tract. In particular, autoimmune gastritis showed interesting remodeling effects in terms of ghrelin expression within neuroendocrine cell hyperplasia by immunohistochemistry. Using confocal laser microscopy, the gastrin/cholecystokinin receptor (CCKB) could be detected on normal ghrelin cells as Well as in autoimmune gastritis. Functionally, we found evidence for a physiological interaction between gastrin and ghrelin in a primary rodent cell culture model. Additionally, we gathered serological data from patients with different basic gastrin levels due to long-term autoimmune gastritis or short-term proton pump inhibitor treatment with slightly reactive plasma gastrin elevations. Total ghrelin plasma levels showed a significantly inverse correlation with gastrin under long-term conditions. Autoimmune gastritis as a relevant condition within gastric carcinogenesis therefore has two effects on ghrelin-positive cells due to hypergastrinemia. On the one hand, gastrin stimulates the proliferation of ghrelin-positive cells as integral part of neuroendocrine cell hyperplasia, while on the other hand, plasma ghrelin is reduced by gastrin and lost in pseudopyloric and intestinal metaplastic areas. Ghrelin is necessary for the maintenance of the mucosal barrier and might play a role in gastric carcinogenesis, if altered under these pre neoplastic conditions.
C1 [Rau, T. T.; Sonst, A.; Hartmann, A.] Univ Erlangen Nurnberg, Inst Pathol, Erlangen, Germany.
   [Burnat, G.; Neumann, H.] Univ Erlangen Nurnberg, Dept Med 1, Erlangen, Germany.
   [Oeckl, K.] Univ Erlangen Nurnberg, Dept Surg, Erlangen, Germany.
   [Neuhuber, W.] Univ Erlangen Nurnberg, Inst Anat, Erlangen, Germany.
   [Dimmler, A.; Faller, G.] St Vincentius Hosp, Inst Pathol, Karlsruhe, Germany.
   [Brzozowski, T.] Jagiellonian Univ, Coll Med, Dept Physiol, Krakow, Poland.
   [Konturek, P. C.] Univ Jena, Teaching Hosp, Thuringia Clin Saalfeld, Dept Med, Saalfeld Saale, Germany.
C3 University of Erlangen Nuremberg; University of Erlangen Nuremberg;
   University of Erlangen Nuremberg; University of Erlangen Nuremberg;
   Jagiellonian University; Collegium Medicum Jagiellonian University;
   Friedrich Schiller University of Jena
RP Rau, TT (corresponding author), Univ Hosp Erlangen, Inst Pathol, Krankenhausstr 8-10, D-91054 Erlangen, Germany.
EM Tilman.Rau@uk-erlangen.de
OI /0000-0002-2300-0850
FU Bavarian Society for Gastroenterology; Interdisciplinary Centre for
   Clinical Research (IZKF) Erlangen
FX The study was supported by grants from the Bavarian Society for
   Gastroenterology and the Interdisciplinary Centre for Clinical Research
   (IZKF) Erlangen. We are grateful to Prof. Prinz, 2nd Department of
   Internal Medicine, Technical University Munich, Germany, who helped us
   to establish the primary culture techniques. Furthermore, we thank Katja
   Sesselmann and Angela Neumann for the excellent technical assistance.
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NR 34
TC 16
Z9 17
U1 0
U2 7
PU POLISH PHYSIOLOGICAL SOC
PI GRZEGORZECKA
PA JAGIELLONIAN UNIV SCHOOL MED, INST PHYSIOLOGY, 31-531 KRAKOW, 16
   GRZEGORZECKA, POLAND
SN 0867-5910
J9 J PHYSIOL PHARMACOL
JI J. Physiol. Pharmacol.
PD DEC
PY 2013
VL 64
IS 6
BP 719
EP 725
PG 7
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 296QI
UT WOS:000330200100005
PM 24388886
DA 2025-06-01
ER

PT J
AU Massironi, S
   Cavalcoli, F
   Zilli, A
   Del Gobbo, A
   Ciafardini, C
   Bernasconi, S
   Felicetta, I
   Conte, D
   Peracchi, M
AF Massironi, Sara
   Cavalcoli, Federica
   Zilli, Alessandra
   Del Gobbo, Alessandro
   Ciafardini, Clorinda
   Bernasconi, Susanna
   Felicetta, Irene
   Conte, Dario
   Peracchi, Maddalena
TI Relevance of vitamin D deficiency in patients with chronic autoimmune
   atrophic gastritis: a prospective study
SO BMC GASTROENTEROLOGY
LA English
DT Article
DE Chronic autoimmune atrophic gastritis; Vitamin D deficiency; Gastric
   carcinoid; Bone health; Osteoporosis
ID PERNICIOUS-ANEMIA; IRON-DEFICIENCY; CALCIUM-ABSORPTION; RISK;
   CLASSIFICATION; BREAST; CANCER; ACHLORHYDRIA; OSTEOPOROSIS; PROGRESSION
AB BackgroundChronic autoimmune atrophic gastritis (CAAG) is an autoimmune disease characterized by hypo/achlorhydria. A role of CAAG in the pathogenesis of nutritional deficiencies has been reported, therefore we hypothesized a possible association between CAAG and 25-OH-Vitamin D [25(OH)D] deficiency. Aim of the present study is to evaluate the prevalence of 25(OH)D deficiency in CAAG patients. Methods: 87 CAAG patients (71 females; mean age 63.512.8years) followed at our Centre from January 2012 to July 2015 were consecutively evaluated. 25(OH)D, vitamin B-12, parathormone, and calcium were measured in all the CAAG patients. The results were compared with a control group of 1232 healthy subjects.ResultsIn the CAAG group the mean 25(OH)D levels were significantly lower than in the control group (18.8 vs. 27.0ng/ml, p<0.0001). 25(OH)D levels <20ng/ml was observed in 57 patients, while levels <12.5ng/ml in 27 patients. A significant correlation between vitamin B-12 values at diagnosis and 25(OH)D levels was observed (r(s)=0.25, p=0.01). Interestingly, the CAAG patients with moderate/severe gastric atrophy had lower 25(OH)D values as compared to those with mild atrophy (11.8 vs. 20ng/ml; p=0.0047). Moreover, the 25(OH)D levels were significantly lower in CAAG patients with gastric carcinoid as compared to those without gastric carcinoid (11.8 vs. 19.8ng/ml; p=0,0041).Conclusion p id=Par3 Data from the present study showed a significant reduction of 25(OH)D levels in CAAG patients and a possible impairment of vitamin D absorption in CAAG may be postulated. Any implication to the genesis of gastric carcinoids remains to be elucidated.
C1 [Massironi, Sara; Cavalcoli, Federica; Zilli, Alessandra; Ciafardini, Clorinda; Bernasconi, Susanna; Conte, Dario; Peracchi, Maddalena] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, Milan, Italy.
   [Cavalcoli, Federica; Zilli, Alessandra] Univ Milan, Dept Pathophysiol & Transplantat, Milan, Italy.
   [Del Gobbo, Alessandro] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Div Pathol, I-20122 Milan, Italy.
   [Felicetta, Irene] Fdn IRCCS Ca Granda Osped Maggiore Policlin, Lab Clin Chem & Microbiol, Milan, Italy.
C3 IRCCS Ca Granda Ospedale Maggiore Policlinico; University of Milan;
   IRCCS Ca Granda Ospedale Maggiore Policlinico; IRCCS Ca Granda Ospedale
   Maggiore Policlinico
RP Cavalcoli, F (corresponding author), Fdn IRCCS Ca Granda Osped Maggiore Policlin, Gastroenterol & Endoscopy Unit, Milan, Italy.; Cavalcoli, F (corresponding author), Univ Milan, Dept Pathophysiol & Transplantat, Milan, Italy.
EM cavalcoli.federica@gmail.com
RI Massironi, Sara/X-2547-2019
OI Massironi, Sara/0000-0003-3214-8192
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NR 38
TC 25
Z9 28
U1 0
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-230X
J9 BMC GASTROENTEROL
JI BMC Gastroenterol.
PD NOV 8
PY 2018
VL 18
AR 172
DI 10.1186/s12876-018-0901-0
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GZ8DL
UT WOS:000449716700001
PM 30409113
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bockerstett, KA
   Osaki, LH
   Petersen, CP
   Cai, CW
   Wong, CF
   Nguyen, TLM
   Ford, EL
   Hoft, DF
   Mills, JC
   Goldenring, JR
   DiPaolo, RJ
AF Bockerstett, Kevin A.
   Osaki, Luciana H.
   Petersen, Christine P.
   Cai, Catherine W.
   Wong, Chun Fung
   Nguyen, Thanh-Long M.
   Ford, Eric L.
   Hoft, Daniel F.
   Mills, Jason C.
   Goldenring, James R.
   DiPaolo, Richard J.
TI Interleukin-17A Promotes Parietal Cell Atrophy by Inducing Apoptosis
SO CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE IL-17A; Atrophy; Metaplasia; Apoptosis
ID REGULATORY T-CELLS; POLYPEPTIDE-EXPRESSING METAPLASIA; GASTRIC-CANCER;
   AUTOIMMUNE GASTRITIS; HELICOBACTER-PYLORI; INCREASED RISK; TH17 CELLS;
   INFLAMMATION; MODEL; PREVALENCE
AB This study reports that interleukin-17A (IL-17A) is an important contributor to parietal cell atrophy and metaplasia during chronic atrophic gastritis. IL-17A induces parietal cell apoptosis, while IL-17A neutralization in the setting of gastritis limits atrophy and metaplasia.
   BACKGROUND & AIMS: Atrophic gastritis caused by chronic inflammation in the gastric mucosa leads to the loss of gastric glandular cells, including acid-secreting parietal cells. Parietal cell atrophy in a setting of chronic inflammation induces spasmolytic polypeptide expressing metaplasia, a critical step in gastric carcinogenesis. However, the mechanisms by which inflammation causes parietal cell atrophy and spasmolytic polypeptide expressing metaplasia are not well defined. We investigated the role of interleukin-17A (IL-17A) in causing parietal cell atrophy.
   METHODS: A mouse model of autoimmune atrophic gastritis was used to examine IL-17A production during early and late stages of disease. Organoids derived from corpus glands were used to determine the direct effects of IL-17A on gastric epithelial cells. Immunofluorescent staining was used to examine IL-17A receptors and the direct effect of signaling on parietal cells. Mice were infected with an IL-17A-producing adenovirus to determine the effects of IL-17A on parietal cells in vivo. Finally, IL-17A neutralizing antibodies were administered to mice with active atrophic gastritis to evaluate the effects on parietal cell atrophy and metaplasia.
   RESULTS: Increased IL-17A correlated with disease severity in mice with chronic atrophic gastritis. IL-17A caused caspase-dependent gastric organoid degeneration, which could not be rescued with a necroptosis inhibitor. Parietal cells expressed IL-17A receptors and IL-17A treatment induced apoptosis in parietal cells. Overexpressing IL-17A in vivo induced caspase-3 activation and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining in parietal cells. Finally, IL-17A neutralizing antibody decreased parietal cell atrophy and metaplasia in mice with chronic atrophic gastritis.
   CONCLUSIONS: These data identify IL-17A as a cytokine that promotes parietal cell apoptosis during atrophic gastritis, a precursor lesion for gastric cancer.
C1 [Bockerstett, Kevin A.; Cai, Catherine W.; Wong, Chun Fung; Nguyen, Thanh-Long M.; Ford, Eric L.; Hoft, Daniel F.; DiPaolo, Richard J.] St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, DRC 707,1100 South Grand Blvd, St Louis, MO 63104 USA.
   [Osaki, Luciana H.; Mills, Jason C.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
   [Osaki, Luciana H.; Mills, Jason C.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63103 USA.
   [Osaki, Luciana H.; Mills, Jason C.] Washington Univ, Sch Med, Dept Dev Biol, St Louis, MO 63103 USA.
   [Petersen, Christine P.; Goldenring, James R.] Vanderbilt Univ, Sch Med, Epithelial Biol Ctr, Nashville VA Med Ctr, Nashville, TN 37212 USA.
   [Petersen, Christine P.; Goldenring, James R.] Vanderbilt Univ, Sch Med, Epithelial Biol Ctr, Dept Surg, Nashville, TN 37212 USA.
   [Petersen, Christine P.; Goldenring, James R.] Vanderbilt Univ, Sch Med, Epithelial Biol Ctr, Dept Cell & Dev Biol, Nashville, TN 37212 USA.
C3 Saint Louis University; Washington University (WUSTL); Washington
   University (WUSTL); Washington University (WUSTL); US Department of
   Veterans Affairs; Veterans Health Administration (VHA); VA Tennessee
   Valley Healthcare System; Vanderbilt University; Vanderbilt University;
   Vanderbilt University
RP DiPaolo, RJ (corresponding author), St Louis Univ, Sch Med, Dept Mol Microbiol & Immunol, DRC 707,1100 South Grand Blvd, St Louis, MO 63104 USA.
EM richard.dipaolo@slu.edu
RI Osaki, Luciana/I-3624-2012; Cai, Catherine/G-8103-2016; Nguyen,
   Thanh-Luan/AAR-7199-2021; Mills, Jason/AAA-6688-2021; Goldenring, James
   R./KYQ-3750-2024
OI DiPaolo, Richard/0000-0002-2191-6689; Osaki,
   Luciana/0000-0003-0665-7567; Mills, Jason/0000-0002-0402-4662;
   Bockerstett, Kevin/0000-0002-5010-4970; Goldenring, James
   R./0000-0002-7833-2940; Cai, Catherine/0000-0003-1855-7950
FU American Cancer Society [RSG-12-171-01-LIB]; National Institutes of
   Health National Institute of Diabetes and Digestive and Kidney Diseases
   [RO1 DK110406, R01 DK094989, R01 DK105129]; Digestive Diseases Research
   Core Center of the Washington University School of Medicine (National
   Institute of Diabetes and Digestive and Kidney Diseases) [P30DK52574];
   American Gastroenterological Association Funderburg Research Award; VA
   Merit Review [1I01BX000930]; National Institutes of Health [DK101332];
   National Institutes of Health National Research Service Award
   Predoctoral Fellowship [F31 DK104600]; Siteman Cancer Center
FX Supported by the American Cancer Society (RSG-12-171-01-LIB) and the
   National Institutes of Health National Institute of Diabetes and
   Digestive and Kidney Diseases (RO1 DK110406) (R.J.D. and J.C.M.); a
   grant from the Digestive Diseases Research Core Center of the Washington
   University School of Medicine (National Institute of Diabetes and
   Digestive and Kidney Diseases grant P30DK52574) and by the American
   Gastroenterological Association Funderburg Research Award (R.J.D.); a VA
   Merit Review (1I01BX000930) and National Institutes of Health grant
   DK101332 (J.R.G.); a National Institutes of Health National Research
   Service Award Predoctoral Fellowship (F31 DK104600 to C.P.P.); and a
   pre-Program Projects Grants award from the Siteman Cancer Center and the
   National Institutes of Health National Institute of Diabetes and
   Digestive and Kidney Diseases (R01 DK094989 and R01 DK105129 to J.C.M.).
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NR 48
TC 42
Z9 47
U1 1
U2 15
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 2352-345X
J9 CELL MOL GASTROENTER
JI Cell. Mol. Gastroenterol. Hepatol.
PY 2018
VL 5
IS 4
BP 678
EP +
DI 10.1016/j.jcmgh.2017.12.012
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GE2QD
UT WOS:000431058800026
PM 29930985
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Calapkulu, M
   Sencar, ME
   Duger, H
   Bayram, SM
   Unsal, IO
   Cakal, E
   Ozbek, M
AF Calapkulu, Murat
   Sencar, Muhammed Erkam
   Duger, Hakan
   Bayram, Seyit Murat
   Unsal, Ilknur Ozturk
   Cakal, Erman
   Ozbek, Mustafa
TI Coexistence of Type-1 Diabetes Mellitus and Papillary Thyroid Carcinoma
SO CURRENT DIABETES REVIEWS
LA English
DT Article
DE Type-1 diabetes; thyroid cancer; papillary thyroid cancer; anti-thyroid
   peroxidase; carcinoma; thyroid gland
ID POPULATION-BASED COHORT; CANCER-RISK; ASSOCIATION
AB Introduction: Type 1 diabetes mellitus (DM) is characterized by selective autoimmune destruction of pancreatic b-cells, resulting in insulin deficiency and associated autoimmune disorders, such as celiac disease, autoimmune thyroiditis, and gastritis, which can coexist in patients with type 1 DM. These disorders are characterized by the presence of antibodies against tissue transglutaminase, thyroglobulin, and thyroid peroxidase (TPO), as well as against gastric parietal cells. Cross-sectional studies have reported that the risk of autoimmune thyroid diseases in patients with type-1 DM is two- to threefold higher than in the general population. However, there are a few studies in the literature that investigated the relationship between malignancy and type-1 DM, and it has been shown that type-1 DM does not increase thyroid cancer. Furthermore, there is a lot of controversy regarding the role of thyroid autoimmunity in the pathogenesis of thyroid cancer. Here, a type-1 DM patient diagnosed with papillary thyroid cancer is presented.
   Case Report: Herein, it was aimed to present a 20-year-old female patient diagnosed with type-1 DM and subsequently with papillary thyroid carcinoma (PTC). Thyroid ultrasound revealed a 10x12x18 mm hypoechoic irregular edges nodule with macrocalcification and microcalcification foci in the left lobe and pathological lymph nodes without echogenic hilus were detected at the fourth level of the left cervical chain. Fine needle aspiration biopsy of the nodule was consistent with papillary thyroid carcinoma. Total thyroidectomy, bilateral central lymph node dissection, and left neck dissection (level II to IV) were performed. Pathological examination revealed a 1.4 x 0.9 cm diameter papillary carcinoma located in the left lobe of the thyroid gland with 13 lymph node metastases.
   Conclusion: Patients with type 1 DM should be examined for thyroid diseases, and patients with suspected thyroid disease should be evaluated with a thyroid ultrasound. Type 1 DM and PTC can coexist, albeit very rare. It should be known that type 1 diabetes can be observed together with thyroid cancer.
C1 [Calapkulu, Murat; Sencar, Muhammed Erkam; Duger, Hakan; Bayram, Seyit Murat; Unsal, Ilknur Ozturk; Cakal, Erman; Ozbek, Mustafa] Univ Hlth Sci, Diskapi Yildirim Beyazit Training & Res Hosp, Dept Endocrinol & Metab, Ankara, Turkey.
C3 University of Health Sciences Turkey; Diskapi Yildirim Beyazit Training
   & Research Hospital
RP Calapkulu, M (corresponding author), Univ Hlth Sci, Diskapi Yildirim Beyazit Training & Res Hosp, Dept Endocrinol & Metab, Ankara, Turkey.
EM calapkulumurat89@gmail.com
RI Düğer, Hakan/IZP-9361-2023; Ustun, Yaprak/KFQ-9767-2024; Ünsal,
   İlknur/AAO-7474-2021; Çalapkulu, Murat/ABF-6267-2020; özbek,
   mustafa/IYS-6564-2023; Sencar, Muhammed/AAN-8807-2021
OI Sencar, Muhammed Erkam/0000-0001-5581-4886; cakal,
   erman/0000-0003-4455-7276; CALAPKULU, MURAT/0000-0002-7445-2275; Duger,
   Hakan/0000-0001-5478-3192
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NR 19
TC 2
Z9 2
U1 0
U2 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1573-3998
EI 1875-6417
J9 CURR DIABETES REV
JI Curr. Diabetes Reviews
PY 2020
VL 16
IS 7
BP 787
EP 789
DI 10.2174/1573399815666191104114551
PG 3
WC Endocrinology & Metabolism
WE Emerging Sources Citation Index (ESCI)
SC Endocrinology & Metabolism
GA NN8VD
UT WOS:000569064900005
PM 31686641
DA 2025-06-01
ER

PT J
AU Miwa, W
   Hiratsuka, T
   Sato, K
   Fujino, T
   Kato, Y
AF Miwa, Wataru
   Hiratsuka, Takashi
   Sato, Ken
   Fujino, Takashi
   Kato, Yo
TI Development of white globe appearance lesions in the noncancerous
   stomach after vonoprazan administration: a report of two cases with a
   literature review
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE White globe appearance; Vonoprazan; Potassium-competitive acid blocker;
   Autoimmune atrophic gastritis
ID GASTRIC-CANCER; MARKER
AB White globe appearance has recently been identified as a novel endoscopic marker useful in the diagnosis of early gastric cancer. Recently, this lesion has also been reported in the noncancerous stomach, including cases with autoimmune atrophic gastritis, although the clinical significance remains unclear. We present the details of a 68-year-old woman who began vonoprazan therapy for severe gastroesophageal reflux disease causing esophageal stricture. On follow-up endoscopy 1 year after beginning vonoprazan, multiple white globe appearance lesions developed in all sections of her stomach, except for the antrum. We also detected lesions during a yearly follow-up in the noncancerous stomach of a 70-year-old man who had received vonoprazan for 3 years. Lesions in both cases constituted cystic gland dilatations containing eosinophilic material. There was no evidence of accompanying autoimmune atrophic gastritis in either patient. This report is the first to our knowledge describing newly developed white globe appearance lesions in the noncancerous stomach during follow-up in two cases who received vonoprazan. Our findings suggest that these lesions in the noncancerous stomach might be associated with vonoprazan treatment. We investigated the two cases endoscopically and histologically, and we report our findings with a literature review.
C1 [Miwa, Wataru; Hiratsuka, Takashi] Hiratsuka Gastroenterol Hosp, Div Internal Med, Toshima Ku, 3-2-16 Nishiikebukuro, Tokyo 1710021, Japan.
   [Sato, Ken] Hiratsuka Gastroenterol Hosp, Div Surg, Tokyo, Japan.
   [Fujino, Takashi] Saitama Med Univ Int Med Ctr, Dept Canc Genom Med, Saitama, Japan.
   [Kato, Yo] Hiratsuka Gastroenterol Hosp, Div Pathol, Tokyo, Japan.
C3 Saitama Medical University
RP Miwa, W (corresponding author), Hiratsuka Gastroenterol Hosp, Div Internal Med, Toshima Ku, 3-2-16 Nishiikebukuro, Tokyo 1710021, Japan.
EM wmiwa@ichou.gr.jp
RI Miwa, Wataru/AAT-4347-2021
OI Fujino, Takashi/0000-0002-0953-7379
CR Ayaki M., 2019, GASTROINTEST ENDOSC, V61, P1226
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NR 17
TC 5
Z9 7
U1 0
U2 9
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1865-7257
EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD FEB
PY 2021
VL 14
IS 1
BP 48
EP 58
DI 10.1007/s12328-020-01243-z
EA OCT 2020
PG 11
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA QI2PP
UT WOS:000575704100003
PM 33025345
DA 2025-06-01
ER

PT J
AU Chang, MC
   Chang, YT
   Wei, SC
   Kuo, CH
   Liang, PC
   Wong, JM
AF Chang, Ming-Chu
   Chang, Yu-Ting
   Wei, Shu-Chen
   Kuo, Chun-Hung
   Liang, Po-Chin
   Wong, Jau-Min
TI Autoimmune Pancreatitis Associated With High Prevalence of Gastric Ulcer
   Independent of Helicobacter pylori Infection Status
SO PANCREAS
LA English
DT Article
DE autoimmune pancreatitis (AIP); chronic pancreatitis; Helicobacter
   pylori; gastric ulcer; Chinese
ID IDIOPATHIC CHRONIC-PANCREATITIS; DUODENAL-ULCER; CARBONIC-ANHYDRASE;
   GENE POLYMORPHISMS; MOLECULAR MIMICRY; PATHOGENESIS; DISEASES; CHINESE;
   RISK
AB Objectives: The relationship between Helicobacter pylori status and host tumor necrosis factor alpha (TNF-alpha) promoter susceptibility in ulcers in autoimmune pancreatitis (AIP) is unknown. We sought to study the frequency of peptic ulcer, the association of peptic ulcer with H. pylori and host TNF-alpha promoter haplotype in AIP and nonautoimmune chronic pancreatitis.
   Methods: Esophagogastroduodenoscopy (EGD) was performed in 40 patients with AIP and 113 patients with nonautoimmune chronic pancreatitis (CP). The status of H. pylori infection was determined. Genotyping and 5-locus haplotype assembly of the TNF-alpha promoter were performed. The correlation between clinical characteristics, endoscopic findings, Helicobacter pylori infection status, and TNF-alpha promoter polymorphism and haplotype was analyzed.
   Results: The frequencies of gastric ulcer (GU) was higher in patients with AIP compared with patients with nonautoimmune CP (22.5% vs 4.4%, P = 0.001). Duodenal ulcer (DU) was more prevalent than GU in both patients with AIP and patients with nonautoimmune CP. There was no difference in the positive status of H. pylori and TNF-alpha promoter polymorphism/haplotype.
   Conclusions: Our results demonstrated that GU was more prevalent in AIP compared with nonautoimmune CP. Positive H. pylori status and host TNF-alpha promoter susceptibility could not explain the pathogenesis of higher GU prevalence and pathogenesis of AIP in our population.
C1 [Chang, Ming-Chu; Chang, Yu-Ting; Wei, Shu-Chen; Kuo, Chun-Hung; Wong, Jau-Min] Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan.
   [Liang, Po-Chin] Natl Taiwan Univ Hosp, Dept Radiol, Taipei 100, Taiwan.
C3 National Taiwan University; National Taiwan University Hospital;
   National Taiwan University; National Taiwan University Hospital
RP Wong, JM (corresponding author), Natl Taiwan Univ Hosp, Dept Internal Med, 7 Chung Shan S Rd, Taipei 100, Taiwan.
EM jmwong@ntu.edu.tw
RI Lai, Chien-Hsien/ABD-9379-2020; Chen, Chien/Q-3826-2018; Li,
   Jenny/GSD-3780-2022; Liang, Po-chin/HKF-7304-2023
OI LIANG, PO-CHIN/0000-0002-6674-2926; WEI, SHU-CHEN/0000-0002-5017-5840;
   CHANG, YU-TING/0000-0002-5912-3406
FU National Science Council [NSC 94-2314-B-002-272]; National Taiwan
   University Hospital [NTUH-95-M-22]
FX This work was supported by grants from the National Science Council (NSC
   94-2314-B-002-272), Taiwan, and National Taiwan University Hospital
   (NTUH-95-M-22).
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NR 25
TC 22
Z9 26
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0885-3177
EI 1536-4828
J9 PANCREAS
JI Pancreas
PD MAY
PY 2009
VL 38
IS 4
BP 442
EP 446
DI 10.1097/MPA.0b013e31819b5f3c
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 439WZ
UT WOS:000265659600014
PM 19276869
DA 2025-06-01
ER

PT J
AU Hiraizumi, K
   Honda, C
   Watanabe, A
   Nakao, T
   Midorikawa, S
   Abe, H
   Matsui, N
   Yamamoto, T
   Sakamoto, T
AF Hiraizumi, Kenji
   Honda, Chikara
   Watanabe, Ayu
   Nakao, Takafumi
   Midorikawa, Shuichi
   Abe, Hiromi
   Matsui, Nobuki
   Yamamoto, Tsunehisa
   Sakamoto, Takahiko
TI Safety of nivolumab monotherapy in five cancer types: pooled analysis of
   post-marketing surveillance in Japan
SO INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article; Early Access
DE Nivolumab; Post-marketing surveillance; Real-world clinical practice;
   Safety; Treatment-related adverse events
ID IMMUNE CHECKPOINT INHIBITORS; SQUAMOUS-CELL CARCINOMA; PREEXISTING
   AUTOIMMUNE; LUNG-CANCER; CLINICAL-OUTCOMES; TUBERCULOSIS; MYOCARDITIS;
   DOCETAXEL; EFFICACY; MELANOMA
AB Background Nivolumab has been approved for treating >= 10 cancer types. However, there is limited information on the incidence of rare, but potentially serious, treatment-related adverse events (TRAEs), as well as notable TRAEs in patients with certain medical disorders or older patients in Japan. Methods We performed pooled analyses of data from published post-marketing surveillance in Japan of nivolumab monotherapy for patients with malignant melanoma, non-small cell lung cancer, renal cell carcinoma, head and neck cancer, and gastric cancer to determine the frequencies of 20 categories of TRAEs of special interest overall and in patient groups with higher perceived safety risks (history of autoimmune disease, interstitial lung disease, tuberculosis, or hepatitis B/C; patients vaccinated during nivolumab treatment; and older patients [>= 75 years]). Results The overall population comprised 7421 patients treated with nivolumab. TRAEs were reported in 49.1% of patients, with grade >= 3 TRAEs in 16.7%. Endocrine disorders (14.4%), hepatobiliary disorders (10.9%), and interstitial lung disease (7.0%) were the three most common categories (any grade). The incidences of rare TRAEs with high risk of becoming serious, which occurred in < 1% of patients, were consistent with those in previous reports. The frequencies of TRAEs were not markedly increased in the specified patient groups relative to the overall population. Conclusion To our knowledge, this is the largest study examining the safety of nivolumab-treated patients in real-world clinical practice including rare but potentially serious TRAEs. We found no new signals in the safety of nivolumab among the patient groups relative to the overall population, and no additional safety measures are required in these groups. Trial registration UMIN000048892 (overall analysis), JapicCTI-163272 (melanoma), Japic-163271 (non-small cell lung cancer), JapicCTI-184071 (head and neck cancer), JapicCTI-184070 (gastric cancer), and JapicCTI-184069 (renal cell cancer). Conclusion To our knowledge, this is the largest study examining the safety of nivolumab-treated patients in real-world clinical practice including rare but potentially serious TRAEs. We found no new signals in the safety of nivolumab among the patient groups relative to the overall population, and no additional safety measures are required in these groups. Trial registration UMIN000048892 (overall analysis), JapicCTI-163272 (melanoma), Japic-163271 (non-small cell lung cancer), JapicCTI-184071 (head and neck cancer), JapicCTI-184070 (gastric cancer), and JapicCTI-184069 (renal cell cancer).
C1 [Hiraizumi, Kenji] Ono Pharmaceut Co Ltd, Oncol Med Affairs, 8-2 Kyutaromachi 1-Chome Chuo Ku, Osaka 5418564, Japan.
   [Honda, Chikara] Ono Pharmaceut Co Ltd, Pharmacovigilance Dept, PV Data Strategy, 2-1-5 Dosho machi,Chuo-ku, Osaka 5418526, Japan.
   [Watanabe, Ayu; Nakao, Takafumi; Sakamoto, Takahiko] Ono Pharmaceut Co Ltd, Safety Management Pharmacovigilance Dept, 2-1-5 Dosho Machi,Chuo Ku, Osaka 5418526, Japan.
   [Midorikawa, Shuichi] Bristol Myers Squibb KK, R&D Dept, Biometr & Data Sci, Otemachi One Tower,1-2-1 Otemachi,Chiyoda ku, Tokyo 1000004, Japan.
   [Abe, Hiromi; Yamamoto, Tsunehisa] Bristol Myers Squibb KK, Oncol Med, Otemachi One Tower,1-2-1 Otemachi,Chiyoda ku, Tokyo 1000004, Japan.
   [Matsui, Nobuki] Bristol Myers Squibb KK, Patient Safety Japan, Otemachi One Tower,1-2-1 Otemachi,Chiyoda ku, Tokyo 1000004, Japan.
C3 Ono Pharmaceutical Co Ltd; Ono Pharmaceutical Co Ltd; Ono Pharmaceutical
   Co Ltd; Bristol-Myers Squibb; Bristol-Myers Squibb; Bristol-Myers Squibb
RP Sakamoto, T (corresponding author), Ono Pharmaceut Co Ltd, Safety Management Pharmacovigilance Dept, 2-1-5 Dosho Machi,Chuo Ku, Osaka 5418526, Japan.
EM t.sakamoto@ono-pharma.com
RI Yamamoto, Tsunehisa/O-2014-2013
OI Yamamoto, Tsunehisa/0000-0002-5241-9482; Honda,
   Chikara/0000-0003-1005-7505; Sakamoto, Takahiko/0000-0002-3518-9574
FU Ono Pharmaceutical; Ono Pharmaceutical Co., Ltd.; Bristol-Myers Squibb
   K.K - Ono Pharmaceutical Co., Ltd.; Bristol-Myers Squibb K.K.
FX We would like to thank all of the patients and their families involved
   in the PMS. This study was funded by Ono Pharmaceutical Co., Ltd. and
   Bristol-Myers Squibb K.K. The authors thank Nicholas D. Smith (EMC K.K.)
   for medical writing support, which was funded by Ono Pharmaceutical Co.,
   Ltd. and Bristol-Myers Squibb K.K.
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NR 51
TC 1
Z9 1
U1 1
U2 1
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1341-9625
EI 1437-7772
J9 INT J CLIN ONCOL
JI Int. J. Clin. Oncol.
PD 2024 JUN 6
PY 2024
DI 10.1007/s10147-024-02515-1
EA JUN 2024
PG 12
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA TS7B1
UT WOS:001243302600001
PM 38844668
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Jain, R
   Chetty, R
AF Jain, Richa
   Chetty, Runjan
TI Gastric Hyperplastic Polyps: A Review
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Review
DE Hyperplastic polyps; Stomach; Gastritis; Juvenile/retention polyps
ID RING CELL-CARCINOMA; MALIGNANT-TRANSFORMATION; HELICOBACTER-PYLORI;
   TRANSPLANT PATIENTS; SERRATED ADENOMA; P53 EXPRESSION; STOMACH;
   DIFFERENTIATION; ADENOCARCINOMA; COLON
AB Hyperplastic polyps represent the commonest polyp encountered in the stomach. They occur in patients of either gender and are commoner in the seventh decade of life. They are usually asymptomatic, small (less than 1 cm in diameter), solitary lesions occurring in the antrum but can present with dyspepsia, heartburn, abdominal pain, or upper gastrointestinal (GI) bleeding leading to anemia. Hyperplastic polyps almost never occur in normal gastric mucosa and are most commonly associated with chronic gastritis (Helicobacter pylori or autoimmune-induced). Pathologically, they are characterized by dilated, tortuous gastric foveoli set within an inflamed, edematous stroma. There is considerable histologic overlap especially with M,n,trier's disease and hamartomatous (juvenile or retention) polyps, and clinical input is mandatory to accomplish separation of these entities. Hyperplastic polyps arise as a by-product of repair to damaged mucosa. Dysplasia and malignancy are rarely associated with these polyps, which show an array of molecular aberrations. The importance of hyperplastic polyps for both gastroenterologist and pathologist lies in their association with other gastric mucosal pathology and mandates biopsy of adjacent mucosa and diligent search for accompanying pathology by the pathologist.
C1 [Chetty, Runjan] Toronto Gen Hosp, Dept Pathol, Univ Hlth Network, Toronto Med Labs, Toronto, ON M5G 2C4, Canada.
   [Jain, Richa; Chetty, Runjan] Univ Toronto, Dept Pathol, Univ Hlth Network, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; Toronto
   General Hospital; University of Toronto; University Health Network
   Toronto
RP Chetty, R (corresponding author), Toronto Gen Hosp, Dept Pathol, Univ Hlth Network, Toronto Med Labs, 200 Elizabeth St,11th Floor, Toronto, ON M5G 2C4, Canada.
EM runjan.chetty@uhn.on.ca
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NR 39
TC 83
Z9 90
U1 2
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0163-2116
EI 1573-2568
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD SEP
PY 2009
VL 54
IS 9
BP 1839
EP 1846
DI 10.1007/s10620-008-0572-8
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 474ZP
UT WOS:000268324000005
PM 19037727
DA 2025-06-01
ER

PT J
AU Park, JK
   Yang, JA
   Ahn, EY
   Chang, SH
   Song, YW
   Curtis, JR
   Lee, EB
AF Park, Jin Kyun
   Yang, Ji Ae
   Ahn, Eun Young
   Chang, Sung Hae
   Song, Yeong Wook
   Curtis, Jeffrey R.
   Lee, Eun Bong
TI Survival rates of cancer patients with and without rheumatic disease: a
   retrospective cohort analysis
SO BMC CANCER
LA English
DT Article
DE Rheumatic diseases; Cancer; Staging; Mortality; Survival
ID INTERSTITIAL LUNG-DISEASE; AUTOIMMUNE-DISEASES; REVISED CRITERIA; RISK;
   MALIGNANCY; ARTHRITIS; DERMATOMYOSITIS; CLASSIFICATION; PATHOGENESIS;
   POLYMYOSITIS
AB Background: To compare the outcomes of gastric, colon, lung, and breast cancer patients with and without rheumatic diseases (RD).
   Methods: This retrospective study compared the cancer survival rates of a cohort of 122 cancer patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), dermatomyositis/polymyositis (DM/PM), or systemic sclerosis with that of a cohort of 366 age-, sex-, and, cancer type-matched patients without RD who received medical care from 2000 to 2014. Staging, comorbidities, and functional status were ascertained. Survival was compared using the Kaplan-Meier method. Relative risk of death was estimated as a hazard ratio (HR) using Cox regression analysis.
   Results: The mean age of the RD patients at the time of cancer diagnosis was 58.7 +/- 11.5 years. The overall survival rate of gastric cancer patients did not differ between the cohorts. The survival of lung or breast cancer was worse in patients with RA or DM/PM than in those without RD (all, p < 0.05). After adjusting for cancer stage, comorbidity index, performance status and age at the time of cancer diagnosis (as well as interstitial lung disease for lung cancer group), the mortality rate among lung cancer patients with RA was significantly higher (HR, 1.81; 95 % CI, 1. 03-3.18) than that of lung cancer patients without RD, whereas SSc was associated with decreased mortality of lung cancer (HR, 0.16; 95 % CI, 0.04-0.58). DM/PM were associated with increased mortality of breast cancer patients (HR, 297.39; 95 % CI, 4.24-20842.33).
   Conclusions: RA and DM/PM seemed to be associated with a higher mortality in patients with lung or breast cancers, whereas SSc seemed to be associated with decreased mortality in patients with lung cancer. It is warranted to explore the survival effect of tailored cancer treatments according to specific RD.
C1 [Park, Jin Kyun; Yang, Ji Ae; Ahn, Eun Young; Song, Yeong Wook; Lee, Eun Bong] Seoul Natl Univ, Div Rheumatol, Dept Internal Med, Coll Med, 101 Daehak Ro, Seoul 03080, South Korea.
   [Chang, Sung Hae] Soonchunhyang Univ, Div Rheumatol, Dept Internal Med, Cheonan Hosp, Cheonan, South Korea.
   [Curtis, Jeffrey R.] Univ Alabama Birmingham, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA.
C3 Seoul National University (SNU); Soonchunhyang University; University of
   Alabama System; University of Alabama Birmingham
RP Lee, EB (corresponding author), Seoul Natl Univ, Div Rheumatol, Dept Internal Med, Coll Med, 101 Daehak Ro, Seoul 03080, South Korea.
EM leb7616@snu.ac.kr
RI Lee, Youngil/AAX-2787-2021; Curtis, Jeffrey/I-6723-2015; Park, Kyung
   Woo/AAX-3046-2020
OI Park, Jin Kyun/0000-0003-2167-9393
FU AHRQ HHS [R01 HS018517] Funding Source: Medline
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NR 36
TC 23
Z9 26
U1 0
U2 1
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2407
J9 BMC CANCER
JI BMC Cancer
PD JUL 4
PY 2016
VL 16
AR 381
DI 10.1186/s12885-016-2444-5
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA VF2ZV
UT WOS:000442463100001
PM 27412038
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Jiang, XX
   Huang, JF
   Huo, Z
   Zhang, QQ
   Jiang, Y
   Wu, XP
   Li, YW
   Jiang, GM
   Zeng, LP
   Yan, XX
   Yu, P
   Cao, RX
AF Jiang, Xiaoxin
   Huang, Ju-Fang
   Huo, Zhi
   Zhang, Qiuqui
   Jiang, Yan
   Wu, Xiaoping
   Li, Yanwen
   Jiang, Guanmin
   Zeng, Leping
   Yan, Xiao-Xin
   Yu, Ping
   Cao, Renxian
TI Elevation of soluble major histocompatibility complex class I related
   chain A protein in malignant and infectious diseases in Chinese patients
SO BMC IMMUNOLOGY
LA English
DT Article
DE MHC; sMICA/B; NKG2D; Cancer diagnosis; Serum
ID CHLAMYDIA-TRACHOMATIS INFECTION; MICA GENE POLYMORPHISMS; SQUAMOUS-CELL
   CARCINOMA; SERUM-LEVELS CORRELATE; NKG2D LIGANDS; MULTIPLE-MYELOMA;
   DOWN-REGULATION; T-CELLS; HEPATOCELLULAR-CARCINOMA; ULCERATIVE-COLITIS
AB Background: Elevation of soluble major histocompatibility complex class I chain-related gene A (sMICA) products in serum has been linked to tissue/organ transplantation, autoimmune diseases and some malignant disorders. Cells infected by microbiological pathogens may release sMICA, whereas less is known whether and to what extent serum sMICA levels may change in infectious diseases.
   Methods: The present study determined serum sMICA levels by enzyme-linked immunosorbent assay (ELISA) in a southern China population, including patients (n = 1041) suffering from several types of malignant and infectious diseases and healthy controls (n = 141).
   Results: Relative to controls, serum sMICA elevation was significant in patients of hepatic cancer, and was approaching statistical significance in patients with lung, gastric and nasopharyngeal cancers. sMICA elevation was also associated with some bacterial (Enterobacteriaceae, Mycobacterium tuberculosis, non-fermenting Gram-negative bacteria and Gram-positive cocci), viral (hepatitis B and C) and the Microspironema pallidum infections.
   Conclusion: Serum sMICA levels may be informative for the diagnosis of some malignant and infectious diseases. The results also indicate that microbiological infections should be considered as a potential confounding clinical condition causing serum sMICA elevation while using this test to evaluate the status of other disorders, such as cancers, host-graft response and autoimmune diseases.
C1 [Jiang, Xiaoxin; Huo, Zhi; Zhang, Qiuqui; Jiang, Yan; Wu, Xiaoping; Li, Yanwen; Jiang, Guanmin; Cao, Renxian] Nanhua Univ, Affiliated Hosp 1, Hengyang 421001, Peoples R China.
   [Jiang, Xiaoxin; Yu, Ping] Cent S Univ, Xiangya Sch Med, Dept Immunol, Changsha 410078, Hunan, Peoples R China.
   [Jiang, Xiaoxin; Huang, Ju-Fang; Zeng, Leping; Yan, Xiao-Xin] Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
C3 University of South China; Central South University; Central South
   University
RP Yan, XX (corresponding author), Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
EM yanxiaoxin@csu.edu.cn; caorenxian@hotmail.com
RI Jufang, Huang/AAW-1847-2020; JIANG, xx/KHV-3752-2024
FU National Natural Science Foundation of China [81172542, 30870135];
   Central South University
FX The authors appreciate the patients for their blood donation, the stuff
   of the in- and out-patient laboratory units of the First Affiliated
   Hospital of Nanhua University for sample collection. We thank Dr. Zou
   Yizhou for kindly providing the anti-MICA 6B3 antibody and the
   recombinant human MICA*008 protein, and Ye Cao for secretary assistance.
   This work was supported in part by the National Natural Science
   Foundation of China (general programs #81172542 and #30870135) and a
   postdoctoral fund from Central South University.
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NR 50
TC 11
Z9 13
U1 0
U2 14
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1471-2172
J9 BMC IMMUNOL
JI BMC Immunol.
PD NOV 26
PY 2012
VL 13
AR 62
DI 10.1186/1471-2172-13-62
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 078HX
UT WOS:000314090500001
PM 23181907
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Dore, MP
   Pes, GM
AF Dore, Maria Pina
   Pes, Giovanni Mario
TI Trained Immunity and Trained Tolerance: The Case of Helicobacter
   pylori Infection
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE trained immunity; Helicobacter pylori; gastritis; immunocompetent cells
ID INDUCTION; CAGA; LIPOPOLYSACCHARIDE; PHAGOCYTOSIS; CHOLESTEROL;
   RESPONSES; PATHOGENESIS; MACROPHAGES; MODULATION; ACTIVATION
AB Trained immunity is a concept in immunology in which innate immune cells, such as monocytes and macrophages, exhibit enhanced responsiveness and memory-like characteristics following initial contact with a pathogenic stimulus that may promote a more effective immune defense following subsequent contact with the same pathogen. Helicobacter pylori, a bacterium that colonizes the stomach lining, is etiologically associated with various gastrointestinal diseases, including gastritis, peptic ulcer, gastric adenocarcinoma, MALT lymphoma, and extra gastric disorders. It has been demonstrated that repeated exposure to H. pylori can induce trained immunity in the innate immune cells of the gastric mucosa, which become more responsive and better able to respond to subsequent H. pylori infections. However, interactions between H. pylori and trained immunity are intricate and produce both beneficial and detrimental effects. H. pylori infection is characterized histologically as the presence of both an acute and chronic inflammatory response called acute-on-chronic inflammation, or gastritis. The clinical outcomes of ongoing inflammation include intestinal metaplasia, gastric atrophy, and dysplasia. These same mechanisms may also reduce immunotolerance and trigger autoimmune pathologies in the host. This review focuses on the relationship between trained immunity and H. pylori and underscores the dynamic interplay between the immune system and the pathogen in the context of gastric colonization and inflammation.
C1 [Dore, Maria Pina; Pes, Giovanni Mario] Univ Sassari, Dipartimento Med Chirurg & Farm, Clin Med, Viale San Pietro 8, I-07100 Sassari, Italy.
   [Dore, Maria Pina] Baylor Coll Med, Dept Med, One Baylor Plaza Blvd, Houston, TX 77030 USA.
C3 University of Sassari; Baylor College of Medicine
RP Dore, MP (corresponding author), Univ Sassari, Dipartimento Med Chirurg & Farm, Clin Med, Viale San Pietro 8, I-07100 Sassari, Italy.; Dore, MP (corresponding author), Baylor Coll Med, Dept Med, One Baylor Plaza Blvd, Houston, TX 77030 USA.
EM mpdore@uniss.it; gmpes@uniss.it
RI DORE, Maria/AAV-7918-2021; Pes, Giovanni Mario/AAH-3340-2019
OI Pes, Giovanni Mario/0000-0003-3265-2823; DORE, Maria
   Pina/0000-0001-7305-3531
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NR 76
TC 3
Z9 3
U1 0
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUN
PY 2024
VL 25
IS 11
AR 5856
DI 10.3390/ijms25115856
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA UG3B1
UT WOS:001246855000001
PM 38892046
OA gold, Green Published
DA 2025-06-01
ER

PT J
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   Chott, A.
   Raderer, M.
TI MALT lymphoma in patients with autoimmune diseases:: a comparative
   analysis of characteristics and clinical course
SO LEUKEMIA
LA English
DT Article
DE MALT lymphoma; autoimmune disease; prognosis
ID B-CELL LYMPHOMA; HELICOBACTER-PYLORI; TISSUE LYMPHOMA; GASTRIC-CANCER;
   CLASSIFICATION; T(11/18)(Q21,Q21); CHEMOTHERAPY; ERADICATION; INFECTION;
   RISK
AB MALT lymphoma, especially of extragastric origin, is thought to be associated with an underlying autoimmune disease (AD) in a significant proportion of patients. No systematic assessment of the clinical characteristics of MALT lymphoma arising in AD as opposed to patients without AD has been performed so far. Therefore, all patients diagnosed and treated for MALT lymphoma at our institution have prospectively undergone routine clinical and serological assessment for AD since 1997. In total, 158 patients were available for analysis, and 61 out of 158 patients (39%) were diagnosed with an underlying AD. Patients with AD were predominantly women and significantly younger at lymphoma diagnosis (56 versus 67 years, P = 0.004), with a significantly higher rate of extragastric lymphomas (P = 0.012). Furthermore, lymphomas in these patients showed a lower frequency of trisomy 3 (P = 0.04) and a significantly lower response rate to Helicobacter pylori eradication therapy in the case of gastric lymphomas (P = 0.03). All other parameters including estimated median time to relapse were comparable between both groups. Our data suggest that patients with AD develop MALT lymphoma significantly earlier in life. The clinical course, however, does not appear to be adversely influenced by the presence of AD, as neither rate of relapse nor times to relapse or survival are significantly different.
C1 Med Univ Vienna, Div Bone Marrow Transplantat, Dept Internal Med 1, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Oncol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Pathol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Internal Med 3, Div Rheumatol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Hematol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Hemostasiol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Otorhinolaryngol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Ophthalmol, A-1090 Vienna, Austria.
   Med Univ Vienna, Dept Nucl Med, A-1090 Vienna, Austria.
C3 Medical University of Vienna; Medical University of Vienna; Medical
   University of Vienna; Medical University of Vienna; Medical University
   of Vienna; Medical University of Vienna; Medical University of Vienna;
   Medical University of Vienna; Medical University of Vienna
RP Raderer, M (corresponding author), Med Univ Vienna, Div Oncol, Dept Internal Med 1, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
EM markus.raderer@meduniwien.ac.at
RI Troch, Marlene/AAS-9067-2020; Mullauer, Leonhard/GSN-9884-2022
OI Mullauer, Leonhard/0000-0002-3399-078X
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NR 32
TC 87
Z9 93
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD AUG
PY 2007
VL 21
IS 8
BP 1812
EP 1818
DI 10.1038/sj.leu.2404782
PG 7
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 191ZI
UT WOS:000248170100024
PM 17554381
DA 2025-06-01
ER

PT J
AU Wu, S
   Li, XF
   Wu, YY
   Yin, SQ
   Huang, C
   Li, J
AF Wu, Sha
   Li, Xiao-Feng
   Wu, Yuan-Yuan
   Yin, Su-Qin
   Huang, Cheng
   Li, Jun
TI N<SUP>6</SUP> -Methyladenosine and Rheumatoid Arthritis: A
   Comprehensive Review
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE N-6; -methyladenosine; rheumatoid arthritis; immune cells; autoimmune
   disease; cancers
ID METHYLTRANSFERASE METTL3 PROMOTES; NATURAL-KILLER-CELLS; MESSENGER-RNA;
   HEPATOCELLULAR-CARCINOMA; STRUCTURAL BASIS; DENDRITIC CELLS;
   NUCLEAR-RNA; M(6)A RNA; CANCER; TRANSLATION
AB Rheumatoid arthritis (RA), one of the most common autoimmune diseases, is characterized by immune cell infiltration, fibroblast-like synovial cell hyperproliferation, and cartilage and bone destruction. To date, numerous studies have demonstrated that immune cells are one of the key targets for the treatment of RA. N-6-methyladenosine (m(6)A) is the most common internal modification to eukaryotic mRNA, which is involved in the splicing, stability, export, and degradation of RNA metabolism. m(6)A methylated-related genes are divided into writers, erasers, and readers, and they are critical for the regulation of cell life. They play a significant role in various biological processes, such as virus replication and cell differentiation by controlling gene expression. Furthermore, a growing number of studies have indicated that m(6)A is associated with the occurrence of numerous diseases, such as lung cancer, bladder cancer, gastric cancer, acute myeloid leukemia, and hepatocellular carcinoma. In this review, we summarize the history of m6A research and recent progress on RA research concerning m(6)A enzymes. The relationship between m(6)A enzymes, immune cells, and RA suggests that m(6)A modification offers evidence for the pathogenesis of RA, which will help in the development of new therapies for RA.
C1 [Wu, Sha; Li, Xiao-Feng; Wu, Yuan-Yuan; Yin, Su-Qin; Huang, Cheng; Li, Jun] Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Key Lab Antiinflammatory & Immune Med, Anhui Inst Innovat Drugs,Minist Educ,Sch Pharm, Hefei, Peoples R China.
   [Li, Xiao-Feng] Anhui Med Univ, Postdoctoral Stn Clin Med, Hefei, Peoples R China.
C3 Ministry of Education - China; Anhui Medical University; Anhui Medical
   University
RP Li, J (corresponding author), Anhui Med Univ, Inflammat & Immune Mediated Dis Lab Anhui Prov, Key Lab Antiinflammatory & Immune Med, Anhui Inst Innovat Drugs,Minist Educ,Sch Pharm, Hefei, Peoples R China.
EM lj@ahmu.edu.cn
RI wu, yunayuan/IST-4642-2023; li, xiaofeng/GXF-9442-2022
FU National Natural Science Foundation of China [82002269]; China
   Postdoctoral Science Foundation [2020M671839]; Postdoctoral Science
   Foundation from Anhui Medical University [BSH201902]; Anhui Provincial
   Science and Technology Major Project [8212929035]
FX This study was supported by the National Natural Science Foundation of
   China (No. 82002269), China Postdoctoral Science Foundation (No.
   2020M671839), Postdoctoral Science Foundation from Anhui Medical
   University (No. BSH201902), and Anhui Provincial Science and Technology
   Major Project (8212929035).
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NR 117
TC 37
Z9 38
U1 1
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 24
PY 2021
VL 12
AR 731842
DI 10.3389/fimmu.2021.731842
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA WE8PK
UT WOS:000705881100001
PM 34630412
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bockerstett, KA
   Wong, CF
   Koehm, S
   Ford, EL
   DiPaolo, RJ
AF Bockerstett, Kevin A.
   Wong, Chun Fung
   Koehm, Sherri
   Ford, Eric L.
   DiPaolo, Richard J.
TI Molecular Characterization of Gastric Epithelial Cells Using Flow
   Cytometry
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE flow cytometry; gastric epithelium; autoimmune gastritis; atrophic
   gastritis
ID HELICOBACTER-PYLORI; PARIETAL-CELLS; APOPTOSIS; MICE; CANCER; MODEL
AB The ability to analyze individual epithelial cells in the gastric mucosa would provide important insight into gastric disease, including chronic gastritis and progression to gastric cancer. However, the successful isolation of viable gastric epithelial cells (parietal cells, neck cells, chief cells, and foveolar cells) from gastric glands has been limited due to difficulties in tissue processing. Furthermore, analysis and interpretation of gastric epithelial cell flow cytometry data has been difficult due to the varying sizes and light scatter properties of the different epithelial cells, high levels of autofluorescence, and poor cell viability. These studies were designed to develop a reliable method for isolating viable single cells from the corpus of stomachs and to optimize analyses examining epithelial cells from healthy and diseased stomach tissue by flow cytometry. We performed a two stage enzymatic digestion in which collagenase released individual gastric glands from the stromal tissue of the corpus, followed by a Dispase II digestion that dispersed these glands into greater than 1 x 10(6) viable single cells per gastric corpus. Single cell suspensions were comprised of all major cell lineages found in the normal gastric glands. A method describing light scatter, size exclusion, doublet discrimination, viability staining, and fluorescently-conjugated antibodies and lectins was used to analyze individual epithelial cells and immune cells. This technique was capable of identifying parietal cells and revealed that gastric epithelial cells in the chronically inflamed mucosa significantly upregulated major histocompatibility complexes (MHC) I and II but not CD80 or CD86, which are costimulatory molecules involved in T cell activation. These studies describe a method for isolating viable single cells and a detailed description of flow cytometric analysis of cells from healthy and diseased stomachs. These studies begin to identify effects of chronic inflammation on individual gastric epithelial cells, a critical consideration for the study of gastric cancer.
C1 [Bockerstett, Kevin A.; Wong, Chun Fung; Koehm, Sherri; Ford, Eric L.; DiPaolo, Richard J.] St Louis Univ, Dept Mol Microbiol & Immunol, Sch Med, St Louis, MO 63104 USA.
C3 Saint Louis University
RP DiPaolo, RJ (corresponding author), St Louis Univ, Dept Mol Microbiol & Immunol, Sch Med, St Louis, MO 63104 USA.
EM kevin.bockerstett@slu.edu; johnny.wong@health.slu.edu;
   sherri.koehm@health.slu.edu; eric.ford@health.slu.edu;
   richard.dipaolo@health.slu.edu
OI koehm, sherri/0000-0002-2947-9321; Bockerstett,
   Kevin/0000-0002-5010-4970; DiPaolo, Richard/0000-0002-2191-6689
FU AGA Funderburg Research Award; American Cancer Society
   [RSG-12-171-01-LIB]; National Institutes of Health (NIH) National
   Institute of Diabetes and Digestive and Kidney Diseases [RO1 DK110406];
   Digestive Diseases Research Core Center of the Washington University
   School of Medicine [NIDDK P30DK52574]
FX The authors thank Joy Eslick for assistance with flow cytometry; Grant
   Kolar, Barbara Nagel, and Katie Phelps from the Saint Louis University
   Research Microscopy and Histology Core for generation of tissue
   sections; and the Saint Louis University Comparative Medicine department
   for assistance in maintaining mouse colonies. Richard J. DiPaolo and is
   supported by the AGA Funderburg Research Award, the American Cancer
   Society (RSG-12-171-01-LIB), the National Institutes of Health (NIH)
   National Institute of Diabetes and Digestive and Kidney Diseases (RO1
   DK110406) and a grant from the Digestive Diseases Research Core Center
   of the Washington University School of Medicine NIDDK P30DK52574.
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NR 24
TC 5
Z9 6
U1 1
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2018
VL 19
IS 4
AR 1096
DI 10.3390/ijms19041096
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA GJ0XU
UT WOS:000434978700175
PM 29642375
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Arai, H
   Hayashi, H
   Ogata, S
   Uto, K
   Saegusa, J
   Takahashi, K
   Koide, S
   Inaguma, D
   Hasegawa, M
   Yuzawa, Y
AF Arai, Haruna
   Hayashi, Hiroki
   Ogata, Soshiro
   Uto, Kenichi
   Saegusa, Jun
   Takahashi, Kazuo
   Koide, Shigehisa
   Inaguma, Daijyo
   Hasegawa, Midori
   Yuzawa, Yukio
TI Progression of immunoglobulin G4-related disease to systematic lupus
   erythematosus after gastric cancer surgery A case report
SO MEDICINE
LA English
DT Article
DE anti-nuclear antibody; IgG4-related disease; systemic lupus
   erythematosus
ID IGG4-RELATED DISEASE; DIAGNOSTIC-CRITERIA; ASSOCIATION
AB Rationale: Immunoglobulin G4 related disease (IgG4-RD) rarely coexists with other autoimmune diseases, though we had a patient whose primary clinical problem was shifted from IgG4-RD to systemic lupus erythematosus (SLE) after gastrectomy. The present paper aimed to report pathological findings and clinical course of the patient.
   Patient concerns: The patient was a male aged 74 years old with gastric cancer characterized by the following symptoms: Raynaud phenomenon, polyarthralgia, and swollen parotid glands on both sides. Before gastrectomy, laboratory examination results showed renal dysfunction, hypocomplementemia, antinuclear antibodies (ANAs) positivity, and elevated serum IgG and IgG4 levels.
   Diagnosis: Based on postoperative renal biopsy showing severe plasma cell infiltration with tubulointerstitial fibrosclerosis, the patient was diagnosed with IgG4-RD. Despite significant improvement in renal function and reduction in parotid gland swelling during the postoperative follow-up period, after 7 months of the gastrectomy, anti-DNA antibody levels were increased and serositis was detected, which indicated the onset of SLE. IgG4-type ANA were also detected in the sera of the patient.
   Interventions: Treatment by oral prednisolone at 30 mg/day was initiated.
   Outcomes: Pericardial fluid, pleural effusions, and thickening of the gallbladder wall improved after 3 months of treatment according to computed tomography.
   Lessons: This study presented a rare case of comorbidity, wherein the patient's primary problem progressed from IgG4-type ANA positive IgG4-RD to SLE after excision of gastric cancer.
C1 [Arai, Haruna; Hayashi, Hiroki; Takahashi, Kazuo; Koide, Shigehisa; Inaguma, Daijyo; Hasegawa, Midori; Yuzawa, Yukio] Fujita Hlth Univ, Sch Med, Dept Nephrol, 1-98 Dengakugakubo,Kutsukake Cho, Toyoake, Aichi 4701192, Japan.
   [Ogata, Soshiro] Fujita Hlth Univ, Sch Healthcare, Fac Nursing, 1-98 Dengakugakubo,Kutsukake Cho, Toyoake, Aichi, Japan.
   [Uto, Kenichi] Kobe Univ, Grad Sch Med, Kobe Univ Hosp, Dept Clin Lab,Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo, Japan.
   [Saegusa, Jun] Kobe Univ, Grad Sch Med, Dept Rheumatol & Clin Immunol, Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo, Japan.
C3 Fujita Health University; Fujita Health University; Kobe University;
   Kobe University
RP Hayashi, H (corresponding author), Fujita Hlth Univ, Sch Med, Dept Nephrol, 1-98 Dengakugakubo,Kutsukake Cho, Toyoake, Aichi 4701192, Japan.
EM hhayashi@fujita-hu.ac.jp
OI Takahashi, Kazuo/0000-0002-5774-4620
FU Aichi Kidney Foundation [H28-18]
FX This work was supported by the Aichi Kidney Foundation (H28-18). The
   funding source had no role in the study design; collection, analysis,
   and interpretation of data; report writing; or decision to submit the
   report for publication.
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TC 8
Z9 9
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0025-7974
EI 1536-5964
J9 MEDICINE
JI Medicine (Baltimore)
PD DEC
PY 2018
VL 97
IS 51
AR e13545
DI 10.1097/MD.0000000000013545
PG 6
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA HI3GA
UT WOS:000456334600033
PM 30572454
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Zhang, ZM
   Xue, ZY
   Liu, Y
   Liu, HK
   Guo, XD
   Li, Y
   Yang, HW
   Zhang, LJ
   Da, YR
   Yao, Z
   Zhang, RX
AF Zhang, Zimu
   Xue, Zhenyi
   Liu, Ying
   Liu, Hongkun
   Guo, Xiangdong
   Li, Yan
   Yang, Hongwei
   Zhang, Lijuan
   Da, Yurong
   Yao, Zhi
   Zhang, Rongxin
TI MicroRNA-181c promotes Th17 cell differentiation and mediates
   experimental autoimmune encephalomyelitis
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE MicroRNA-181c; Multiple sclerosis; Experimental autoimmune;
   encephalomyelitis; TGF-beta signaling; Th17 cell
ID REGULATORY T-CELLS; MULTIPLE-SCLEROSIS; GASTRIC-CANCER; EXPRESSION;
   DISEASE; SIGNALS; GROWTH; SMAD; INFLAMMATION; METASTASIS
AB Among T helper (Th) cell subsets differentiated from naive CD4(+) T cells, IL-17-producing Th17 cells are closely associated with the pathogenesis of autoimmune diseases, including multiple sclerosis (MS) and the MS animal model, experimental autoimmune encephalomyelitis (EAE). The modulation of Th17 differentiation offers a potential avenue for treatment. Although a series of microRNAs (miRNAs) that modulate autoimmune disease development have been reported, further studies on miRNA roles in Th17 differentiation and MS pathogenesis are still warranted. Here, we demonstrated that mice with miR-181c knockdown presented with delayed EAE and slowed disease progression, along with a decreased Th17 cell population. We also found that miR-181c was a Th17 cell-associated miRNA and that Smad7, a negative regulator of TGF-beta signaling, was a potential target of miR-181c. miR-181c knockdown rendered T cells less sensitive to TGF-beta-induced Smad2/3, enhancing the expression of IL-2 which has been reported to inhibit Th17 cell differentiation. Moreover, through the analysis of published miRNA expression profiles from the Gene Expression Omnibus database, increased miR-181c levels were found in peripheral blood from MS patients. Our results identified a novel miRNA that promotes Th17 cell differentiation and autoimmunity, thus miR-181c may serve as a potential treatment target in patients with MS. (C) 2018 Elsevier Inc. All rights reserved.
C1 [Zhang, Zimu; Xue, Zhenyi; Liu, Ying; Liu, Hongkun; Guo, Xiangdong; Li, Yan; Zhang, Lijuan; Da, Yurong; Zhang, Rongxin] Tianjin Med Univ, Sch Basic Med Sci,Dept Immunol, Tianjin Key Lab Cellular & Mol Immunol,Lab Immuno, Educ Minist China,Key Lab Immune Microenvironm &, Tianjin 300070, Peoples R China.
   [Liu, Ying] Tianjin First Cent Hosp, Dept Neurol, Tianjin, Peoples R China.
   [Yang, Hongwei] Tianjin Med Univ, Gen Hosp, Dept Neurol, Tianjin, Peoples R China.
   [Yang, Hongwei] Tianjin Med Univ, Gen Hosp, Tianjin Neurol Inst, Tianjin, Peoples R China.
   [Yao, Zhi] Tianjin Med Univ, Sch Basic Med Sci, Educ Minist China, Key Lab Immune Microenvironment & Dis,Dept Immuno, Tianjin 300070, Peoples R China.
   [Zhang, Rongxin] Guangdong Pharmaceut Univ, Sch Life Sci & Biopharmaceut, Guangdong Prov Key Lab Biotechnol Drug Candidates, Lab Immunol & Inflammat, Guangzhou, Guangdong, Peoples R China.
C3 Tianjin Medical University; Tianjin Medical University; Tianjin Medical
   University; Tianjin Medical University; Tianjin Medical University;
   Guangdong Pharmaceutical University
RP Da, YR; Zhang, RX (corresponding author), Tianjin Med Univ, Sch Basic Med Sci,Dept Immunol, Tianjin Key Lab Cellular & Mol Immunol,Lab Immuno, Educ Minist China,Key Lab Immune Microenvironm &, Tianjin 300070, Peoples R China.
EM dayr@tmu.edu.cn; rxzhang@gdpu.edu.cn
RI Zhang, Rongxin/ABG-3679-2021; Liu, Hongkun/AAP-4231-2021; Yang,
   Hongwei/AGX-5467-2022; Li, Yan/JQI-3638-2023
OI Zhang, Rongxin/0000-0002-4083-374X
FU National Natural Science Foundation of China [81272317, 81302568,
   81301026, 81501036, 81541032, 31600730, 81602496]; Natural Science
   Foundation of Tianjin [16JCYBJC24600, 16JCYBJC24800, 16JCYBJC26900];
   Postdoctoral Science Foundation of China [201620162016]
FX This work was supported by the National Natural Science Foundation of
   China through grant nos. 81272317, 81302568, 81301026, 81501036,
   81541032, 31600730, and 81602496; the Natural Science Foundation of
   Tianjin through grant nos. 16JCYBJC24600, 16JCYBJC24800, and
   16JCYBJC26900; and the Postdoctoral Science Foundation of China through
   grant no. 201620162016.
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NR 41
TC 53
Z9 58
U1 0
U2 23
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
EI 1090-2139
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD MAY
PY 2018
VL 70
BP 305
EP 314
DI 10.1016/j.bbi.2018.03.011
PG 10
WC Immunology; Neurosciences; Psychiatry
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Neurosciences & Neurology; Psychiatry
GA GH4US
UT WOS:000433400900029
PM 29545117
DA 2025-06-01
ER

PT J
AU Kishikawa, H
   Nakamura, K
   Takarabe, S
   Katayama, T
   Sasaki, A
   Miura, S
   Hayashi, Y
   Hoshi, H
   Kanai, T
   Nishida, J
AF Kishikawa, Hiroshi
   Nakamura, Kenji
   Takarabe, Sakiko
   Katayama, Tadashi
   Sasaki, Aya
   Miura, Soichiro
   Hayashi, Yukie
   Hoshi, Hitomi
   Kanai, Takahiro
   Nishida, Jiro
TI Clinical Characteristics of Patients With Previous Helicobacter pylori
   Infection-Induced Atrophic Gastritis
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE helicobacter pylori; atrophic gastritis; pepsinogen; autoimmune
   gastritis; gastric cancer screening
ID IGG ANTIBODY; CANCER RISK; PEPSINOGEN; CLASSIFICATION; ERADICATION;
   PREDICTORS
AB Aims: Patients with atrophic gastritis unrelated to autoimmune gastritis (AIG) and without active Helicobacter pylori ( H.pylori ) infection or previous eradication therapy are considered to have previous Helicobacter pylori infection -induced atrophic gastritis (PHIG). This study aimed to clarify the clinical characteristics of patients with PHIG. Methods: Consecutive patients who underwent upper gastrointestinal endoscopy during the study period were enrolled in the study. Pepsinogen and gastrin levels, H. pylori serology, and endoscopic atrophic grade were assessed. Patients were divided into five groups based on their H. pylori status and disease history (PHIG, without H. pylori infection, with active H. pylori infection, with successful H. pylori eradication, and AIG). Their gastric cancer risk status was classified according to the ABC method of serological gastric cancer screening. Results: Of 536 consecutive patients who underwent upper gastrointestinal endoscopy during the study period, 318 were included (31 with PHIG, 77 without H. pylori infection, 101 with active H. pylori infection, 80 with successful H. pylori eradication, and 29 with AIG). Of the 31 patients with PHIG, 21 (68%) were H. pylori -seronegative , and 20 (65%) were classified as group A (normal pepsinogen, H. pylori -seronegative). Patients with PHIG accounted for 90.1% of the patients at high risk for gastric cancer misclassified as group A. The pepsinogen and H. pylori serological profiles of patients with PHIG were similar to those of patients with successful H. pylori eradication more than six years previously. A receiver -operating characteristic curve (ROC) analysis that included 13 patients with AIG and without active H. pylori infection and no previous eradication therapy and 31 patients with PHIG revealed that an endoscopic atrophy grade of O -III or greater according to the Kimura-Takemoto classification can predict AIG. Conclusions: Two-thirds of the patients with PHIG were misclassified as being at low risk (group A) according to the ABC method, suggesting that endoscopy is necessary for group A patients. The results of the serological evaluation of PHIG indicated that patients with PHIG may have experienced spontaneous H. pylori eradication, possibly because of the use of antibiotics for other conditions. Autoimmune gastritis should be considered in the presence of grade 0 -III or greater gastric mucosal atrophy in patients with suspected PHIG, even if the autoantibody and histological findings are not available.
C1 [Kishikawa, Hiroshi; Nakamura, Kenji; Takarabe, Sakiko; Katayama, Tadashi; Nishida, Jiro] Tokyo Dent Coll, Ichikawa Gen Hosp, Gastroenterol, Chiba, Japan.
   [Sasaki, Aya] Tokyo Dent Coll, Ichikawa Gen Hosp, Clin Lab, Chiba, Japan.
   [Miura, Soichiro] Int Univ Hlth & Welf, Grad Sch, Tokyo, Japan.
   [Hayashi, Yukie; Hoshi, Hitomi; Kanai, Takahiro] Keio Univ, Gastroenterol & Hepatol, Tokyo, Japan.
C3 Tokyo Dental College; Tokyo Dental College; International University of
   Health & Welfare; Keio University
RP Kishikawa, H (corresponding author), Tokyo Dent Coll, Ichikawa Gen Hosp, Gastroenterol, Chiba, Japan.
EM kisikawa@tdc.ac.jp
FX The data generated and/or analyzed during the current study are not
   publicly available due to privacy reasons but are available from the
   corresponding author on reasonable request. We thank Dr. Masataka
   Ichikawa of Tokyo Dental College, Ichikawa General Hospital, for
   constructive criticism. We are also grateful to Editage (
   www.editage.jp) for assistance with editing the manuscript.
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TC 1
Z9 1
U1 2
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD JUN 28
PY 2024
VL 16
IS 6
AR e63368
DI 10.7759/cureus.63368
PG 12
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA XY3J9
UT WOS:001265199000012
PM 39070512
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Santhosh, S
   Musinsky, J
   Tracey, M
   Capustin, M
AF Santhosh, Sharon
   Musinsky, Jacob
   Tracey, Matthew
   Capustin, Matthew
TI High-grade neuroendocrine carcinoma presenting as dermatomyositis
SO BMJ CASE REPORTS
LA English
DT Article
DE Cancer - see Oncology; Dermatology; General practice / family medicine;
   Gastric cancer
ID POLYMYOSITIS
AB Dermatomyositis is a class of autoimmune connective tissue diseases characterised by skin rash and proximal myopathy. Research to date has shown a strong association between dermatomyositis and underlying malignancy. This report presents a case of rapidly progressing neuroendocrine carcinoma manifesting as paraneoplastic dermatomyositis in a relatively healthy middle-aged man. We aim to highlight the importance of having medical professionals be comfortable with identifying signs and symptoms of dermatomyositis in a timely and efficient manner. This report highlights the importance of being aware of the possibility of an underlying malignancy in a patient with dermatomyositis and being proficient in its workup
C1 [Santhosh, Sharon] Northwell Hlth, Internal Med, New Hyde Pk, NY 11040 USA.
   [Musinsky, Jacob; Capustin, Matthew] Northwell Hlth, New Hyde Pk, NY USA.
   [Tracey, Matthew] Northwell Hlth, Dept Radiol, New Hyde Pk, NY USA.
C3 Northwell Health; Northwell Health; Northwell Health
RP Santhosh, S (corresponding author), Northwell Hlth, Internal Med, New Hyde Pk, NY 11040 USA.
EM sharonsanthosh@yahoo.com; jmusinsky@northwell.edu;
   mtracey1@northwell.edu; mcapustin@northwell.edu
CR Dalakas MC, 2003, LANCET, V362, P971, DOI 10.1016/S0140-6736(03)14368-1
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NR 10
TC 0
Z9 0
U1 0
U2 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
EI 1757-790X
J9 BMJ CASE REP
JI BMJ Case Rep.
PD MAY 7
PY 2025
VL 18
IS 5
AR e264148
DI 10.1136/bcr-2024-264148
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 2IO1K
UT WOS:001483495400001
PM 40341082
DA 2025-06-01
ER

PT J
AU Richter, JE
AF Richter, Joel E.
TI How to manage refractory GERD
SO NATURE CLINICAL PRACTICE GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE eosinophilic esophagitis; GERD; nonacid reflux; pill esophagitis; PPIs
ID GASTROESOPHAGEAL-REFLUX DISEASE; EOSINOPHILIC ESOPHAGITIS; DOUBLE-BLIND;
   ACID REFLUX; SYMPTOMS; HEARTBURN; TERM
AB Patients who are unresponsive to 4-8 weeks' treatment with PPIs twice daily might have so-called refractory GERD. The first investigation these patients should undergo is upper endoscopy to exclude a diagnosis of peptic ulcer disease or cancer and identify the presence of esophagitis. The presence of esophagitis in these patients is suggestive of a pill-induced injury, an autoimmune skin disease involving the esophagus, eosinophilic esophagitis or, less likely, a hypersecretory syndrome or a genotype that confers altered metabolism of PPls. Refractory reflux syndromes associated with normal endoscopy findings are more problematic to diagnose and further testing may be required, including prolonged 48 h pH testing, impedance measurements (for nonacid reflux), esophageal manometry and gastric function tests. For patients with refractory GERD who do not have esophagitis, possible etiologies include nocturnal gastric acid breakthrough, nonacid GER, missed GER or other diseases such as achalasia, gastroparesis or functional heartburn.
C1 Temple Univ, Sch Med, Dept Med, Philadelphia, PA 19140 USA.
C3 Pennsylvania Commonwealth System of Higher Education (PCSHE); Temple
   University
RP Richter, JE (corresponding author), Temple Univ, Sch Med, Dept Med, Philadelphia, PA 19140 USA.
EM jrichter@temple.edu
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NR 40
TC 45
Z9 56
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1743-4378
J9 NAT CLIN PRACT GASTR
JI Nat. Clin. Pract. Gastroenterol. Hepatol.
PD DEC
PY 2007
VL 4
IS 12
BP 658
EP 664
DI 10.1038/ncpgasthep0979
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 235PE
UT WOS:000251246000008
PM 18043675
DA 2025-06-01
ER

PT J
AU Bimczok, D
   Smythies, LE
   Waites, KB
   Grams, JM
   Stahl, RD
   Mannon, PJ
   Peter, S
   Wilcox, CM
   Harris, PR
   Das, S
   Ernst, PB
   Smith, PD
AF Bimczok, Diane
   Smythies, Lesley E.
   Waites, Ken B.
   Grams, Jayleen M.
   Stahl, Richard D.
   Mannon, Peter J.
   Peter, Shajan
   Wilcox, C. Mel
   Harris, Paul R.
   Das, Soumita
   Ernst, Peter B.
   Smith, Phillip D.
TI Helicobacter pylori Infection Inhibits Phagocyte Clearance of
   Apoptotic Gastric Epithelial Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID NECROSIS-FACTOR-ALPHA; CYTOKINE PRODUCTION; SMALL-INTESTINE; TH1
   RESPONSE; IN-VITRO; MACROPHAGES; RECEPTOR; ACTIVATION; CANCER;
   RECOGNITION
AB Increased apoptotic death of gastric epithelial cells is a hallmark of Helicobacter pylori infection, and altered epithelial cell turnover is an important contributor to gastric carcinogenesis. To address the fate of apoptotic gastric epithelial cells and their role in H. pylori mucosal disease, we investigated phagocyte clearance of apoptotic gastric epithelial cells in H. pylori infection. Human gastric mononuclear phagocytes were analyzed for their ability to take up apoptotic epithelial cells (AECs) in vivo using immunofluorescence analysis. We then used primary human gastric epithelial cells induced to undergo apoptosis by exposure to live H. pylori to study apoptotic cell uptake by autologous monocyte-derived macrophages. We show that HLA-DR+ mononuclear phagocytes in human gastric mucosa contain cytokeratin-positive and TUNEL-positive AEC material, indicating that gastric phagocytes are involved in AEC clearance. We further show that H. pylori both increased apoptosis in primary gastric epithelial cells and decreased phagocytosis of the AECs by autologous monocyte-derived macrophages. Reduced macrophage clearance of apoptotic cells was mediated in part by H. pylori-induced macrophage TNF-alpha, which was expressed at higher levels in H. pyloriinfected, compared with uninfected, gastric mucosa. Importantly, we show that H. pylori-infected gastric mucosa contained significantly higher numbers of AECs and higher levels of nonphagocytosed TUNEL-positive apoptotic material, consistent with a defect in apoptotic cell clearance. Thus, as shown in other autoimmune and chronic inflammatory diseases, insufficient phagocyte clearance may contribute to the chronic and self-perpetuating inflammation in human H. pylori infection.
C1 [Bimczok, Diane; Smythies, Lesley E.; Mannon, Peter J.; Peter, Shajan; Wilcox, C. Mel; Smith, Phillip D.] Univ Alabama Birmingham, Dept Med, Birmingham, AL 35294 USA.
   [Waites, Ken B.] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA.
   [Grams, Jayleen M.; Stahl, Richard D.] Univ Alabama Birmingham, Dept Surg, Birmingham, AL 35294 USA.
   [Harris, Paul R.] Pontificia Univ Catolica Chile, Sch Med, Div Pediat, Unit Gastroenterol & Nutr, Santiago 6510273, Chile.
   [Das, Soumita; Ernst, Peter B.] Univ Calif San Diego, Dept Pathol, San Diego, CA 92093 USA.
   [Smith, Phillip D.] Vet Adm Med Ctr, Birmingham, AL 35233 USA.
C3 University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   University of Alabama System; University of Alabama Birmingham;
   Pontificia Universidad Catolica de Chile; University of California
   System; University of California San Diego; US Department of Veterans
   Affairs; Veterans Health Administration (VHA)
RP Smith, PD (corresponding author), Univ Alabama Birmingham, 1720 2nd Ave South,SHEL 611, Birmingham, AL 35294 USA.
EM pdsmith@uab.edu
RI Harris, Paul/HKF-7359-2023
OI Ernst, Peter/0000-0001-7777-1813; Harris, Paul/0000-0001-6226-0957
FU National Institutes of Health [DK-5449, AI-079145, AI-07047, DK-084063,
   AI-083539, DK-097144, RR-20136, DK-064400]; Mucosal HIV and
   Immunobiology Center; University of Alabama at Birmingham (UAB);
   Autoimmunity, Immunology and Transplantation Steering Committee Pilot
   Program; Clinical and Translational Science Pilot Program [UL1
   TR000165]; Fondo Nacional de Desarrollo Cientifico y Tecnologico
   [1130387]; Research Service of the Veterans Administration; Analytic and
   Preparative Cytometry Facility [P30 AR48311]; Digestive Diseases
   Research Development Center Human Cell/Tissue Core [DK-64400]; UAB High
   Resolution Imaging Facility
FX This work was supported by National Institutes of Health Grants DK-54495
   (to P.D.S.), AI-079145 and AI-07047 (to P.B.E.), DK-084063 (to P. B. E.
   and P. D. S.), AI-083539 (to L.E.S.), DK-097144 (to D.B.), RR-20136, and
   DK-064400, the Mucosal HIV and Immunobiology Center (to P.D.S. and
   L.E.S.), the University of Alabama at Birmingham (UAB) Autoimmunity,
   Immunology and Transplantation Steering Committee Pilot Program (to
   D.B.), UAB Center for Clinical and Translational Science Pilot Program
   Grant UL1 TR000165 (to D.B.), Fondo Nacional de Desarrollo Cientifico y
   Tecnologico Grant 1130387 (P.R.H.), and the Research Service of the
   Veterans Administration (P.D.S.). Support was also provided by the
   Analytic and Preparative Cytometry Facility (Grant P30 AR48311), the
   Digestive Diseases Research Development Center Human Cell/Tissue Core
   (Grant DK-64400), and the UAB High Resolution Imaging Facility.
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NR 47
TC 21
Z9 24
U1 0
U2 5
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD JUN 15
PY 2013
VL 190
IS 12
BP 6626
EP 6634
DI 10.4049/jimmunol.1203330
PG 9
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 163YE
UT WOS:000320373700076
PM 23686492
OA Green Accepted, Bronze
DA 2025-06-01
ER

PT J
AU Cao, JG
   Mu, QC
   Huang, HY
AF Cao, Junguo
   Mu, Qingchun
   Huang, Haiyan
TI The Roles of Insulin-Like Growth Factor 2 mRNA-Binding Protein 2 in
   Cancer and Cancer Stem Cells
SO STEM CELLS INTERNATIONAL
LA English
DT Review
ID CHRONIC LIVER-DISEASE; LONG NONCODING RNA; FACTOR-II; COLORECTAL-CANCER;
   BREAST-CANCER; HEPATOCELLULAR-CARCINOMA; TRANSCRIPTION FACTOR;
   AUTOIMMUNE-RESPONSE; GASTRIC-CANCER; KH DOMAINS
AB RNA-binding proteins (RBPs) mediate the localization, stability, and translation of the target transcripts and fine-tune the physiological functions of the proteins encoded. The insulin-like growth factor (IGF) 2 mRNA-binding protein (IGF2BP, IMP) family comprises three RBPs, IGF2BP1, IGF2BP2, and IGF2BP3, capable of associating with IGF2 and other transcripts and mediating their processing. IGF2BP2 represents the least understood member of this family of RBPs; however, it has been reported to participate in a wide range of physiological processes, such as embryonic development, neuronal differentiation, and metabolism. Its dysregulation is associated with insulin resistance, diabetes, and carcinogenesis and may potentially be a powerful biomarker and candidate target for relevant diseases. This review summarizes the structural features, regulation, and functions of IGF2BP2 and their association with cancer and cancer stem cells.
C1 [Cao, Junguo; Huang, Haiyan] Jilin Univ, Hosp 1, Dept Neurosurg, Xinmin St 71, Changchun, Jilin, Peoples R China.
   [Mu, Qingchun] Mudanjiang Med Univ, Hongqi Hosp, Mudanjiang, Peoples R China.
C3 Jilin University; Mudanjiang Medical University
RP Huang, HY (corresponding author), Jilin Univ, Hosp 1, Dept Neurosurg, Xinmin St 71, Changchun, Jilin, Peoples R China.; Mu, QC (corresponding author), Mudanjiang Med Univ, Hongqi Hosp, Mudanjiang, Peoples R China.
EM muqc@qq.com; huanghy@jlu.edu.cn
OI Mu, Qingchun/0000-0001-7578-5381
FU S&T Development Planning Program of Jilin Province [20150312005ZG]
FX This study was supported by grants from the S&T Development Planning
   Program of Jilin Province (nos. 20150312005ZG).
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NR 148
TC 117
Z9 123
U1 0
U2 26
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-966X
EI 1687-9678
J9 STEM CELLS INT
JI Stem Cells Int.
PY 2018
VL 2018
AR 4217259
DI 10.1155/2018/4217259
PG 15
WC Cell & Tissue Engineering
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA GA5DZ
UT WOS:000428353600001
PM 29736175
OA Green Submitted, Green Published, gold
DA 2025-06-01
ER

PT J
AU Egg, D
   Schwab, C
   Gabrysch, A
   Arkwright, PD
   Cheesman, E
   Giulino-Roth, L
   Neth, O
   Snapper, S
   Okada, S
   Moutschen, M
   Delvenne, P
   Pecher, AC
   Wolff, D
   Kim, YJ
   Seneviratne, S
   Kim, KM
   Kang, JM
   Ojaimi, S
   McLean, C
   Warnatz, K
   Seidl, M
   Grimbacher, B
AF Egg, David
   Schwab, Charlotte
   Gabrysch, Annemarie
   Arkwright, Peter D.
   Cheesman, Edmund
   Giulino-Roth, Lisa
   Neth, Olaf
   Snapper, Scott
   Okada, Satoshi
   Moutschen, Michel
   Delvenne, Philippe
   Pecher, Ann-Christin
   Wolff, Daniel
   Kim, Yae-Jean
   Seneviratne, Suranjith
   Kim, Kyoung-Mee
   Kang, Ji-Man
   Ojaimi, Samar
   McLean, Catriona
   Warnatz, Klaus
   Seidl, Maximilian
   Grimbacher, Bodo
TI Increased Risk for Malignancies in 131 Affected CTLA4 Mutation
   Carriers
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE CTLA4; combined immunodeficiency; primary immunodeficiency; malignancy;
   cancer predisposition; EBV; CMV
ID IMMUNE DYSREGULATION; GASTRIC-CANCER; LRBA; DEFICIENCY; IPILIMUMAB;
   NIVOLUMAB; MELANOMA; DISEASES
AB Background: Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) is a negative immune regulator on the surface of T cells. In humans, heterozygous germline mutations in CTLA4 can cause an immune dysregulation syndrome. The phenotype comprises a broad spectrum of autoinflammatory, autoimmune, and immunodeficient features. An increased frequency of malignancies in primary immunodeficiencies is known, but their incidence in CTLA-4 insufficiency is unknown.
   Methods: Clinical manifestations and details of the clinical history were assessed in a worldwide cohort of 184 CTLA4 mutation carriers. Whenever a malignancy was reported, a malignancy-specific questionnaire was filled.
   Results: Among the 184 CTLA4 mutation carriers, 131 were considered affected, indicating a penetrance of 71.2%. We documented 17 malignancies, which amounts to a cancer prevalence of 12.9% in affected CTLA4 mutation carriers. There were ten lymphomas, five gastric cancers, one multiple myeloma, and one metastatic melanoma. Seven lymphomas and three gastric cancers were EBV-associated.
   Conclusion: Our findings demonstrate an elevated cancer risk for patients with CTLA-4 insufficiency. As more than half of the cancers were EBV-associated, the failure to control oncogenic viruses seems to be part of the CTLA-4-insufficient phenotype. Hence, lymphoproliferation and EBV viral load in blood should be carefully monitored, especially when immunosuppressing affected CTLA4 mutation carriers.
C1 [Egg, David; Schwab, Charlotte; Gabrysch, Annemarie; Warnatz, Klaus; Seidl, Maximilian; Grimbacher, Bodo] Univ Freiburg, Univ Hosp, Med Ctr, Fac Med,Ctr Chron Immunodeficiency, Freiburg, Germany.
   [Arkwright, Peter D.; Cheesman, Edmund] Univ Manchester, Royal Manchester Childrens Hosp, Manchester, Lancs, England.
   [Giulino-Roth, Lisa] Weill Cornell Med, Dept Pediat, Div Pediat Hematol Oncol, New York, NY USA.
   [Neth, Olaf] Hosp Virgen Rocio, Inst Biomed Sevilla, Unidad Pediat, Secc Infectol & Inmunopatol, Seville, Spain.
   [Snapper, Scott] Childrens Hosp Boston, Dept Med, Div Pediat Gastroenterol Hepatol & Nutr, Boston, MA USA.
   [Okada, Satoshi] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Pediat, Hiroshima, Japan.
   [Moutschen, Michel; Delvenne, Philippe] Univ Hosp Liege, Dept Infect Dis & Gen Internal Med, Liege, Belgium.
   [Pecher, Ann-Christin] Univ Hosp Tubingen, Dept Internal Med 2, Tubingen, Germany.
   [Wolff, Daniel] Univ Hosp Regensburg, Dept Internal Med 3, Regensburg, Germany.
   [Kim, Yae-Jean] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Div Infect Dis & Immunodeficiency, Seoul, South Korea.
   [Seneviratne, Suranjith] UCL, Royal Free Hosp, Inst Immun & Transplantat, London, England.
   [Kim, Kyoung-Mee] Sungkyunkwan Univ, Samsung Med Ctr, Sch Med, Dept Pathol & Translat Genom, Seoul, South Korea.
   [Kang, Ji-Man] Natl Canc Ctr, Goyang, South Korea.
   [Ojaimi, Samar] Monash Univ, Dept Paediat, Clayton, Vic, Australia.
   [McLean, Catriona] Alfred Hlth, Prahran, Vic, Australia.
C3 University of Freiburg; University of Manchester; Manchester University
   NHS Foundation Trust; Royal Manchester Children's Hospital; Cornell
   University; Weill Cornell Medicine; Consejo Superior de Investigaciones
   Cientificas (CSIC); University of Sevilla; CSIC-JA-USE - Instituto de
   Biomedicina de Sevilla (IBIS); Virgen del Rocio University Hospital;
   Harvard University; Harvard University Medical Affiliates; Boston
   Children's Hospital; Hiroshima University; University of Liege; Eberhard
   Karls University of Tubingen; Eberhard Karls University Hospital;
   University of Regensburg; Sungkyunkwan University (SKKU); Samsung
   Medical Center; University of London; University College London; UCL
   Medical School; Royal Free London NHS Foundation Trust; Sungkyunkwan
   University (SKKU); Samsung Medical Center; National Cancer Center -
   Korea (NCC); Monash University; Alfred Health
RP Grimbacher, B (corresponding author), Univ Freiburg, Univ Hosp, Med Ctr, Fac Med,Ctr Chron Immunodeficiency, Freiburg, Germany.
EM bodo.grimbacher@uniklinik-freiburg.de
RI Seidl, Maxmilian/ABF-3322-2021; Seneviratne, Suranjith/N-2617-2018;
   Cheesman, Edmund/AAN-3717-2021; Arkwright, Peter/C-5149-2012; Pecher,
   Ann-Christin/AAC-4429-2022; Kim, Junetae/AAS-1234-2021; Warnatz,
   Klaus/AAD-3464-2022; Neth, Olaf/F-1167-2015; Okada, Satoshi/B-8901-2011
OI McLean, Catriona/0000-0002-0302-5727; Egg, David/0000-0002-7467-8960;
   Kang, Ji-Man/0000-0002-0678-4964; Seidl, Maxmilian/0000-0002-5559-4980;
   Neth, Olaf/0000-0001-5018-0466; Okada, Satoshi/0000-0002-4622-5657
FU German Ministry of Education and Research (BMBF) [01E01303, 01ZX1306F];
   German Research Society (DFG) [SFB1160-IMPATH]; German Research
   Foundation (DFG); University of Freiburg
FX The financial support for the conduct of the research came from the
   German Ministry of Education and Research (BMBF, grants # 01E01303 and
   01ZX1306F), and the German Research Society (DFG; SFB1160-IMPATH). The
   article processing charge was funded by the German Research Foundation
   (DFG) and the University of Freiburg in the funding programme Open
   Access Publishing. The grant agencies had no role in study design, the
   collection, analysis, and interpretation of data, the writing of the
   report, nor in the decision to submit the paper for publication. The
   authors are responsible for the content of this research.
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NR 31
TC 72
Z9 74
U1 0
U2 13
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD SEP 10
PY 2018
VL 9
AR 2012
DI 10.3389/fimmu.2018.02012
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GT0KQ
UT WOS:000444129100001
PM 30250467
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Gadiparthi, C
   Hans, A
   Potts, K
   Ismail, MK
AF Gadiparthi, Chiranjeevi
   Hans, Amneet
   Potts, Kyle
   Ismail, Mohammad K.
TI Gastrointestinal and Hepatic Disease in the Inflammatory Myopathies
SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA
LA English
DT Article
DE Corticosteroids; Creatine kinase; Dermatomyositis; Inclusion body
   myositis; Oropharyngeal dysphagia; Polymyositis
ID INCLUSION-BODY MYOSITIS; CANCER-ASSOCIATED MYOSITIS;
   PNEUMATOSIS-CYSTOIDES-INTESTINALIS; ONSET POLYMYOSITIS-DERMATOMYOSITIS;
   POPULATION-BASED COHORT; JUVENILE DERMATOMYOSITIS; ADULT
   DERMATOMYOSITIS; AUTOIMMUNE HEPATITIS; ULCERATIVE-COLITIS; CLINICAL
   CHARACTERISTICS
AB Although muscle weakness is the pathognomonic feature of idiopathic inflammatory myopathies, systemic organ involvement is not uncommon. The gastrointestinal and hepatic manifestations are well known. Oropharyngeal dysphagia is the most common gastrointestinal symptom and can be severe. Gastric and small intestinal motility disorders, including chronic intestinal pseudoobstruction, celiac disease, and inflammatory bowel disease, have been described. Comprehensive cancer screening is warranted soon after the diagnosis of inflammatory myopathies because of high risk of occult malignancies. Elevated levels of aminotransferases may suggest muscular injury rather than hepatic dysfunction. Knowledge regarding the systemic involvement of inflammatory myopathies can assist in timely diagnosis of these complex disorders.
C1 [Gadiparthi, Chiranjeevi] Univ Tennessee, Hlth Sci Ctr, Div Gastroenterol & Hepatol, 1211 Union Ave,Suite 340, Memphis, TN 38104 USA.
   [Hans, Amneet; Potts, Kyle] Univ Colorado, Sch Med, 13001 E 17th Pl, Aurora, CO 80045 USA.
   [Ismail, Mohammad K.] Univ Tennessee, Hlth Sci Ctr, Div Gastroenterol & Hepatol, 1211 Union Ave,Suite 460, Memphis, TN 38104 USA.
C3 University of Tennessee System; University of Tennessee Health Science
   Center; University of Colorado System; University of Colorado Anschutz
   Medical Campus; University of Tennessee System; University of Tennessee
   Health Science Center
RP Ismail, MK (corresponding author), Univ Tennessee, Hlth Sci Ctr, Div Gastroenterol & Hepatol, 1211 Union Ave,Suite 460, Memphis, TN 38104 USA.
EM mismail@uthsc.edu
RI Gadiparthi, Chiranjeevi/AAF-5194-2019
OI Gadiparthi, Chiranjeevi/0000-0002-8905-6742
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NR 98
TC 17
Z9 18
U1 0
U2 7
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-857X
EI 1558-3163
J9 RHEUM DIS CLIN N AM
JI Rheum. Dis. Clin. North Am.
PD FEB
PY 2018
VL 44
IS 1
BP 113
EP +
DI 10.1016/j.rdc.2017.09.006
PG 19
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA FS8YJ
UT WOS:000422700300009
PM 29149920
DA 2025-06-01
ER

PT J
AU Ness-Abramof, R
   Nabriski, DA
   Braverman, LE
   Shilo, L
   Weiss, E
   Reshef, T
AF Ness-Abramof, Rosane
   Nabriski, Dan A.
   Braverman, Lewis E.
   Shilo, Lotan
   Weiss, Eliahu
   Reshef, Tamar
TI Prevalence and evaluation of B12 deficiency in patients with autoimmune
   thyroid disease
SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES
LA English
DT Article
DE vitamin B12 deficiency; autoimmune thyroid disease; gastrin; parietal
   cell antibodies
ID GASTRIC AUTOIMMUNITY; COBALAMIN DEFICIENCY; PERNICIOUS-ANEMIA;
   MANIFESTATIONS; VITAMIN-B-12; ASSOCIATION; TUMORS
AB Background. Patients with autoimmune thyroid disease (AITD) have a higher prevalence of pernicious anemia compared with the general population. Clinical signs of B12 deficiency may be subtle and missed, particularly in patients with known autoimmune disease. We assessed the prevalence of vitamin B12 deficiency in patients with AITD and whether their evaluation may be simplified by measuring fasting gastrin levels. Methods: Serum B12 levels was measured in 115 patients with AITD (7 men and 108 women), with a mean age of 47 +/- 15 years. In patients with low serum B12 levels (<= 133 pmol/L), fasting serum gastrin and parietal cell antibodies (PCA) were measured. Results: Thirty-two patients (28%) with AITD had low B12 levels. Fasting serum gastrin was measured in 26 and was higher than normal in 8 patients. PCA were also measured in 27 patients with B12 deficiency and were positive in 8 patients. Five patients with high gastrin levels underwent gastroscopy with biopsy, and atrophic gastritis was diagnosed in all. The prevalence of pernicious anemia as assessed by high serum gastrin levels in patients with low B12 was 31%. Conclusions: Patients with AITD have a high prevalence of B12 deficiency and particularly of pernicious anemia. The evaluation of B12 deficiency can be simplified by measuring fasting serum gastrin and, if elevated, referring the patient for gastroscopy.
C1 Tel Aviv Univ, Endocrine Unit, Sapir Med Ctr, IL-44261 Kefar Sava, Israel.
   Tel Aviv Univ, Endocrine Lab, Sapir Med Ctr, IL-44261 Kefar Sava, Israel.
   Tel Aviv Univ, Immunol Lab, Sapir Med Ctr, IL-44261 Kefar Sava, Israel.
   Boston Med Ctr, Div Endocrinol Diabet & Nutr, Boston, MA USA.
C3 Tel Aviv University; Sackler Faculty of Medicine; Tel Aviv University;
   Sackler Faculty of Medicine; Tel Aviv University; Sackler Faculty of
   Medicine; Boston Medical Center
RP Ness-Abramof, R (corresponding author), Tel Aviv Univ, Endocrine Unit, Sapir Med Ctr, Tchernikovsky 53, IL-44261 Kefar Sava, Israel.
EM Rosane-Abramof.Ness@clalit.org.il
OI Braverman, Lewis/0000-0003-1263-1099
CR Allen LH, 2004, NUTR REV, V62, pS29, DOI 10.1111/j.1753-4887.2004.tb00069.x
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NR 20
TC 48
Z9 50
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0002-9629
J9 AM J MED SCI
JI Am. J. Med. Sci.
PD SEP
PY 2006
VL 332
IS 3
BP 119
EP 122
DI 10.1097/00000441-200609000-00004
PG 4
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 168FE
UT WOS:000246507700004
PM 16969140
DA 2025-06-01
ER

PT J
AU Sasahara, GL
   Gouveia, FS
   Rodrigues, RD
   Zampieri, DS
   Fonseca, SGC
   Gonçalves, RDR
   Athaydes, BR
   Kitagawa, RR
   Santos, FA
   Sousa, EHS
   Nagao-Dias, AT
   Lopes, LGD
AF Sasahara, Greyce Luri
   Gouveia Junior, Florencio Sousa
   Rodrigues, Raphael de Oliveira
   Zampieri, Davila Souza
   Cruz Fonseca, Said Goncalves
   Ribeiro Goncalves, Rita de Cassia
   Athaydes, Brena Ramos
   Kitagawa, Rodrigo Rezende
   Santos, Flavia Almeida
   Silva Sousa, Eduardo Henrique
   Nagao-Dias, Aparecida Tiemi
   de Franca Lopes, Luiz Gonzaga
TI Nitro-imidazole-based ruthenium complexes with antioxidant and
   anti-inflammatory activities
SO JOURNAL OF INORGANIC BIOCHEMISTRY
LA English
DT Article
DE Ruthenium; Metallodrugs; Anti-inflammatory; ROS; Helicobacter pylori
ID LIPID-PEROXIDATION; GASTRIC-ULCER; DNA; MALONDIALDEHYDE; CYTOTOXICITY;
   RESISTANCE; INHIBITION; EXPRESSION; 2,2-BIPYRIDINE; INVOLVEMENT
AB Inflammation is a physiological process triggered in response to tissue damage, and involves events related to cell recruitment, cytokines release and reactive oxygen species (ROS) production. Failing to control the process duration lead to chronification and may be associated with the development of various pathologies, including autoimmune diseases and cancer. Considering the pharmacological potential of metal-based compounds, two new ruthenium complexes were synthesized: cis-[Ru(NO2)(bpy)(2)(5NIM)]PF6 (1) and cis-[RuCl(bpy)(2)(MTZ)]PF6 (2), where bpy = 2,2'-bipyridine, 5NIM = 5-nitroimidazole and MTZ = metronidazole. Both products were characterized by spectroscopic techniques, followed by Density Functional Theory (DFT) calculations in order to support experimental findings. Afterwards, their in vitro cytotoxic, antioxidant and anti-inflammatory activities were investigated. Compounds 1 and 2 presented expressive in vitro antioxidant activity, reducing lipid peroxidation and decreasing intracellular ROS levels with comparable effectiveness to the standard steroidal drug dexamethasone or alpha-tocopherol. These complexes showed no noticeable cytotoxicity on the tested cancer cell lines. Bactericidal assay against metronidazole-resistant Helicobacter pylori, a microorganism able to disrupt oxidative balance, unraveled compound 1 moderate activity over that strain. Besides this, it was able to inhibit interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) production as well as interleukin-beta (IL-beta) and cyclooxygenase-2 (COX-2) expression in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. This latter activity is remarkable, which has not been reported for other ruthenium-based complexes. Altogether, these results suggest cis-[Ru(NO2)(bpy)(2)(5NIM)]PF6 complex has potential pharmacological application as an anti-inflammatory agent that deserve further biological investigation.
C1 [Sasahara, Greyce Luri; Rodrigues, Raphael de Oliveira; Nagao-Dias, Aparecida Tiemi] Univ Fed Ceara, Fac Pharm Dent & Nursing, Dept Clin & Toxicol Anal, Fortaleza, Ceara, Brazil.
   [Gouveia Junior, Florencio Sousa; Zampieri, Davila Souza; Silva Sousa, Eduardo Henrique; de Franca Lopes, Luiz Gonzaga] Univ Fed Ceara, Dept Organ & Inorgan Chem, POB 6021, Fortaleza, Ceara, Brazil.
   [Cruz Fonseca, Said Goncalves] Univ Fed Ceara, Fac Pharm Dent & Nursing, Dept Pharm, Fortaleza, Ceara, Brazil.
   [Ribeiro Goncalves, Rita de Cassia; Athaydes, Brena Ramos; Kitagawa, Rodrigo Rezende] Univ Fed Espirito Santo, Fac Pharm, Dept Pharmaceut Sci, Vitoria, ES, Brazil.
   [Santos, Flavia Almeida] Univ Fed Ceara, Fac Med, Dept Physiol & Pharmacol, Fortaleza, Ceara, Brazil.
C3 Universidade Federal do Ceara; Universidade Federal do Ceara;
   Universidade Federal do Ceara; Universidade Federal do Espirito Santo;
   Universidade Federal do Ceara
RP Lopes, LGD (corresponding author), Univ Fed Ceara, Dept Organ & Inorgan Chem, POB 6021, Fortaleza, Ceara, Brazil.
EM lopeslu@dqoi.ufc.br
RI Sasahara, Greyce/GLS-1037-2022; Goncalves, Rita/AAI-6760-2021; Athaydes,
   Brena/LZH-5516-2025; Zampieri, Davila/P-3857-2016; de Franca Lopes, Luiz
   Gonzaga/J-4385-2015; Kitagawa, Rodrigo Rezende/E-8639-2019; Santos,
   Flavia/S-5321-2016; Sousa, Eduardo/J-8167-2014
OI SASAHARA, GREYCE LURI/0000-0001-6944-7247; Zampieri,
   Davila/0000-0002-2702-7268; de Franca Lopes, Luiz
   Gonzaga/0000-0002-3641-1835; Ribeiro Goncalves, Rita de
   Cassia/0000-0001-9352-2454; Kitagawa, Rodrigo
   Rezende/0000-0002-2208-6699; Santos, Flavia/0000-0003-3625-8540; Sousa,
   Eduardo/0000-0002-0007-8452
FU Brazilian agency CAPES; Brazilian agency CNPq [303355/2018-2,
   308383/2018-4, 01/2016 403866/20162]; Brazilian agency FUNCAP
   [PPSUS12535691-9, PRONEX PR2-0101-00030.01.00/15 SPU, 3265612/2015];
   Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior -Brasil
   (CAPES) [001]
FX The authors thank CENAPAD-UFC for computer facilities, CENAUREN-UFC for
   the acquisition of NMR spectra, Clinical and Toxicological Analysis
   Laboratory (LACT, Federal University of Ceara) for technical support in
   PCR analysis. Additionally, we are thankful to the Brazilian agencies
   CAPES, CNPq (L. G. F. Lopes 303355/2018-2, E. H. S. Sousa 308383/2018-4,
   Edital Universal 01/2016 403866/20162), FUNCAP (PPSUS12535691-9, PRONEX
   PR2-0101-00030.01.00/15 SPU No: 3265612/2015) for financial support.
   This study was financed in part by the Coordenacao de Aperfeicoamento de
   Pessoal de Nivel Superior -Brasil (CAPES) -Finance Code 001.
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NR 94
TC 28
Z9 28
U1 1
U2 25
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0162-0134
EI 1873-3344
J9 J INORG BIOCHEM
JI J. Inorg. Biochem.
PD MAY
PY 2020
VL 206
AR 111048
DI 10.1016/j.jinorgbio.2020.111048
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA LH2PX
UT WOS:000528630900023
PM 32151873
DA 2025-06-01
ER

PT J
AU Engler, DB
   Leonardi, I
   Hartung, ML
   Kyburz, A
   Spath, S
   Becher, B
   Rogler, G
   Müller, A
AF Engler, Daniela B.
   Leonardi, Irina
   Hartung, Mara L.
   Kyburz, Andreas
   Spath, Sabine
   Becher, Burkhard
   Rogler, Gerhard
   Mueller, Anne
TI Helicobacter pylori-specific Protection Against Inflammatory
   Bowel Disease Requires the NLRP3 Inflammasome and IL-18
SO INFLAMMATORY BOWEL DISEASES
LA English
DT Article
DE chronic intestinal inflammation; microbial immunomodulation;
   autoimmunity; mucus production; inflammasome activation
ID TRICHURIS-SUIS THERAPY; REGULATORY T-CELLS; DENDRITIC CELLS;
   CROHNS-DISEASE; INTESTINAL INFLAMMATION; ULCERATIVE-COLITIS; IMMUNE
   TOLERANCE; GASTRIC-CANCER; INFECTION; METAANALYSIS
AB Background:The Gram-negative bacterium Helicobacter pylori is a constituent of the human gastric microbiota. Chronic infection with H. pylori causes gastritis and predisposes to gastric carcinoma but has also been inversely linked to various allergic and chronic inflammatory conditions. In particular, large meta-analyses have documented an inverse association between H. pylori infection and the risk of developing ulcerative colitis and Crohn's disease.Methods:We investigated possible protective effects of experimental H. pylori infection and of regular treatment with H. pylori extract in 2 mouse models of colitis and in mouse models of type I diabetes and multiple sclerosis. The mechanism of protection was examined in mouse strains lacking specific innate immune recognition pathways and cytokines.Results:We show here that experimental infection with H. pylori and administration of regular doses of H. pylori extract both alleviate the clinical and histopathological features of dextran sodium sulfate-induced chronic colitis and of T-cell transfer-induced colitis. High resolution endoscopy of the protected animals revealed the accumulation of large amounts of colonic mucus upon H. pylori exposure, which could be attributed to transcriptional activation of the mucin 2 gene. The protection against dextran sodium sulfate-induced colitis was dependent on the NLRP3 inflammasome and interleukin-18 signaling. Other autoimmune diseases, i.e., experimental autoimmune encephalomyelitis and type I diabetes, were not controlled by H. pylori.Conclusions:In summary, we propose here that the immunomodulatory activity of an ancient constituent of the gut microbiota, H. pylori, may be exploited for the prevention and/or treatment of inflammatory bowel diseases.
C1 [Engler, Daniela B.; Hartung, Mara L.; Kyburz, Andreas; Mueller, Anne] Univ Zurich, Inst Mol Canc Res, CH-8057 Zurich, Switzerland.
   [Spath, Sabine; Becher, Burkhard] Univ Zurich, Expt Immunol, CH-8057 Zurich, Switzerland.
   [Leonardi, Irina; Rogler, Gerhard] Univ Zurich Hosp, Div Gastroenterol & Hepatol, CH-8091 Zurich, Switzerland.
C3 University of Zurich; University of Zurich; University of Zurich;
   University Zurich Hospital
RP Müller, A (corresponding author), Univ Zurich, Inst Mol Canc Res, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
EM mueller@imcr.uzh.ch
RI Leonardi, Irina/AAW-7480-2020; Becher, Burkhard/ABE-4225-2020; Rogler,
   Gerhard/O-5308-2015
OI Leonardi, Irina/0000-0002-0369-7371; Becher,
   Burkhard/0000-0002-1541-7867; Muller, Anne/0000-0002-1368-8276; Spath,
   Sabine/0000-0002-2689-1951; Rogler, Gerhard/0000-0002-1733-9188
FU Gebert Ruf Foundation [GRS-043/11]
FX Supported by the Gebert Ruf Foundation (Grant number GRS-043/11 to
   A.M.).
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NR 37
TC 71
Z9 74
U1 0
U2 36
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 1078-0998
EI 1536-4844
J9 INFLAMM BOWEL DIS
JI Inflamm. Bowel Dis.
PD APR
PY 2015
VL 21
IS 4
BP 854
EP 861
DI 10.1097/MIB.0000000000000318
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA CE2TM
UT WOS:000351671500018
PM 25742401
OA Bronze, Green Published
DA 2025-06-01
ER

PT J
AU Ceeraz, S
   Nowak, EC
   Noelle, RJ
AF Ceeraz, Sabrina
   Nowak, Elizabeth C.
   Noelle, Randolph J.
TI B7 family checkpoint regulators in immune regulation and disease
SO TRENDS IN IMMUNOLOGY
LA English
DT Review
ID T-CELL-ACTIVATION; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
   MONOCLONAL-ANTIBODY TGN1412; DEATH-1 PD-1 PATHWAY; LUNG-CANCER CELL;
   PROGRAMMED DEATH-1; CD28 COSTIMULATION; PROSTATE-CANCER; GASTRIC-CANCER;
   NOD MICE
AB Fine-tuning the immune response and maintaining tolerance to self-antigens involves a complex network of co-stimulatory and co-inhibitory molecules. The recent FDA approval of ipilimumab, a monoclonal antibody blocking cytotoxic T lymphocyte antigen (CTLA)-4, demonstrates the impact of checkpoint regulators in disease. This is reinforced by ongoing clinical trials targeting not only CTLA-4, but also the programmed death (PD)-1 and B7-H4 pathways in various disease states. Recently, two new B7 family inhibitory ligands, V-domain Ig suppressor of T cell activation (VISTA) and B7-H6 were identified. Here, we review recent understanding of B7 family members and their concerted regulation of the immune response to either self or foreign pathogens. We also discuss clinical developments in targeting these pathways in different disease settings, and introduce VISTA as a putative therapeutic target.
C1 [Ceeraz, Sabrina; Nowak, Elizabeth C.; Noelle, Randolph J.] Geisel Sch Med Dartmouth, Dept Microbiol & Immunol, Norris Cotton Canc Ctr, Lebanon, NH 03756 USA.
   [Noelle, Randolph J.] Kings Coll London, Guys Hosp, MRC, Ctr Transplantat, London SE1 9RT, England.
C3 Dartmouth College; Norris Cotton Cancer Center; University of London;
   King's College London; Guy's & St Thomas' NHS Foundation Trust
RP Noelle, RJ (corresponding author), Geisel Sch Med Dartmouth, Dept Microbiol & Immunol, Norris Cotton Canc Ctr, 1 Med Ctr Dr, Lebanon, NH 03756 USA.
EM Randolph.J.Noelle@Dartmouth.edu
OI Nowak, Elizabeth/0000-0001-8791-6166
FU National Institutes of Health [R01AI098007]; Wellcome Trust; National
   Institute for Health Research (NIHR) Biomedical Research Centre based at
   Guy's and St Thomas' NHS Foundation Trust; King's College London; MRC
   [G0802651] Funding Source: UKRI
FX This research was supported by the National Institutes of Health
   R01AI098007, Wellcome Trust (principle research fellowship to RJN), and
   National Institute for Health Research (NIHR) Biomedical Research Centre
   based at Guy's and St Thomas' NHS Foundation Trust and King's College
   London. The views expressed are those of the author(s) and not
   necessarily those of the NIH, NHS, the NIHR or the Department of Health.
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NR 114
TC 247
Z9 294
U1 2
U2 59
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4906
EI 1471-4981
J9 TRENDS IMMUNOL
JI Trends Immunol.
PD NOV
PY 2013
VL 34
IS 11
BP 556
EP 563
DI 10.1016/j.it.2013.07.003
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 256AS
UT WOS:000327282700005
PM 23954143
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Osmola, M
   Hemont, C
   Chapelle, N
   Vibet, MA
   Tougeron, D
   Moussata, D
   Lamarque, D
   Bigot-Corbel, E
   Masson, D
   Blin, J
   Leroy, M
   Josien, R
   Mosnier, JF
   Martin, J
   Matysiak-Budnik, T
AF Osmola, Malgorzata
   Hemont, Caroline
   Chapelle, Nicolas
   Vibet, Marie-Anne
   Tougeron, David
   Moussata, Driffa
   Lamarque, Dominique
   Bigot-Corbel, Edith
   Masson, Damien
   Blin, Justine
   Leroy, Maxime
   Josien, Regis
   Mosnier, Jean-Francois
   Martin, Jerome
   Matysiak-Budnik, Tamara
TI Atrophic Gastritis and Autoimmunity: Results from a Prospective,
   Multicenter Study
SO DIAGNOSTICS
LA English
DT Article
DE autoimmune gastritis; chronic atrophic gastritis; autoimmunity; gastric
   cancer; H.pylori
ID HELICOBACTER-PYLORI INFECTION; ANTINUCLEAR ANTIBODIES; AUTOANTIBODIES;
   CANCER; PREVALENCE; DISEASES
AB Despite a global decrease, gastric cancer (GC) incidence appears to be increasing recently in young, particularly female, patients. The causal mechanism for this "new" type of GC is unknown, but a role for autoimmunity is suggested. A cascade of gastric precancerous lesions, beginning with chronic atrophic gastritis (CAG), precedes GC. To test the possible existence of autoimmunity in patients with CAG, we aimed to analyze the prevalence of several autoantibodies in patients with CAG as compared to control patients. Sera of 355 patients included in our previous prospective, multicenter study were tested for 19 autoantibodies (anti-nuclear antibodies, ANA, anti-parietal cell antibody, APCA, anti-intrinsic factor antibody, AIFA, and 16 myositis-associated antibodies). The results were compared between CAG patients (n = 154), including autoimmune gastritis patients (AIG, n = 45), non-autoimmune gastritis patients (NAIG, n = 109), and control patients (n = 201). ANA positivity was significantly higher in AIG than in NAIG or control patients (46.7%, 29%, and 27%, respectively, p = 0.04). Female gender was positively associated with ANA positivity (OR 0.51 (0.31-0.81), p = 0.005), while age and H. pylori infection status were not. Myositis-associated antibodies were found in 8.9% of AIG, 5.5% of NAIG, and 4.4% of control patients, without significant differences among the groups (p = 0.8). Higher APCA and AIFA positivity was confirmed in AIG, and was not associated with H. pylori infection, age, or gender in the multivariate analysis. ANA antibodies are significantly more prevalent in AIG than in control patients, but the clinical significance of this finding remains to be established. H. pylori infection does not affect autoantibody seropositivity (ANA, APCA, AIFA). The positivity of myositis-associated antibodies is not increased in patients with CAG as compared to control patients. Overall, our results do not support an overrepresentation of common autoantibodies in patients with CAG.
C1 [Osmola, Malgorzata] Med Univ Warsaw, Dept Hematol Transplantat & Internal Med, PL-02097 Warsaw, Poland.
   [Hemont, Caroline; Josien, Regis; Martin, Jerome] Univ Hosp Nantes, Dept Immunol, F-44093 Nantes, France.
   [Chapelle, Nicolas; Matysiak-Budnik, Tamara] Univ Hosp Nantes, Inst Malad Appareil Digest IMAD, Hepatogastroenterol & Digest Oncol, Hotel Dieu, Pl Alexis Ricordeau, F-44093 Nantes 1, France.
   [Chapelle, Nicolas; Josien, Regis; Martin, Jerome; Matysiak-Budnik, Tamara] Inst Natl Sante & Rech Med INSERM, Ctr Rech Translat Transplantat & Immunol CR2TI, U1064, F-44093 Nantes, France.
   [Chapelle, Nicolas; Bigot-Corbel, Edith; Masson, Damien; Blin, Justine; Josien, Regis; Mosnier, Jean-Francois; Martin, Jerome; Matysiak-Budnik, Tamara] Univ Nantes, Fac Med, F-44300 Nantes, France.
   [Vibet, Marie-Anne; Leroy, Maxime] Ctr Hosp Univ Nantes, Dept Biostat, F-44093 Nantes, France.
   [Tougeron, David] Univ Poitiers, Poitiers Univ Hosp, Dept Hepatogastroenterol, F-86000 Poitiers, France.
   [Moussata, Driffa] Univ Hosp Tours, Dept Hepatogastroenterol, F-37044 Tours, France.
   [Lamarque, Dominique] Paris Saclay Univ, Univ Versailles St Quentin En Yvelines, Inst Natl Sante & Rech Med INSERM, Ambroise Pare Hosp,AP HP,Dept Hepatogastroenterol,, F-91190 Paris, France.
   [Bigot-Corbel, Edith; Masson, Damien; Blin, Justine] Univ Hosp Nantes, Dept Biochem, F-44093 Nantes, France.
   [Blin, Justine] Inst Natl Sante & Rech Med INSERM, U1235 Enter Nervous Syst Gut & Brain Disorders TEN, F-44300 Nantes, France.
   [Mosnier, Jean-Francois] Univ Hosp Nantes, Dept Pathol, F-44093 Nantes, France.
C3 Medical University of Warsaw; Nantes Universite; CHU de Nantes; Nantes
   Universite; CHU de Nantes; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Nantes Universite; Nantes Universite; CHU
   de Nantes; CHU Poitiers; Universite de Poitiers; CHU Tours; Assistance
   Publique Hopitaux Paris (APHP); Hopital Universitaire Ambroise-Pare -
   APHP; Universite Paris Saclay; Institut National de la Sante et de la
   Recherche Medicale (Inserm); Nantes Universite; CHU de Nantes; Institut
   National de la Sante et de la Recherche Medicale (Inserm); Nantes
   Universite; CHU de Nantes
RP Matysiak-Budnik, T (corresponding author), Univ Hosp Nantes, Inst Malad Appareil Digest IMAD, Hepatogastroenterol & Digest Oncol, Hotel Dieu, Pl Alexis Ricordeau, F-44093 Nantes 1, France.; Matysiak-Budnik, T (corresponding author), Inst Natl Sante & Rech Med INSERM, Ctr Rech Translat Transplantat & Immunol CR2TI, U1064, F-44093 Nantes, France.; Matysiak-Budnik, T (corresponding author), Univ Nantes, Fac Med, F-44300 Nantes, France.
EM mosmola@wum.edu.pl; tamara.matysiakbudnik@chu-nantes.fr
RI tougeron, david/ABF-3217-2020; Chapelle, Nicolas/JSL-6988-2023; Martin,
   Jerome/GZG-4189-2022; Osmola, Malgorzata/ABB-3318-2021
OI Lamarque, Dominique/0000-0002-0899-2222; , Blin/0000-0003-2695-610X;
   Chapelle, Nicolas/0000-0003-4834-9693; Osmola,
   Malgorzata/0000-0001-6188-7328; tougeron, david/0000-0002-8065-9635
FU FARE grant from Societe Nationale Francaise de Gastroenterologie (SNFGE)
   in 2019; Ligue contre le Cancer; BIOHIT; FUJIREBIO; SanteDige foundation
FX This research was financed by FARE grant from Societe Nationale
   Francaise de Gastroenterologie (SNFGE) in 2019, la Ligue contre le
   Cancer, and unrestricted grants from BIOHIT and FUJIREBIO, and the
   SanteDige foundation.
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NR 51
TC 8
Z9 10
U1 0
U2 7
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD APR 30
PY 2023
VL 13
IS 9
AR 1599
DI 10.3390/diagnostics13091599
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA G1YL3
UT WOS:000987195600001
PM 37174990
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Tiaka, EK
   Manolakis, AC
   Kapsoritakis, AN
   Potamianos, SP
AF Tiaka, Elisavet K.
   Manolakis, Anastassios C.
   Kapsoritakis, Andreas N.
   Potamianos, Spyros P.
TI The implication of adiponectin and resistin in gastrointestinal diseases
SO CYTOKINE & GROWTH FACTOR REVIEWS
LA English
DT Review
DE Adipokines; Adiponectin; Resistin; Obesity; Gastrointestinal diseases
ID MESENTERIC ADIPOSE-TISSUE; ACTIVATED RECEPTOR-GAMMA;
   INFLAMMATORY-BOWEL-DISEASE; LOW PLASMA ADIPONECTIN; BONE-MINERAL
   DENSITY; HUMAN COLON-CANCER; INSULIN-RESISTANCE; COLORECTAL-CANCER;
   MOLECULE-BETA; CELL-PROLIFERATION
AB Adiponectin and resistin, members of the adipokine family, are multi-task hormones involved in several disorders, including those of the alimentary tract. In the present review, eligible studies focusing on the role of adiponectin and resistin in gastrointestinal diseases are manifested together and classified according to anatomic criteria. In addition, similarities and common patterns have been recognized, ultimately revealing an inverse association: the down-regulation of adiponectin and up-regulation of resistin - both in vitro and in vivo - in gastrointestinal disorders, irrespective of their diverse nature inflammatory, autoimmune or malignant - or anatomic position - esophageal, gastric, of the small intestine, colonic. Finally, a potential role for both adipokines in alimentary tract-related carcinogenesis has been identified, possibly representing a missing link between obesity and cancer. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Tiaka, Elisavet K.; Manolakis, Anastassios C.; Kapsoritakis, Andreas N.; Potamianos, Spyros P.] Univ Thessaly, Univ Hosp Larissa, Sch Med, Dept Gastroenterol, Larisa 41110, Greece.
C3 General University Hospital of Larissa; University of Thessaly
RP Kapsoritakis, AN (corresponding author), Univ Thessaly, Univ Hosp Larissa, Sch Med, Dept Gastroenterol, Larisa 41110, Greece.
EM kapsoritakis@med.uth.gr
OI MANOLAKIS, ANASTASSIOS/0000-0001-8661-6997
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NR 149
TC 26
Z9 26
U1 0
U2 9
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6101
EI 1879-0305
J9 CYTOKINE GROWTH F R
JI Cytokine Growth Factor Rev.
PD APR
PY 2011
VL 22
IS 2
BP 109
EP 119
DI 10.1016/j.cytogfr.2011.04.002
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 791KU
UT WOS:000292664900006
PM 21531165
DA 2025-06-01
ER

PT J
AU Venerito, M
   Varbanova, M
   Röhl, FW
   Reinhold, D
   Frauenschläger, K
   Jechorek, D
   Weigt, J
   Link, A
   Malfertheiner, P
AF Venerito, Marino
   Varbanova, Mariya
   Roehl, Friedrich-Wilhelm
   Reinhold, Dirk
   Frauenschlaeger, Katrin
   Jechorek, Doerthe
   Weigt, Jochen
   Link, Alexander
   Malfertheiner, Peter
TI Oxyntic gastric atrophy in Helicobacter pylori gastritis is
   distinct from autoimmune gastritis
SO JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
ID PERNICIOUS-ANEMIA; THYROID-DISEASE; CANCER; LESIONS; CLASSIFICATION;
   PATHOGENESIS; MANAGEMENT; INFECTION; DIAGNOSIS; PATHOLOGY
AB Aim To assess characteristics of oxyntic gastric atrophy (OGA) in autoimmune gastritis (AIG) compared with OGA as a consequence of Helicobacter pylori infection.
   Methods Patients undergoing oesophagogastroduodenoscopy from July 2011 to October 2014 were prospectively included (N = 452). Gastric biopsies were obtained for histology and H. pylori testing. Serum gastrin-17 (G17), pepsinogen (PG) I, PGII and antibodies against H. pylori and cytotoxin-associated gene A protein were determined in all patients. Antibodies against parietal cells and intrinsic factor were determined in patients with advanced (moderate to severe) OGA. Areas under the receiver operating characteristic curves (AUCs) were calculated for serum biomarkers and compared with histology.
   Results Overall, 34 patients (8.9%) had advanced OGA by histology (22 women, age 61 +/- 15 years). Current or past H. pylori infection and AIG were present in 14/34 and 22/34 patients, respectively. H. pylori-negative AIG patients (N = 18) were more likely to have another autoimmune disease (OR 6.3; 95% CI 1.3 to 29.8), severe corpus atrophy (OR 10.1; 95% CI 1.9 to 54.1) and corpus intestinal metaplasia (OR 26.9; 95% CI 5.3 to 136.5) compared with H. pylori-positive patients with advanced OGA. Antrum atrophy was present in 39% of H. pylori-negative AIG patients. The diagnostic performance of G17, PG I and PGI/II was excellent for AIG patients (AUC = 0.83, 0.95 and 0.97, respectively), but limited for H. pylori-positive patients with advanced OGA (AUC = 0.62, 0.75 and 0.67, respectively).
   Conclusions H. pylori-negative AIG has a distinct clinical, morphological and serological phenotype compared with advanced OGA in H. pylori gastritis.
C1 [Venerito, Marino; Varbanova, Mariya; Weigt, Jochen; Link, Alexander; Malfertheiner, Peter] Otto von Guericke Univ Hosp, Dept Gastroenterol Hepatol & Infect Dis, Magdeburg, Germany.
   [Roehl, Friedrich-Wilhelm] Otto von Guericke Univ Hosp, Inst Biometr & Med Informat, Magdeburg, Germany.
   [Reinhold, Dirk] Otto von Guericke Univ Hosp, Inst Mol & Clin Immunol, Magdeburg, Germany.
   [Frauenschlaeger, Katrin; Jechorek, Doerthe] Otto von Guericke Univ Hosp, Inst Pathol, Magdeburg, Germany.
C3 University Hospital Magdeburg; Otto von Guericke University; Otto von
   Guericke University; University Hospital Magdeburg; University Hospital
   Magdeburg; Otto von Guericke University; University Hospital Magdeburg;
   Otto von Guericke University
RP Malfertheiner, P (corresponding author), Univ Magdeburg, Dept Gastroenterol Hepatol & Infect Dis, Leipziger Str 44, D-39120 Magdeburg, Germany.
EM peter.malfertheiner@med.ovgu.de
RI Malfertheiner, Peter/AEZ-6553-2022; Venerito, Marino/AAF-4493-2020;
   Link, Alexander/AFK-7535-2022; Jechorek, Doerthe/J-4716-2014
OI Weigt, Jochen/0000-0002-3334-2168; Link, Alexander/0000-0002-9514-4562;
   Jechorek, Doerthe/0000-0002-1480-5200; Malfertheiner,
   Peter/0000-0001-8439-9036; Venerito, Prof. Dr. med.
   Marino/0000-0001-8581-0974
FU Bundesministerium fur Bildung und Frauen [BMBF-0315905D]
FX Supported in part by a research grant from the Bundesministerium fur
   Bildung und Frauen (BMBF-0315905D) to PM in the frame of ERA-NET
   PathoGenoMics.
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NR 28
TC 32
Z9 34
U1 0
U2 13
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0021-9746
EI 1472-4146
J9 J CLIN PATHOL
JI J. Clin. Pathol.
PD AUG
PY 2016
VL 69
IS 8
BP 677
EP 685
DI 10.1136/jclinpath-2015-203405
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA DS5EE
UT WOS:000380803000003
PM 26729016
DA 2025-06-01
ER

PT J
AU Kirchner, T
   Faller, G
   Price, A
AF Kirchner, T
   Faller, G
   Price, A
TI Pathology and autoimmunity
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; MONOCLONAL-ANTIBODIES; ATROPHIC
   GASTRITIS; ACID-SECRETION; DISEASES; IMMUNOPATHOLOGY; ERADICATION;
   EXPRESSION; CELLS; BODY
AB One of the present tasks of pathology is to define distinct topographical patterns and phenotypes of Helicobacter pylori gastritis with clinical and prognostic implications. There are indications that a diffuse antral-predominant gastritis is associated with duodenal and prepyloric ulcers, that pangastritis with progressive intestinal metaplasia and atrophy predispose to gastric ulcers or cancer, and that a non-ulcer pangastritis without intestinalization follows an uncomplicated course in the majority of patients. Gastritis risk indices reflecting these patterns can be useful for the evaluation of such phenotypes in routine diagnosis, even though the exact histological criteria for the diagnosis and grading of atrophy still need to be improved. A decisive pathogenic cofactor for the development of atrophy and intestinal metaplasia in H. pylori gastritis seems to be an antigastric autoimmunity. Autoantibodies with major specificities for the canalicular folds of parietal cells and the gastric H+,K+-ATPase are significantly associated with H. pylori infection and indicate a link between bacterial and classical autoimmune gastritis, Molecular mimicry involving Lewis antigens is probably relevant in the pathogenesis of the anti-gastric autoreactivity in animal experimental models, but not in human H. pylori infection, Apparently, the H. pylori-induced immune and cytokine response itself initiates changes of the gastric microenvironment in infected patients, which predispose to the local autoimmune attacks. Curr Opin Gastroenterol 14 (suppl 1):S35-S39 (C) 1998 Lippincott Williams & Wilkins.
C1 Univ Erlangen Nurnberg, Inst Pathol, D-91054 Erlangen, Germany.
   Northwick Pk Hosp & Clin Res Ctr, Dept Cellular Pathol, Harrow HA1 3UJ, Middx, England.
   St Marks Hosp, Dept Cellular Pathol, Harrow, Middx, England.
C3 University of Erlangen Nuremberg; Imperial College London; Imperial
   College London
RP Univ Erlangen Nurnberg, Inst Pathol, D-91054 Erlangen, Germany.
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NR 46
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PY 1998
VL 14
SU 1
BP S35
EP S39
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 126GT
UT WOS:000076286100008
DA 2025-06-01
ER

PT J
AU Ernst, PB
   Crowe, SE
   Reyes, VE
AF Ernst, PB
   Crowe, SE
   Reyes, VE
TI How does Helicobacter pylori cause mucosal damage? The inflammatory
   response
SO GASTROENTEROLOGY
LA English
DT Article
ID EPITHELIAL-CELL LINES; NECROSIS-FACTOR-ALPHA; INTERLEUKIN-8 PRODUCTION;
   IN-VITRO; ORAL IMMUNIZATION; INTERFERON-GAMMA; MONOCLONAL-ANTIBODIES;
   CYTOKINE PRODUCTION; ADHESION MOLECULES; SURFACE-PROTEINS
AB The role for Helicobacter pylori in the pathogenesis of disease provides the conundrum that only a subset of subjects infected with H. pylori will ever develop peptic ulcer or gastric cancer. Thus, variation in strain as well as environmental or host factors converge in the gastroduodenal milieu and control the final outcome of infection. The host immune and inflammatory response is emerging as an important element in the pathogenesis of these gastric diseases. The ideal host response provides protection to clear an infection without causing excessive amounts of inflammation that could compromise the integrity and function of host cells. This review will cover four main questions: (1) What are the mucosal immune/inflammatory responses that confer protection without damaging the host? (2) How do the gastric immune responses during infection with H. pylori differ from this ideal scenario? (3) Do these responses contribute to autoimmune-mediated damage to gastric tissue? (4) Can immunomodulation through vaccination enhance protective, nondestructive responses that prevent or treat infection or, at least, attenuate inflammation?
C1 UNIV TEXAS,MED BRANCH,DEPT PEDIAT,CHILD HLTH RES CTR,GALVESTON,TX 77550.
   UNIV TEXAS,MED BRANCH,DEPT MICROBIOL & IMMUNOL,GALVESTON,TX 77550.
   UNIV TEXAS,MED BRANCH,DEPT INTERNAL MED,GALVESTON,TX 77550.
C3 University of Texas System; University of Texas Medical Branch
   Galveston; University of Texas System; University of Texas Medical
   Branch Galveston; University of Texas System; University of Texas
   Medical Branch Galveston
OI Ernst, Peter/0000-0001-7777-1813
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NR 63
TC 98
Z9 105
U1 0
U2 8
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD DEC
PY 1997
VL 113
IS 6
SU S
BP S35
EP S42
DI 10.1016/S0016-5085(97)80009-1
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA YJ608
UT WOS:A1997YJ60800009
PM 9394758
DA 2025-06-01
ER

PT J
AU El-Zimaity, H
AF El-Zimaity, Hala
TI Gastritis and gastric atrophy
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE atrophy; gastritis; staging
ID HELICOBACTER-PYLORI GASTRITIS; DUODENAL-ULCER PATIENTS; INTESTINAL
   METAPLASIA; PEPTIC-ULCER; PERNICIOUS-ANEMIA; MAJOR AUTOANTIGEN; CORPUS
   GASTRITIS; HIGH PREVALENCE; SYDNEY SYSTEM; PEPSINOGEN-I
AB Purpose of review
   The majority of problems in interpreting gastritis remain Helicobacter related, but their nature has changed. The present review covers gastritis historically through cancer risk staging systems.
   Recent findings
   Key points to remember are: Helicobacter is associated with several forms of gastritis; in the present review, I am focusing on the two ends of the disease, Helicobacter pylori infection', that starts with antral predominant gastritis but can continue to oxyntic predominant disease with atrophy; the role Helicobacter pylori plays in autoimmune gastritis with pernicious anemia remains unresolved; gastritis staging systems for cancer risk, namely Baylor and Operative Link on Gastritis Assessment, are currently available.
   Summary
   As most gastric carcinomas arise on a background of atrophic gastritis, and the risk increases with the extent of atrophy, an index of atrophy location and extent could be useful in predicting patients at greatest risk for carcinoma. It is now possible to stage patients for cancer risk. Nonetheless, in a field such as gastritis in which many issues remain unresolved, a classification or staging system that is more descriptive will likely prove more useful.
C1 [El-Zimaity, Hala] McMaster Univ, Dept Pathol, Hamilton, ON, Canada.
   [El-Zimaity, Hala] Baylor Coll Med, Dept Med, Michael E DeBakey Vet Affairs Med Ctr, Houston, TX 77030 USA.
C3 McMaster University; US Department of Veterans Affairs; Veterans Health
   Administration (VHA); Michael E DeBakey VA Medical Center; Baylor
   College of Medicine
RP El-Zimaity, H (corresponding author), McMaster Div, 1200 Main St W,RM 2N31, Hamilton, ON L8S 3Z5, Canada.
EM zimaity@mcmaster.ca
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NR 50
TC 27
Z9 34
U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD NOV
PY 2008
VL 24
IS 6
BP 682
EP 686
DI 10.1097/MOG.0b013e328311d1cc
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 374AE
UT WOS:000261013800005
PM 19122515
DA 2025-06-01
ER

PT J
AU Tas, SK
   Kirkik, D
   Öztürk, K
   Tanoglu, A
AF Tas, Sevgi Kalkanli
   Kirkik, Duygu
   Ozturk, Kubra
   Tanoglu, Alpaslan
TI Determination of B- and T- cell epitopes for
   Helicobacter pylori cagPAI: An in silico approach
SO TURKISH JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE CagA protein; Helicobacter pylori; computational biology
AB Background/Aims: Helicobacter pylori is classified as a gram-negative bacteria and can cause significant diseases, including gastric cancer, mucosa-associated lymphoid tumor, peptic ulcer, and chronic gastritis. Recent studies have shown that some autoimmune diseases are also associated with H. pylori. In the past decades, polymorphisms of certain genes of H. pylori, mechanisms and strains of H. pylon, and new therapeutic approaches have continued to be defined. Bioinformatic tools continue to be used in drug design and vaccine design. This study aimed to investigate the cag pathogenicity island (cagPAI) of H. pylori using an in silico approach, which could contribute to vaccine studies.
   Materials and Methods: The pathogenicity island of H. pylon was obtained from GenBank and analyzed with ClustalW software. Structures of cog Virb11 (Hp0525) and an inhibitory protein (-10451) were obtained, and colon optimization and secondary and tertiary structure prediction for the cagPAI of H. pylori were analyzed using Garnier-Osguthorpe-Rabson IV secondary structure prediction method and self-optimized prediction method with alignment software. The BcePred prediction server was used to distinguish linear B-cell epitopes, and prediction of T-cell was obtained with NetCTL and MHCPred.
   Results: According to the physicochemical parameters, the cagPAI of H. pylori was analyzed and found to be stable, and 2 B-cell epitopes of cagPAI of H. pylori and 2 T-cell epitopes of cagPAI were found in this study.
   Conclusion: B- and T-cell epitopes that we have identified can induce both humoral and cellular immune responses. Thus, these epitopes have a potential for vaccine studies.Consequently, this in silica analysis should be combined with other pieces of evidence, including experimental data, to assign function.
C1 [Tas, Sevgi Kalkanli] Hlth Sci Univ, Dept Immunol, Sch Med, Istanbul, Turkey.
   [Kirkik, Duygu; Ozturk, Kubra] Hlth Sci Univ, Dept Med Biol, Sch Med, Istanbul, Turkey.
   [Tanoglu, Alpaslan] Sultan Abdulhamit Training & Res Hosp, Dept Gastroenterol, Istanbul, Turkey.
C3 University of Health Sciences Turkey; University of Health Sciences
   Turkey
RP Kirkik, D (corresponding author), Hlth Sci Univ, Dept Med Biol, Sch Med, Istanbul, Turkey.
EM dygkirkik@gmail.com
RI Kırkık, Duygu/AAA-7305-2021; Tanoglu, Alpaslan/AAI-5138-2020; ÖZTÜRK,
   Kübra/GRF-4182-2022; KALKANLI TAS, SEVGI/AAS-7395-2020
OI Tanoglu, Alpaslan/0000-0002-7477-6640; KIRKIK,
   Duygu/0000-0003-1417-6915; KALKANLI TAS, SEVGI/0000-0001-5288-6040
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NR 25
TC 2
Z9 2
U1 0
U2 6
PU AVES
PI SISLI
PA BUYUKDERE CAD 105-9, MECIDIYEKOY, SISLI, ISTANBUL 34394, TURKEY
EI 2148-5607
J9 TURK J GASTROENTEROL
JI Turk. J. Gastroenterol.
PD OCT
PY 2020
VL 31
IS 10
BP 713
EP 720
DI 10.5152/tjg.2020.19154
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA OV5CR
UT WOS:000592228300006
PM 33169709
OA Green Published
DA 2025-06-01
ER

PT J
AU Zheng, ZH
   Huang, G
   Gao, T
   Huang, TY
   Zou, MS
   Zou, YH
   Duan, SW
AF Zheng, Zhonghua
   Huang, Gang
   Gao, Tong
   Huang, Tianyi
   Zou, Mengsha
   Zou, Yuhao
   Duan, Shiwei
TI Epigenetic Changes Associated With Interleukin-10
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE DNA methylation; epigenetics; interleukin-10; immune inflammatory
   disease; histone modification; microRNA; lncRNA
ID PERIPHERAL B-CELLS; BLOOD MONONUCLEAR-CELLS; DNA METHYLATION;
   HEPATOCELLULAR-CARCINOMA; IL-10 EXPRESSION; T-CELLS; PROMOTER
   POLYMORPHISM; GASTRIC-CANCER; BREAST-CANCER; GENE
AB IL-10 is a regulator of inflammation and immunosuppression. IL-10 regulates a variety of immune cells to limit and stop the inflammatory response, and thus plays an important role in autoimmune diseases, inflammatory diseases and cancer. IL-10 is closely related to epigenetic modification, in which changes in DNA methylation of IL-10 gene can affect mRNA and protein levels of IL-10. In addition, changes in histone modifications, especially histone acetylation, can also lead to abnormal expression of IL-10 mRNA. At the same time, a handful of IL-10 related microRNAs (miRNAs) are found to be aberrantly expressed in multiple diseases. Besides, long non-coding RNA (lncRNA) growth arrest specific transcript 5 (GAS5) also inhibits IL-10 expression. Here, we reviewed the epigenetic changes related to IL-10 in various diseases, as well as the regulation of IL-10 gene expression in various diseases by epigenetic modifications such as DNA methylation, histone modification, miRNA, and lncRNA.
C1 [Zheng, Zhonghua; Huang, Gang; Gao, Tong; Huang, Tianyi; Zou, Mengsha; Zou, Yuhao; Duan, Shiwei] Ningbo Univ, Sch Med, Ctr Med Genet, Ningbo, Peoples R China.
C3 Ningbo University
RP Duan, SW (corresponding author), Ningbo Univ, Sch Med, Ctr Med Genet, Ningbo, Peoples R China.
EM duanshiwei@nbu.edu.cn
RI Duan, Shiwei/AAA-4782-2022; Zou, Yuhao/MIW-2223-2025; Zou,
   Mengsha/GQR-2114-2022
OI Duan, Shiwei/0000-0001-7682-2877
FU K. C. Wong Magna Fund in Ningbo University
FX This research was supported by the grants from K. C. Wong Magna Fund in
   Ningbo University.
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NR 79
TC 30
Z9 35
U1 1
U2 17
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JUN 4
PY 2020
VL 11
AR 1105
DI 10.3389/fimmu.2020.01105
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA MC2YW
UT WOS:000543160000001
PM 32582189
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Delitala, AP
   Pes, GM
   Errigo, A
   Maioli, M
   Delitala, G
   Dore, MP
AF Delitala, A. P.
   Pes, G. M.
   Errigo, A.
   Maioli, M.
   Delitala, G.
   Dore, M. P.
TI Helicobacter pylori CagA antibodies and thyroid function in
   latent autoimmune diabetes in adults
SO EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES
LA English
DT Article
DE Latent autoimmune diabetes in adults; CagA; Antibodies against
   thyroperoxidase; Thyrotropin
ID GRAVES-DISEASE; CARDIOVASCULAR-DISEASE; GASTRIC-CANCER; HEPATITIS-C;
   INFECTION; METAANALYSIS; DISORDERS; AUTOANTIBODIES; SEROPOSITIVITY;
   ASSOCIATION
AB OBJECTIVE: H. pylori infection is reportedly associated with autoimmune diseases such as chronic thyroiditis and autoimmune diabetes. The aim of this study is to determine the association between H. pylori infection and its virulent strain CagA with antibodies against thyroperoxidase (TPO Ab) and thyrotropin (TSH) in a cohort of latent autoimmune diabetes in adult (LADA) patients.
   PATIENTS AND METHODS: We included 234 LADA patients (53.8% women). Antibodies against H. pylori whole antigens and CagA, TPO Ab and TSH were assessed in all patients.
   RESULTS: Prevalence of IgG against H. pylori and GagA was 52.1% and 20.9% respectively. Antibodies against H. pylori were not associated with TPO Ab and TSH (rho = 0.067, p = 0.620 and rho = 0.156, p = 0.099, respectively). Antibodies against CagA showed a positive association with TSH and TPO Ab (respectively rho = 0.309, p = 0.036 and rho = 0.419, p = 0.037). Subjects with hypothyroidism (TSH >= 3.5 mu U/ml) had an increased frequency of Ab anti CagA (p = 0.059).
   CONCLUSIONS: The infection by H. pylori strains expressing CagA is associated with increased TPO Ab and TSH levels in LADA patients, suggesting a possible mechanism involved in thyroid autoimmunity and dysfunction of the gland. Further research is needed to test this hypothesis.
C1 [Delitala, A. P.] Azienda Osped Univ Sassari, Sassari, Italy.
   [Pes, G. M.; Errigo, A.; Delitala, G.; Dore, M. P.] Univ Sassari, Dept Clin & Expt Med, Sassari, Italy.
   [Maioli, M.] Univ Sassari, Dept Biomed Sci, Sassari, Italy.
   [Maioli, M.] CNR, Ist Ric Genet & Biomed, Cagliari, Italy.
C3 University of Sassari; University of Sassari; University of Sassari;
   Consiglio Nazionale delle Ricerche (CNR); Istituto di Ricerca Genetica e
   Biomedica (IRGB-CNR)
RP Delitala, AP (corresponding author), Azienda Osped Univ Sassari, Sassari, Italy.
EM aledelitala@tiscali.it
RI Delitala, Alessandro/AAH-2697-2020; DORE, Maria/AAV-7918-2021; Errigo,
   Alessandra/ABI-2812-2020; Pes, Giovanni Mario/AAH-3340-2019
OI Errigo, Alessandra/0000-0002-9911-7270; DORE, Maria
   Pina/0000-0001-7305-3531; Pes, Giovanni Mario/0000-0003-3265-2823
FU Regione Autonoma della Sardegna [CRP-27076]
FX This work was done by using a grant from Regione Autonoma della Sardegna
   (Genetic and immunologic markers in the pathogenesis of LADA and type 2
   diabetes mellitus), n: CRP-27076, scientific coordinator Prof. Giuseppe
   Delitala.
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NR 47
TC 8
Z9 10
U1 0
U2 5
PU VERDUCI PUBLISHER
PI ROME
PA VIA GREGORIO VII, ROME, 186-00165, ITALY
SN 1128-3602
J9 EUR REV MED PHARMACO
JI Eur. Rev. Med. Pharmacol. Sci.
PD OCT
PY 2016
VL 20
IS 19
BP 4041
EP 4047
PG 7
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA EA4FB
UT WOS:000386564500015
PM 27775795
DA 2025-06-01
ER

PT J
AU Cid-Gallegos, MS
   Corzo-Rios, LJ
   Jimenez-Martinez, C
   Sanchez-Chino, XM
AF Cid-Gallegos, M. S.
   Corzo-Rios, L. J.
   Jimenez-Martinez, C.
   Sanchez-Chino, X. M.
TI Protease Inhibitors from Plants as Therapeutic Agents- A Review
SO PLANT FOODS FOR HUMAN NUTRITION
LA English
DT Review
DE Proteolytic activity; Protease inhibitors; Legumes seeds; Cancer
ID BOWMAN-BIRK INHIBITOR; SERINE PROTEINASE-INHIBITOR; KUNITZ
   TRYPSIN-INHIBITOR; COLORECTAL-CANCER CELLS; GROWTH; INACTIVATION;
   CONCENTRATE; MECHANISMS; INVASION; RELEASE
AB Plant-based diets are a great source of protease inhibitors (PIs). Two of the most well-known families of PIs are Bowman-Birk inhibitors (BBI) and Kunitz-type inhibitors (KTI). The first group acts mainly on trypsin, chymotrypsin, and elastase; the second is on serine, cysteine, and aspartic proteases. PIs can retard or inhibit the catalytic action of enzymes; therefore, they are considered non-nutritional compounds; nevertheless, animal studies and cell line experiments showed promising results of PIs in treating human illnesses such as obesity, cardiovascular diseases, autoimmune diseases, inflammatory processes, and different types of cancer (gastric, colorectal, breast, and lung cancer). Anticarcinogenic activity's proposed mechanisms of action comprise several inhibitory effects at different molecular levels, i.e., transcription, post-transcription, translation, post-translation, and secretion of cancer cells. This work reviews the potential therapeutic applications of PIs as anticarcinogenic and anti-inflammatory agents in human diseases and the mechanisms by which they exert these effects.
C1 [Cid-Gallegos, M. S.; Jimenez-Martinez, C.] Escuela Nacl Ciencias Biol, Inst Politecn Nacional, Unidad Profes Adolfo Lopez Mateos, Delega Gustavo Madero,Av Wilfrido Massieu Esq C, Mexico City 07738, DF, Mexico.
   [Corzo-Rios, L. J.] Inst Politecn Nacional, Dept Bioproc, Unidad Profes Interdisciplinaria Biotecnol, Av Acueducto S-N,Barrio Laguna,Col Ticoman, Mexico City 07340, DF, Mexico.
   [Sanchez-Chino, X. M.] CONACYT, Dept Salud, Villahermosa, Tabasco, Mexico.
C3 Consejo Nacional de Ciencia y Tecnologia (CONACyT)
RP Sanchez-Chino, XM (corresponding author), CONACYT, Dept Salud, Villahermosa, Tabasco, Mexico.
EM xsanchez@ecosur.mx
RI Chino, Xariss/ADF-4010-2022; Corzo-Rios, Luis Jorge/AAB-2987-2019
OI Jimenez Martinez, Cristian/0000-0001-8921-9858; Corzo-Rios, Luis
   Jorge/0000-0003-0987-7522; Cid Gallegos, Maria
   Stephanie/0000-0001-9523-4376
FU Instituto Politecnico Nacional [20210017]
FX The authors thank the Instituto Politecnico Nacional for the financial
   support through grant SIP project 20210017.
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NR 80
TC 36
Z9 40
U1 7
U2 51
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0921-9668
EI 1573-9104
J9 PLANT FOOD HUM NUTR
JI Plant Food Hum. Nutr.
PD MAR
PY 2022
VL 77
IS 1
BP 20
EP 29
DI 10.1007/s11130-022-00949-4
EA JAN 2022
PG 10
WC Plant Sciences; Chemistry, Applied; Food Science & Technology; Nutrition
   & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Plant Sciences; Chemistry; Food Science & Technology; Nutrition &
   Dietetics
GA 0L3GJ
UT WOS:000740421600001
PM 35000105
DA 2025-06-01
ER

PT J
AU Schubert, ML
AF Schubert, Mitchell L.
TI Gastric secretion
SO CURRENT OPINION IN GASTROENTEROLOGY
LA English
DT Article
DE acid secretion; gastrin; H. pylori; histamine; parietal cell;
   somatostatin
ID HELICOBACTER-PYLORI; ACID-SECRETION; BIOLOGICAL-ACTIVITY; AFFERENT
   NEURONS; PARIETAL-CELLS; EXPRESSION; HISTAMINE; RECEPTOR; GHRELIN;
   STOMACH
AB Purpose of review This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion. Recent findings Gastric acid secretion is tightly regulated by overlapping neural, hormonal, paracrine, and intracellular pathways in order to achieve the correct amount of acid secretion required by the specific situation. Too little acid can interfere with the absorption of iron, calcium, vitamin B-12, and certain drugs as well as predispose to enteric infection, bacterial overgrowth, and gastric malignancy. Too much acid can induce esophageal, gastric, and duodenal injury. Gastrin, histamine, acetylcholine, and ghrelin stimulate whereas somatostatin, cholecystokinin, atrial natriuretic peptide, and nitric oxide inhibit acid secretion. Most patients infected with Helicobacter pylori manifest a pangastritis and produce less than normal amounts of acid; those with antral predominant gastritis, however, are hypergastrinemic and produce increased amounts of acid. Improved understanding of the channels and receptors that are required for and regulate H+K+-ATPase activity should lead to the development of novel antisecretory agents. Summary A better understanding of the pathways regulating gastric secretions should lead to new strategies to prevent and treat a variety of gastric disorders such as gastroesophageal reflux disease, autoimmune gastritis, gastric cancer, and functional dyspepsia.
C1 Vet Adm Med Ctr, Div Gastroenterol, Richmond, VA 23249 USA.
   Virginia Commonwealth Univ, Med Coll Virginia, McGuire Vet Affairs Med Ctr, Dept Med,Div Gastroenterol, Richmond, VA USA.
C3 Virginia Commonwealth University; Hunter Holmes McGuire Veterinary
   Affairs Medical Center; US Department of Veterans Affairs; Veterans
   Health Administration (VHA); Hunter Holmes McGuire Veterinary Affairs
   Medical Center; Virginia Commonwealth University
RP Schubert, ML (corresponding author), Vet Adm Med Ctr, Div Gastroenterol, Code 111N,1201 Broad Rock Blvd, Richmond, VA 23249 USA.
EM Mitchell.Schubert@va.gov
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NR 51
TC 35
Z9 44
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0267-1379
EI 1531-7056
J9 CURR OPIN GASTROEN
JI Curr. Opin. Gastroenterol.
PD NOV
PY 2007
VL 23
IS 6
BP 595
EP 601
DI 10.1097/MOG.0b013e3282f03462
PG 7
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 223IR
UT WOS:000250364000002
PM 17906434
DA 2025-06-01
ER

PT J
AU Rugge, M
   Fassan, M
   Pizzi, M
   Zorzetto, V
   Maddalo, G
   Realdon, S
   DeBernard, M
   Betterle, C
   Cappellesso, R
   Pennelli, G
   de Boni, M
   Farinati, F
AF Rugge, M.
   Fassan, M.
   Pizzi, M.
   Zorzetto, V.
   Maddalo, G.
   Realdon, S.
   DeBernard, M.
   Betterle, C.
   Cappellesso, R.
   Pennelli, G.
   de Boni, M.
   Farinati, F.
TI Autoimmune gastritis: histology phenotype and OLGA staging
SO ALIMENTARY PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID ATROPHIC GASTRITIS; OPERATIVE LINK; FOLLOW-UP; METAPLASIA; RISK;
   MANAGEMENT; DYSPLASIA; NEOPLASMS; CELLS
AB Background
   Among Western populations, the declining incidence of Helicobacter pylori infection coincides with a growing clinical impact of autoimmune gastritis.
   Aims
   To describe the histological phenotype of autoimmune gastritis, also to test the prognostic impact of OLGA staging in the autoimmune setting.
   Methods
   A single-institutional series (spanning the years 2003-2011) of 562 consecutive patients (M:F ratio: 1:3.7; mean age = 57.6 +/- 14.4 years) with serologically confirmed autoimmune gastritis underwent histology review and OLGA staging.
   Results
   Helicobacter pylori infection was ascertained histologically in 44/562 cases (7.8%). Forty six biopsy sets (8.2%) featured OLGA stages IIIIV; they included all four cases of incidental epithelial neoplasia (three intraepithelial and one invasive; three of these four cases had concomitant H. pylori infection). There were 230 (40.9%) and 139 (24.7%) cases, respectively, of linear and micro-nodular enterochromaffin-like cell hyperplasia; 19 (3.4%) type I carcinoids were detected. The series included 116 patients who underwent repeated endoscopy/biopsy sampling (mean time elapsing between the two procedures = 54 months; range 24108). Paired histology showed a significant (P = 0.009) trend towards a stage progression [the stage increased in 25/116 cases (22%); it remained unchanged in 87/116 cases (75%)].
   Conclusions
   In autoimmune gastritis, the cancer risk is restricted to high-risk gastritis stages (IIIIV), and is associated mainly with concomitant H. pylori infection. OLGA staging consistently depicts the time-dependent organic progression of the autoimmune disease and provides key information for secondary gastric cancer prevention strategies.
C1 [Rugge, M.] Univ Padua, Dept Med DIMED, Ist Oncol Veneto, IRCCS, I-35121 Padua, PD, Italy.
   [Fassan, M.; Pizzi, M.; Zorzetto, V.; Maddalo, G.; Farinati, F.] Univ Padua, Dept Surg Oncol & Gastroenterol Sci DiSCOG, I-35121 Padua, PD, Italy.
   [DeBernard, M.] VIMM, Padua, PD, Italy.
   [de Boni, M.] Feltre Hosp, Dept Gastroenterol, Feltre, BL, Italy.
C3 IRCCS Istituto Oncologico Veneto (IOV); University of Padua; University
   of Padua; Veneto Institute Molecular Medicine; ULSS 1 Dolomiti; Ospedale
   di Feltre
RP Rugge, M (corresponding author), Univ Padua, Dept Med DIMED, Ist Oncol Veneto, IRCCS, Via Aristide Gabelli 61, I-35121 Padua, PD, Italy.
EM massimo.rugge@unipd.it
RI Farinati, Fabio/A-8267-2012; Rugge, Massimo/K-7525-2016; Pizzi,
   Marco/LIA-7766-2024; Fassan, Matteo/F-5152-2012; PENNELLI,
   GIANMARIA/J-9937-2016; Realdon, Stefano/K-8664-2016; Pizzi,
   Marco/H-6273-2016; CAPPELLESSO, Rocco/L-5463-2016
OI Fassan, Matteo/0000-0001-6515-5482; PENNELLI,
   GIANMARIA/0000-0003-0210-165X; Realdon, Stefano/0000-0001-6843-7637;
   FARINATI, FABIO/0000-0002-2944-1374; de Bernard,
   Marina/0000-0002-0091-4502; Pizzi, Marco/0000-0003-4006-7317;
   CAPPELLESSO, Rocco/0000-0002-0480-3412
FU AIRC; "Guido Berlucchi" Foundation; "Morgagni" Association for
   Oncological Research (Padua)
FX This research was supported by the AIRC grant Veneto Region, 2008; the
   "Guido Berlucchi" Foundation, and the "Morgagni" Association for
   Oncological Research (Padua). The funding agencies had no role in the
   design and performance of the study.
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NR 33
TC 70
Z9 73
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-2813
EI 1365-2036
J9 ALIMENT PHARM THER
JI Aliment. Pharmacol. Ther.
PD JUN
PY 2012
VL 35
IS 12
BP 1460
EP 1466
DI 10.1111/j.1365-2036.2012.05101.x
PG 7
WC Gastroenterology & Hepatology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Pharmacology & Pharmacy
GA 941QX
UT WOS:000303978800012
PM 22519568
OA Bronze
DA 2025-06-01
ER

PT J
AU Antico, A
   Tampoia, M
   Villalta, D
   Tonutti, E
   Tozzoli, R
   Bizzaro, N
AF Antico, Antonio
   Tampoia, Marilina
   Villalta, Danilo
   Tonutti, Elio
   Tozzoli, Renato
   Bizzaro, Nicola
TI Clinical Usefulness of the Serological Gastric Biopsy for the Diagnosis
   of Chronic Autoimmune Gastritis
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; ATROPHIC GASTRITIS; PERNICIOUS-ANEMIA;
   MOLECULAR MIMICRY; DISEASE; AUTOANTIBODIES; PREDICTORS; CANCER
AB Aim. To assess the predictive value for chronic autoimmune gastritis (AIG) of the combined assay of anti-parietal-cell antibodies (PCA), anti-intrinsic-factor antibodies (IFA), anti-Helicobacter pylori (Hp) antibodies, and measurement of blood gastrin. Methods. We studied 181 consecutive patients with anemia, due to iron deficiency resistant to oral replacement therapy or to vitamin B12 deficiency. Results. 83 patients (45.8%) tested positive for PCA and underwent gastroscopy with multiple gastric biopsies. On the basis of the histological diagnosis, PCA-positive patients were divided into 4 groups: (1) 30 patients with chronic atrophic gastritis; they had high concentrations of PCA and gastrin and no detectable IFA; (2) 14 subjects with metaplastic gastric atrophy; they had high PCA, IFA, and gastrin; (3) 18 patients with nonspecific lymphocytic inflammation with increased PCA, normal gastrin levels, and absence of IFA; (4) 21 patients with multifocal atrophic gastritis with "borderline" PCA, normal gastrin, absence of IFA and presence of anti-Hp in 100% of the cases. Conclusions. The assay of four serological markers proved particularly effective in the diagnostic classification of gastritis and highly correlated with the histological profile. As such, this laboratory diagnostic profile may be considered an authentic "serological biopsy."
C1 [Bizzaro, Nicola] Osped San Antonio, Lab Patol Clin, I-33028 Tolmezzo, Italy.
   [Antico, Antonio] Osped Civile, Lab Anal Chimicoclin, I-35013 Cittadella, Italy.
   [Tampoia, Marilina] Azienda Osped Univ, Lab Patol Clin, Policlin Bari, I-70124 Bari, Italy.
   [Villalta, Danilo] Azienda Osped S Maria degli Angeli, Allergol & Immunol Clin, I-33170 Pordenone, Italy.
   [Tonutti, Elio] Univ S Maria della Misericordia, Azienda Osped, I-33100 Udine, Italy.
   [Tozzoli, Renato] Azienda Ospedaliera S Maria degli Angeli, Lab Patol Clin, I-33170 Pordenone, Italy.
C3 Universita degli Studi di Bari Aldo Moro; Hospital Santa Maria della
   Misericordia
RP Bizzaro, N (corresponding author), Osped San Antonio, Lab Patol Clin, I-33028 Tolmezzo, Italy.
EM nicola.bizzaro@ass3.sanita.fvg.it
RI Tozzoli, Renato/AAG-4067-2020; Tampoia, Marilina/P-1811-2015
OI Tampoia, Marilina/0000-0001-9067-8808
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NR 29
TC 36
Z9 39
U1 0
U2 4
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1740-2522
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2012
AR 520970
DI 10.1155/2012/520970
PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 050CF
UT WOS:000312029500001
PM 23251219
OA Green Published, Green Submitted, gold
DA 2025-06-01
ER

PT J
AU Zandvakili, I
   Lazaridis, KN
AF Zandvakili, Inuk
   Lazaridis, Konstantinos N.
TI Cell-free DNA testing: future applications in gastroenterology and
   hepatology
SO THERAPEUTIC ADVANCES IN GASTROENTEROLOGY
LA English
DT Review
DE cell-free DNA; gastroenterology and hepatology; individualized medicine
ID METASTATIC COLORECTAL-CANCER; GASTRIC-CANCER; METHYLATION CHANGES;
   CLINICAL-RELEVANCE; PANCREATIC-CANCER; PROGNOSTIC MARKER;
   PERIPHERAL-BLOOD; CIRCULATING DNA; PLASMA DNA; SERUM DNA
AB The application of next-generation sequencing in clinical practice is increasing as accuracy and interpretation have improved and the cost continues to decline rapidly. Cell-free DNA is a unique source for next-generation sequencing that could change routine clinical practice in gastroenterology and hepatology. Testing of cell-free DNA in blood and fecal samples is an easy, rapid, and noninvasive method to assess for premalignant, malignant, metabolic, infectious, inflammatory, and autoimmune gastrointestinal and liver diseases. In this review, we describe cell-free DNA technologies, current applications of cell-free DNA testing, and proposed cell-free DNA targets for gastrointestinal and hepatic diseases, with a specific focus on malignancy. In addition, we provide commentary on how cell-free DNA can be integrated into clinical practice and help guide diagnosis, prognosis, disease management, and therapeutic response.
C1 [Lazaridis, Konstantinos N.] Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
   [Zandvakili, Inuk] Mayo Clin, Div Internal Med, Rochester, MN 55905 USA.
C3 Mayo Clinic; Mayo Clinic
RP Lazaridis, KN (corresponding author), Mayo Clin, Div Gastroenterol & Hepatol, 200 First St SW, Rochester, MN 55905 USA.
EM lazaridis.konstantinos@mayo.edu
RI ; Zandvakili, Inuk/C-8496-2011
OI Lazaridis, Konstantinos/0000-0002-0437-681X; Zandvakili,
   Inuk/0000-0003-3409-0019
FU Catharine Nicole Jockisch Carlos Endowment Fund in Primary Sclerosing
   Cholangitis (PSC)
FX Chris M. Carlos and Catharine Nicole Jockisch Carlos Endowment Fund in
   Primary Sclerosing Cholangitis (PSC).
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NR 90
TC 9
Z9 9
U1 3
U2 13
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1756-283X
EI 1756-2848
J9 THER ADV GASTROENTER
JI Ther. Adv. Gastroenterol.
PD APR
PY 2019
VL 12
AR 1756284819841896
DI 10.1177/1756284819841896
PG 13
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA IN7MG
UT WOS:000478865900001
PM 31019553
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Spanou, E
   Kalisperati, P
   Pateras, IS
   Papalampros, A
   Barbouti, A
   Tzioufas, AG
   Kotsinas, A
   Sougioultzis, S
AF Spanou, Evagelia
   Kalisperati, Polyxeni
   Pateras, Ioannis S.
   Papalampros, Alexandros
   Barbouti, Alexandra
   Tzioufas, Athanasios G.
   Kotsinas, Athanassios
   Sougioultzis, Stavros
TI Genetic Variability as a Regulator of TLR4 and NOD Signaling in Response
   to Bacterial Driven DNA Damage Response (DDR) and Inflammation: Focus on
   the Gastrointestinal (GI) Tract
SO FRONTIERS IN GENETICS
LA English
DT Review
DE toll-like receptors (TLRs); nod-like receptors (NLRs); DNA damage
   response (DDR); single nucleotide polymorphism (SNP); mutation;
   inflammation and tumorigenesis
ID TOLL-LIKE RECEPTORS; HELICOBACTER-PYLORI; GASTRIC-CANCER;
   COLORECTAL-CANCER; INNATE IMMUNITY; GENOMIC INSTABILITY; 3020INSC
   MUTATION; CROHNS-DISEASE; LUNG-CANCER; POLYMORPHISMS
AB The fundamental role of human Toll-like receptors (TLRs) and NOD-like receptors (NLRs), the two most studied pathogen recognition receptors (PRRs), is the protection against pathogens and excessive tissue injury. Recent evidence supports the association between TLR/NLR gene mutations and susceptibility to inflammatory, autoimmune, and malignant diseases. PRRs also interfere with several cellular processes, such as cell growth, apoptosis, cell proliferation, differentiation, autophagy, angiogenesis, cell motility and migration, and DNA repair mechanisms. We briefly review the impact of TLR4 and NOD1/NOD2 and their genetic variability in the process of inflammation, tumorigenesis and DNA repair, focusing in the gastrointestinal tract. We also review the available data on new therapeutic strategies utilizing TLR/NLR agonists and antagonists for cancer, allergic diseases, viral infections and vaccine development against both infectious diseases and cancer.
C1 [Spanou, Evagelia; Kalisperati, Polyxeni; Sougioultzis, Stavros] Univ Athens, Laikon Gen Hosp, Gastroenterol Div, Dept Pathophysiol, Athens, Greece.
   [Pateras, Ioannis S.; Kotsinas, Athanassios] Univ Athens, Dept Histol & Embryol, Athens, Greece.
   [Papalampros, Alexandros] Univ Athens, Laikon Gen Hosp, Dept Surg 1, Athens, Greece.
   [Barbouti, Alexandra] Univ Ioannina, Dept Anat Histol Embryol, Ioannina, Greece.
   [Tzioufas, Athanasios G.] Univ Athens, Laikon Gen Hosp, Dept Pathophysiol, Athens, Greece.
C3 National & Kapodistrian University of Athens; Laiko General Hospital;
   National & Kapodistrian University of Athens; National & Kapodistrian
   University of Athens; Laiko General Hospital; University of Ioannina;
   Laiko General Hospital; National & Kapodistrian University of Athens
RP Kotsinas, A (corresponding author), Univ Athens, Dept Histol & Embryol, Athens, Greece.
EM akotsin@med.uoa.gr
RI Kotsinas, Thanos/JJC-9655-2023; Barbouti, Alexandra/ADP-4365-2022;
   TZIOUFAS, ATHANASIOS/A-1690-2008
OI Tzioufas, Athanasios/0000-0001-6666-8642; BARBOUTI,
   ALEXANDRA/0000-0001-6730-359X
FU NKUA SARG [12128, 8916]
FX This work was supported by NKUA SARG grants 12128, 8916.
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NR 80
TC 8
Z9 9
U1 1
U2 23
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA PO BOX 110, EPFL INNOVATION PARK, BUILDING I, LAUSANNE, 1015,
   SWITZERLAND
SN 1664-8021
J9 FRONT GENET
JI Front. Genet.
PD MAY 29
PY 2017
VL 8
AR 65
DI 10.3389/fgene.2017.00065
PG 10
WC Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity
GA EW7ZN
UT WOS:000402737700001
PM 28611823
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Lenti, MV
   Facciotti, F
   Miceli, E
   Vanoli, A
   Fornasa, G
   Lahner, E
   Spadoni, I
   Giuffrida, P
   Arpa, G
   Pasini, A
   Rovedatti, L
   Caprioli, F
   Travelli, C
   Lattanzi, G
   Conti, L
   Klersy, C
   Vecchi, M
   Paulli, M
   Annibale, B
   Corazza, GR
   Rescigno, M
   Di Sabatino, A
AF Lenti, Marco Vincenzo
   Facciotti, Federica
   Miceli, Emanuela
   Vanoli, Alessandro
   Fornasa, Giulia
   Lahner, Edith
   Spadoni, Ilaria
   Giuffrida, Paolo
   Arpa, Giovanni
   Pasini, Alessandra
   Rovedatti, Laura
   Caprioli, Flavio
   Travelli, Cristina
   Lattanzi, Georgia
   Conti, Laura
   Klersy, Catherine
   Vecchi, Maurizio
   Paulli, Marco
   Annibale, Bruno
   Corazza, Gino Roberto
   Rescigno, Maria
   Di Sabatino, Antonio
TI Mucosal Overexpression of Thymic Stromal Lymphopoietin and
   Proinflammatory Cytokines in Patients With Autoimmune Atrophic Gastritis
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; NATURAL-KILLER-CELLS; HELICOBACTER-PYLORI
   INFECTION; PERNICIOUS-ANEMIA; DISEASE; MODELS; BOWEL; GAMMA
AB INTRODUCTION:The immune mechanisms underlying human autoimmune atrophic gastritis (AAG) are poorly understood. We sought to assess immune mucosal alterations in patients with AAG.METHODS:In 2017-2021, we collected gastric corpus biopsies from 24 patients with AAG (median age 62 years, interquartile range 56-67, 14 women), 26 age-matched and sex-matched healthy controls (HCs), and 14 patients with Helicobacter pylori infection (HP). We investigated the lamina propria mononuclear cell (LPMC) populations and the mucosal expression of thymic stromal lymphopoietin (TSLP) and nicotinamide phosphoribosyltransferase (NAMPT). Ex vivo cytokine production by organ culture biopsies, under different stimuli (short TSLP and zinc-l-carnosine), and the gastric vascular barrier through plasmalemma vesicle-associated protein-1 (PV1) were also assessed.RESULTS:In the subset of CD19+ LPMC, CD38+ cells (plasma cells) were significantly higher in AAG compared with HC. Ex vivo production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-15, and transforming growth factor beta 1 was significantly higher in AAG compared with HC. At immunofluorescence, both IL-7R and TSLP were more expressed in AAG compared with HC and HP, and short TSLP transcripts were significantly increased in AAG compared with HC. In the supernatants of AAG corpus mucosa, short TSLP significantly reduced TNF-alpha, while zinc-l-carnosine significantly reduced interferon-gamma, TNF-alpha, IL-21, IL-6, and IL-15. NAMPT transcripts were significantly increased in AAG compared with HC. PV1 was almost absent in AAG, mildly expressed in HC, and overexpressed in HP.DISCUSSION:Plasma cells, proinflammatory cytokines, and altered gastric vascular barrier may play a major role in AAG. TSLP and NAMPT may represent potential therapeutic targets, while zinc-l-carnosine may dampen mucosal inflammation.
C1 [Lenti, Marco Vincenzo; Miceli, Emanuela; Giuffrida, Paolo; Pasini, Alessandra; Rovedatti, Laura; Corazza, Gino Roberto; Di Sabatino, Antonio] Univ Pavia, IRCCS San Matteo Hosp Fdn, Dept Internal Med 1, Pavia, Italy.
   [Facciotti, Federica; Lattanzi, Georgia] IRCCS European Inst Oncol, Dept Expt Oncol, Milan, Italy.
   [Facciotti, Federica] Univ Milano Bicocca, Dept Biotechnol & Biosci, Milan, Italy.
   [Vanoli, Alessandro; Arpa, Giovanni; Paulli, Marco] Univ Pavia, IRCCS San Matteo Hosp Fdn, Unit Anat Pathol, Pavia, Italy.
   [Fornasa, Giulia; Rescigno, Maria] IRCCS Humanitas Res Hosp, Milan, Italy.
   [Lahner, Edith; Conti, Laura; Annibale, Bruno] Univ Roma La Sapienza, St Andrea Hosp, Dept Med Surg Sci & Translat Med, Rome, Italy.
   [Spadoni, Ilaria; Rescigno, Maria] Humanitas Univ, Dept Biomed Sci, Milan, Italy.
   [Caprioli, Flavio; Vecchi, Maurizio] Univ Milan, IRCCS Ca Granda Hosp Fdn, Gastroenterol & Endoscopy Unit, Milan, Italy.
   [Travelli, Cristina] Univ Pavia, Dept Pharmaceut Sci, Pavia, Italy.
   [Klersy, Catherine] IRCCS San Matteo Hosp Fdn, Clin Epidemiol & Biometry, Pavia, Italy.
C3 University of Pavia; IRCCS Fondazione San Matteo; IRCCS European
   Institute of Oncology (IEO); University of Milano-Bicocca; University of
   Pavia; IRCCS Fondazione San Matteo; Sapienza University Rome; Azienda
   Ospedaliera Sant'Andrea; Humanitas University; University of Milan;
   University of Pavia; IRCCS Fondazione San Matteo
RP Di Sabatino, A (corresponding author), Univ Pavia, IRCCS San Matteo Hosp Fdn, Dept Internal Med 1, Pavia, Italy.
EM marco.lenti@unipv.it; federica.facciotti@unimib.it;
   e.miceli@smatteo.pv.it; alessandro.vanoli@unipv.it;
   giulia.fornasa@humanitasresearch.it; edith.lahner@uniroma1.it;
   ilaria.spadoni@hunimed.eu; paolo.giuffrida01@gmail.com;
   giovanni.arpa90@gmail.com; ale.pasini18@gmail.com;
   l.rovedatti@smatteo.pv.it; flavio.caprioli@unimi.it;
   cristina.travelli@unipv.it; georgia.lattanzi@ieo.it;
   lau88conti@gmail.com; klersy@smatteo.pv.it; maurizio.vecchi@unimi.it;
   marco.paulli@unipv.it; bruno.annibale@uniroma1.it;
   gr.corazza@smatteo.pv.it; maria.rescigno@hunimed.eu;
   a.disabatino@smatteo.pv.it
RI Travelli, Cristina/AAA-9450-2022; Pasini, Alessandra/AAP-8573-2021;
   klersy, catherine/AAA-3003-2019; Spadoni, Ilaria/K-1054-2018; Di
   Sabatino, Antonio/K-8015-2016; Fornasa, Giulia/AAB-8912-2019; Vanoli,
   Alessandro/J-4469-2016; Lenti, Marco/F-9044-2018; Lahner,
   Edith/AAM-1039-2021; Corazza, Gino/K-8500-2016; Caprioli,
   Flavio/AAB-5176-2019; Annibale, Bruno/A-5372-2008; Rescigno,
   Maria/J-9704-2012
OI Caprioli, Flavio/0000-0002-8077-8175; Arpa,
   Giovanni/0000-0001-7226-381X; Lattanzi, Georgia/0000-0002-1444-2489;
   Rescigno, Maria/0000-0002-6464-509X; Fornasa, Giulia/0000-0002-2250-7983
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NR 42
TC 9
Z9 9
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
EI 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD JUL
PY 2022
VL 13
IS 7
AR e00510
DI 10.14309/ctg.0000000000000510
PG 12
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 8W4OS
UT WOS:000931314900002
PM 35905420
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Flanagan, EP
   Saito, YA
   Lennon, VA
   McKeon, A
   Fealey, RD
   Szarka, LA
   Murray, JA
   Foxx-Orenstein, AE
   Fox, JC
   Pittock, SJ
AF Flanagan, E. P.
   Saito, Y. A.
   Lennon, V. A.
   McKeon, A.
   Fealey, R. D.
   Szarka, L. A.
   Murray, J. A.
   Foxx-Orenstein, A. E.
   Fox, J. C.
   Pittock, S. J.
TI Immunotherapy trial as diagnostic test in evaluating patients with
   presumed autoimmune gastrointestinal dysmotility
SO NEUROGASTROENTEROLOGY AND MOTILITY
LA English
DT Article
DE autonomic nervous system; autonomic neuropathy; celiac disease;
   immunoglobulin; scintigraphy; thyroid disease; transit study
ID RANDOMIZED CONTROLLED-TRIAL; ACETYLCHOLINE-RECEPTORS; CLINICAL-COURSE;
   LUNG-CANCER; AUTOANTIBODIES; PROFILES; IMMUNOGLOBULIN; IMMUNIZATION;
   DISORDERS; MOTILITY
AB Background Chronic gastrointestinal dysmotility greatly impacts the quality of life. Treatment options are limited and generally symptomatic. Neural autoimmunity is an under-recognized etiology. We evaluated immunotherapy as an aid to diagnosing autoimmune gastrointestinal dysmotility (AGID). Methods Twenty-three subjects evaluated at the Mayo Clinic for suspected AGID (August 2006-February 2014) fulfilled the following criteria: (1) prominent symptoms of gastrointestinal dysmotility with abnormalities on scintigraphy-manometry; (2) serological evidence or personal/family history of autoimmune disease; (3) treated by immunotherapy on a trial basis, 6-12 weeks (intravenous immune globulin, 16; or methylprednisolone, 5; or both, 2). Response was defined subjectively (symptomatic improvement) and objectively (gastrointestinal scintigraphy/manometry studies). Key Results Symptoms at presentation: constipation, 18/23; nausea or vomiting, 18/23; weight loss, 17/23; bloating, 13/23; and early satiety, 4/23. Thirteen patients had personal/family history of autoimmunity. Sixteen had neural autoantibodies and 19 had extra-intestinal autonomic testing abnormalities. Cancer was detected in three patients. Preimmunotherapy scintigraphy revealed slowed transit (19/21 evaluated; gastric, 11; small bowel, 12; colonic, 11); manometry studies were abnormal in 7/8. Postimmunotherapy, 17 (74%) had improvement both symptomatic and scintigraphic, five; symptomatic alone, eight; scintigraphic alone, four). Nine responders re-evaluated had scintigraphic evidence of improvement. The majority of responders who were re-evaluated had improvement in autonomic testing (six of seven) or manometry (two of two). Conclusions & Inferences This proof of principle study illustrates the importance of considering an autoimmune basis for idiopathic gastrointestinal dysmotility and supports the utility of a diagnostic trial of immunotherapy.
C1 [Flanagan, E. P.; Lennon, V. A.; McKeon, A.; Fealey, R. D.; Pittock, S. J.] Mayo Clin, Dept Neurol, Rochester, MN 55905 USA.
   [Saito, Y. A.; Szarka, L. A.; Murray, J. A.; Fox, J. C.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN 55905 USA.
   [Lennon, V. A.; McKeon, A.; Pittock, S. J.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
   [Lennon, V. A.] Mayo Clin, Dept Immunol, Rochester, MN 55905 USA.
   [Foxx-Orenstein, A. E.] Mayo Clin, Div Gastroenterol & Hepatol, Scottsdale, AZ USA.
C3 Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo Clinic; Mayo
   Clinic Phoenix
RP Pittock, SJ (corresponding author), Mayo Clin, Dept Neurol, 200 First St SW, Rochester, MN 55905 USA.
EM pittock.sean@mayo.edu
RI Pittock, Sean/AEL-3538-2022; McKeon, Andrew/AAY-9214-2021
OI McKeon, Andrew/0000-0001-6856-8143; Flanagan, Eoin/0000-0002-6661-2910;
   Pittock, Sean/0000-0002-6140-5584
FU National Institutes of Health [DK71209]
FX This work was supported in part by grant DK71209 from the National
   Institutes of Health (V.A.L.).
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NR 29
TC 54
Z9 55
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1350-1925
EI 1365-2982
J9 NEUROGASTROENT MOTIL
JI Neurogastroenterol. Motil.
PD SEP
PY 2014
VL 26
IS 9
BP 1285
EP 1297
DI 10.1111/nmo.12391
PG 13
WC Gastroenterology & Hepatology; Clinical Neurology; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Neurosciences & Neurology
GA AO8SQ
UT WOS:000341625000008
PM 25039328
OA Green Accepted, Bronze
DA 2025-06-01
ER

PT J
AU Kos, M
   Tomaka, P
   Mertowska, P
   Mertowski, S
   Wojnicka, J
   Blazewicz, A
   Grywalska, E
   Bojarski, K
AF Kos, Marek
   Tomaka, Piotr
   Mertowska, Paulina
   Mertowski, Sebastian
   Wojnicka, Julia
   Blazewicz, Anna
   Grywalska, Ewelina
   Bojarski, Krzysztof
TI The Many Faces of Immune Thrombocytopenia: Mechanisms, Therapies, and
   Clinical Challenges in Oncological Patients
SO JOURNAL OF CLINICAL MEDICINE
LA English
DT Review
DE autoimmune mechanisms; immunosuppressive treatment; ITP; cancer; immune
   system
ID HIGH-DOSE DEXAMETHASONE; HEPARIN-INDUCED THROMBOCYTOPENIA;
   TRANSITIONAL-CELL CARCINOMA; DNA METHYLATION; GASTRIC-CANCER; AUTOIMMUNE
   THROMBOCYTOPENIA; BREAST-CANCER; ACID THERAPY; PURPURA; ITP
AB The pathogenesis of immune thrombocytopenia (ITP) is complex and involves the dysregulation of immune cells, such as T and B lymphocytes, and several cytokines that promote the production of autoantibodies. In the context of cancer patients, ITP can occur in both primary and secondary forms related to anticancer therapies or the disease itself. Objective: In light of these data, we decided to prepare a literature review that will explain the classification and immunological determinants of the pathogenesis of ITP and present the clinical implications of this condition, especially in patients with cancer. Materials and methods: We reviewed the literature on immunological mechanisms, therapies, and challenges in treating ITP, particularly on cancer patients. Results: The results of the literature review show that ITP in cancer patients can be both primary and secondary, with secondary ITP being more often associated with anticancer therapies such as chemotherapy and immunotherapy. Innovative therapies such as TPO-RA, rituximab, Bruton's kinase inhibitors, and FcRn receptor inhibitors have shown promising results in treating refractory ITP, especially in patients with chronic disease. Conclusions: ITP is a significant clinical challenge, especially in the context of oncology patients, where both the disease and treatment can worsen thrombocytopenia and increase the risk of bleeding complications. Treatment of oncology patients with ITP requires an individualized approach, and new therapies offer effective tools for managing this condition. Future research into immunological mechanisms may bring further advances in treating ITP and improve outcomes in cancer patients.
C1 [Kos, Marek] Med Univ Lublin, Dept Publ Hlth, PL-20400 Lublin, Poland.
   [Tomaka, Piotr] SP ZOZ Leczna, Dept Anesthesiol & Intens Care, PL-21010 Leczna, Poland.
   [Mertowska, Paulina; Mertowski, Sebastian; Grywalska, Ewelina] Med Univ Lublin, Dept Expt Immunol, PL-20093 Lublin, Poland.
   [Wojnicka, Julia; Blazewicz, Anna] Med Univ Lublin, Dept Pathobiochem & Interdisciplinary Applicat Ion, PL-20093 Lublin, Poland.
   [Bojarski, Krzysztof] SP ZOZ Leczna, Gen Surg Dept, PL-21010 Leczna, Poland.
C3 Medical University of Lublin; Medical University of Lublin; Medical
   University of Lublin
RP Mertowski, S (corresponding author), Med Univ Lublin, Dept Expt Immunol, PL-20093 Lublin, Poland.
EM sebastian.mertowski@umlub.pl
RI Mertowska, Paulina/AAA-6693-2022; Mertowski, Sebastian/GZM-4663-2022;
   Bojarski, Krzysztof Kamil/ISA-6428-2023; Kos, Marek/AAU-1513-2020;
   Grywalska, Ewelina/MSX-0772-2025; Blazewicz, Anna/ABD-8690-2020
OI Blazewicz, Anna/0000-0001-9758-5831; Grywalska,
   Ewelina/0000-0002-0451-4741; , Piotr Tomaka/0009-0002-8024-7646;
   Mertowski, Sebastian/0000-0002-7121-1396
FU Medical University of Lublin;  [DS640]
FX This research was funded by the Medical University of Lublin (grant
   number: DS640).
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NR 252
TC 1
Z9 1
U1 4
U2 4
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2077-0383
J9 J CLIN MED
JI J. Clin. Med.
PD NOV
PY 2024
VL 13
IS 22
AR 6738
DI 10.3390/jcm13226738
PG 34
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA N6J3W
UT WOS:001365376000001
PM 39597882
OA gold
DA 2025-06-01
ER

PT J
AU Ni, P
   Zhang, YJ
   Liu, YQ
   Lin, X
   Su, XL
   Lu, HX
   Shen, HL
   Xu, WL
   Xu, HX
   Su, ZL
AF Ni, Ping
   Zhang, Yongjian
   Liu, Yueqin
   Lin, Xin
   Su, Xiaolian
   Lu, Hongxiang
   Shen, Huiling
   Xu, Wenlin
   Xu, Huaxi
   Su, Zhaoliang
TI HMGB1 silence could promote MCF-7 cell apoptosis and inhibit invasion
   and metastasis
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY
LA English
DT Article
DE HMGB1; migration; apoptosis; proliferation
ID GROUP BOX 1; MOBILITY GROUP BOX-1; INCREASED EXPRESSION; GASTRIC-CANCER;
   UP-REGULATION; PROTEIN; RAGE; SIGNAL; INFLAMMATION; CONTRIBUTES
AB High mobility group box 1 (HMGB1), a non-histone nuclear protein, was associated with a variety of biological important processes, such as transcription, differentiation, extracellular signaling. As a cytokine or inflammatory mediator, more and more data showed that HMGB1 was involved in inflammatory diseases, cancers or autoimmune disease. However, few data focused on nucleic or cytoplasmic function of HMGB1. Therefore, the present study focused on cancer cells biological characteristics following HMGB1 silence. HMGB1 siRNAs were designed and chemically synthesized, and then transfected into the breast cancer cell line MCF-7 with lipofectamine 2000. The transcription and translation level of HMGB1 expression, proliferation, apoptosis, migration of MCF-7 were determined. The results demonstrated that HMGB1 silence inhibit invasion and migration and promote apoptosis of human breast cells; which indicated that HMGB1 silence might be a potential therapy targets.
C1 [Ni, Ping; Zhang, Yongjian; Su, Xiaolian; Lu, Hongxiang; Xu, Huaxi; Su, Zhaoliang] Jiangsu Univ, Dept Immunol, 301 Xuefu Rd, Zhenjiang 212013, Jiangsu, Peoples R China.
   [Liu, Yueqin; Lin, Xin; Shen, Huiling; Xu, Wenlin] Jiangsu Univ, Affiliated Peoples Hosp 4, Zhenjiang 212001, Peoples R China.
C3 Jiangsu University; Jiangsu University
RP Su, ZL (corresponding author), Jiangsu Univ, Dept Immunol, 301 Xuefu Rd, Zhenjiang 212013, Jiangsu, Peoples R China.
EM szl30@yeah.net
RI SU, Zhaoliang/ABD-9062-2021
CR Akaike H, 2007, ANTICANCER RES, V27, P449
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NR 28
TC 19
Z9 23
U1 0
U2 1
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1936-2625
J9 INT J CLIN EXP PATHO
JI Int. J. Clin. Exp. Pathol.
PY 2015
VL 8
IS 12
BP 15940
EP 15946
PG 7
WC Oncology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pathology
GA DF4VW
UT WOS:000371350600048
PM 26884867
DA 2025-06-01
ER

PT J
AU Wang, SQ
   Hou, HL
   Bie, LY
   Nie, CY
   Wang, LN
   Gao, SB
   Hu, TT
   Chen, XB
AF Wang, Sai-Qi
   Hou, Hong-Lin
   Bie, Liang-Yu
   Nie, Cai-Yun
   Wang, Luo-Nan
   Gao, Shaobing
   Hu, Ting-Ting
   Chen, Xiao-Bing
TI Mechanistic studies of the apoptosis induced by the macrocyclic natural
   product tetrandrine in MGC 803 cells
SO MEDICINAL CHEMISTRY RESEARCH
LA English
DT Article
DE Tetrandrine; Apoptosis; Cell cycle arrest; Migration
ID CANCER CELLS; MULTIDRUG-RESISTANCE; DRUG DISCOVERY; BCL-2 FAMILY; CYCLE
   ARREST; IN-VITRO; PROLIFERATION; FANGCHINOLINE; COMBINATION; INHIBITION
AB Tetrandrine (Tet) is a macrocyclic tetrahydroisoquinoline alkaloid isolated from Stephania tetrandra S. Moore along with other Chinese and Japanese herbs. It has been used extensively for the treatment of silicosis, autoimmune disorders, inflammatory diseases and cardiovascular diseases. Of late, Tet has garnered increasing attention for its anticancer activity and its efficacy to reverse chemoresistance. In this study, we evaluated the cytotoxicity of Tet on MGC 803 gastric cancer cells using the methyl thiazolyl tetrazolium (MTT) assay. In addition, apoptosis and cell cycle were analyzed through flow cytometry, mitochondrial membrane potential (MMP) was measured using fluorescence microscopy and migration of cells was determined by transwell assay. It was observed that Tet efficiently inhibited the proliferation of MGC 803 cells in a concentration-dependent and time-dependent manner and reduced the number of colonies at low concentrations. It induced apoptosis through mitochondrial dysfunction, which may be related with upregulated Bcl-2-associated X protein (Bax), and downregulated of B cell lymphoma 2 (Bcl-2). On the other hand, Tet blocked the cell cycle at Gap 2 (G2)/mitosis (M) phase, which was associated with the upregulation of p21(CIP1/WAF1). Furthermore, Tet elevated the intracellular reactive oxygen species (ROS) level and suppressed the migration of MGC 803 cells. Altogether, we demonstrated that Tet inhibited the proliferation and migration of gastric cancer MGC 803 cells and thus might be a potential drug candidate for the treatment of gastric cancer.
C1 [Wang, Sai-Qi; Hou, Hong-Lin; Bie, Liang-Yu; Nie, Cai-Yun; Hu, Ting-Ting; Chen, Xiao-Bing] Zhengzhou Univ, Henan Canc Hosp, Dept Oncol, Affiliated Canc Hosp, Zhengzhou 450008, Henan, Peoples R China.
   [Wang, Luo-Nan] Xinxiang Med Univ, Dept Oncol, Affiliated Hosp 1, Xinxiang 453100, Henan, Peoples R China.
   [Gao, Shaobing] Zhengzhou Univ, Henan Canc Hosp, Cent Lab, Affiliated Canc Hosp, Zhengzhou 450008, Henan, Peoples R China.
C3 Zhengzhou University; Xinxiang Medical University; Zhengzhou University
RP Chen, XB (corresponding author), Zhengzhou Univ, Henan Canc Hosp, Dept Oncol, Affiliated Canc Hosp, Zhengzhou 450008, Henan, Peoples R China.
EM 2290773710@qq.com
RI Wang, Jiahao/ABA-3280-2021; tingting, hu/AGX-8728-2022; 高,
   绍冰/GQA-8216-2022
OI Gao, Shaobing/0000-0002-8307-9281
FU National Natural Science Foundation of China [81472714]; Key Medical
   Technologies Research & Development Program of Henan Provence
   [201502027]
FX This study was supported by National Natural Science Foundation of China
   (NO. 81472714 for Xiao-Bing Chen).; the Key Medical Technologies
   Research & Development Program of Henan Provence (No. 201502027 for
   Xiao-Bing Chen).
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NR 44
TC 1
Z9 1
U1 0
U2 22
PU SPRINGER BIRKHAUSER
PI NEW YORK
PA 233 SPRING STREET, 6TH FLOOR, NEW YORK, NY 10013 USA
SN 1054-2523
EI 1554-8120
J9 MED CHEM RES
JI Med. Chem. Res.
PD FEB
PY 2019
VL 28
IS 2
BP 107
EP 115
DI 10.1007/s00044-018-2268-8
PG 9
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA HI4WU
UT WOS:000456453700001
DA 2025-06-01
ER

PT J
AU De Re, V
   Repetto, O
   De Zorzi, M
   Casarotto, M
   Tedeschi, M
   Giuffrida, P
   Lenti, MV
   Magris, R
   Miolo, G
   Mazzon, C
   Zanette, G
   Alessandrini, L
   Canzonieri, V
   Caggiari, L
   Zanussi, S
   Steffan, A
   Di Sabatino, A
   Cannizzaro, R
AF De Re, Valli
   Repetto, Ombretta
   De Zorzi, Mariangela
   Casarotto, Mariateresa
   Tedeschi, Massimo
   Giuffrida, Paolo
   Lenti, Marco Vincenzo
   Magris, Raffaella
   Miolo, Gianmaria
   Mazzon, Cinzia
   Zanette, Giorgio
   Alessandrini, Lara
   Canzonieri, Vincenzo
   Caggiari, Laura
   Zanussi, Stefania
   Steffan, Agostino
   Di Sabatino, Antonio
   Cannizzaro, Renato
TI Polymorphism in Toll-Like Receptors and Helicobacter Pylori
   Motility in Autoimmune Atrophic Gastritis and Gastric Cancer
SO CANCERS
LA English
DT Article
DE autoimmune gastritis; flagellin A; Helicobacter pylori; toll-like
   receptor 5 (TLR5); toll-like receptor 9 (TLR9)
ID KAPPA-B; FLAGELLIN GLYCOSYLATION; GENE POLYMORPHISMS; T-CELLS; TLR5;
   ACTIVATION; INFECTION; DISEASES; INNATE; INFLAMMASOME
AB Autoimmune atrophic gastritis (AAG) is associated with an increased risk of certain types of gastric cancer (GC). Helicobacter pylori (H. pylori) infection may have a role in the induction and/or maintenance of AAG and GC. Toll-like receptors (TLR) are essential for H. pylori recognition and subsequent innate and adaptive immunity responses. This study therefore aimed to characterize TLR polymorphisms, and features of bacterial flagellin A in samples from patients with AAG (n = 67), GC (n = 114) and healthy donors (HD; n = 97). TLR5 rs5744174 C/C genotype was associated with GC, lower IgG anti H. pylori response and a higher H. pylori flagellin A abundance and motility. In a subset of patients with AAG, H. pylori strains showed a reduction of the flagellin A abundance and a moderate motility compared with strains from GC patients, a prerequisite for active colonization of the deeper layers of the mucosa, host immune response and inflammation. TLR9 rs5743836 T allele showed an association with serum gastrin G17. In conclusion, our study suggests that alterations of flaA protein, moderate motility in H. pylori and two polymorphisms in TLR5 and TLR9 may favor the onset of AAG and GC, at least in a subset of patients. These findings corroborate the function of pathogen-host cell interactions and responses, likely influencing the pathogenetic process.
C1 [De Re, Valli; Repetto, Ombretta; De Zorzi, Mariangela; Casarotto, Mariateresa; Tedeschi, Massimo; Caggiari, Laura; Zanussi, Stefania; Steffan, Agostino] IRCCS, Immunopatol & Biomarcatori Oncol Bioprote Facil, Ctr Riferimento Oncol Aviano CRO, I-33081 Aviano, Italy.
   [Giuffrida, Paolo; Lenti, Marco Vincenzo; Di Sabatino, Antonio] Univ Pavia, San Matteo Hosp Fdn, Dept Internal Med 1, I-27100 Pavia, Italy.
   [Magris, Raffaella; Cannizzaro, Renato] IRCCS, Ctr Riferimento Oncol Aviano CRO, Gastroenterol Oncol Sperimentale, I-33081 Aviano, Italy.
   [Miolo, Gianmaria] IRCCS, Ctr Riferimento Oncol Aviano CRO, Prevent Med Oncol, I-33081 Aviano, Italy.
   [Mazzon, Cinzia; Zanette, Giorgio] Azienda Assistenza Sanitaria 5 Friuli Occidentale, SSD Endocrinol & Malattie Metab, I-33170 Pordenone, Italy.
   [Alessandrini, Lara; Canzonieri, Vincenzo] IRCCS, Natl Canc Inst, Pathol Dept CRO Aviano, I-33081 Aviano, Italy.
   [Alessandrini, Lara] Azienda Osped Padova, Pathol, Dept Med DIMED, I-35121 Padua, Italy.
   [Canzonieri, Vincenzo] Univ Trieste, Dept Med Surg & Hlth Sci, I-34127 Trieste, Italy.
C3 IRCCS Aviano (CRO); University of Pavia; IRCCS Aviano (CRO); IRCCS
   Aviano (CRO); University of Padua; Azienda Ospedaliera - Universita di
   Padova; University of Trieste
RP De Re, V (corresponding author), IRCCS, Immunopatol & Biomarcatori Oncol Bioprote Facil, Ctr Riferimento Oncol Aviano CRO, I-33081 Aviano, Italy.
EM vdere@cro.it; orepetto@cro.it; mdezorzi@cro.it; mtcasarotto@cro.it;
   massimo.tedeschi@cro.it; paolo.giuffrida01@universitadipavia.it;
   marco.lenti@unipv.it; raffaella.magris@cro.it; gmiolo@cro.it;
   cinzia.mazzon@aas5.sanita.fvg.it; giorgio.zanette@aas5.sanita.fvg.it;
   lara.alessandrini@aopd.veneto.it; vcanzonieri@cro.it; lcaggiari@cro.it;
   szanussi@cro.it; asteffan@cro.it; a.disabatino@smatteo.pv.it;
   rcannizzaro@cro.it
RI Canzonieri, Vincenzo/AAA-7951-2019; De Re, Valli/K-4121-2016; Di
   Sabatino, Antonio/K-8015-2016; Magris, Raffaella/ABD-7791-2020;
   Canzonieri, Vincenzo/K-3141-2018; ZANUSSI, STEFANIA/I-2558-2018;
   CASAROTTO, MARIATERESA/D-3947-2019; DE RE, VALLI/AAA-1374-2019;
   Cannizzaro, Renato/V-3804-2018; Repetto, Ombretta/V-6342-2019; Miolo,
   Gianmaria/AAC-2351-2020; Lenti, Marco Vincenzo/F-9044-2018; CAGGIARI,
   LAURA/Q-6125-2019; De Zorzi, Mariangela/AAA-8832-2019; Steffan,
   Agostino/ABE-5972-2020
OI Canzonieri, Vincenzo/0000-0001-6010-0976; ZANUSSI,
   STEFANIA/0000-0003-0608-9766; CASAROTTO,
   MARIATERESA/0000-0001-5832-2895; DE RE, VALLI/0000-0001-6100-9373;
   Cannizzaro, Renato/0000-0002-2020-222X; Repetto,
   Ombretta/0000-0002-0785-5066; GIUFFRIDA, PAOLO/0000-0001-7164-2439;
   Miolo, Gianmaria/0000-0001-5084-295X; Lenti, Marco
   Vincenzo/0000-0002-6654-4911; CAGGIARI, LAURA/0000-0003-1651-6653; De
   Zorzi, Mariangela/0000-0002-3794-270X; Steffan,
   Agostino/0000-0002-6320-3054
FU CRO 5X1000_2010_MdS, Italy
FX This research work was supported by the CRO 5X1000_2010_MdS, Italy.
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NR 61
TC 22
Z9 22
U1 1
U2 14
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD MAY
PY 2019
VL 11
IS 5
AR 648
DI 10.3390/cancers11050648
PG 22
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA IF0AP
UT WOS:000472738300061
PM 31083432
OA Green Published, Green Submitted, gold
DA 2025-06-01
ER

PT J
AU Dhuriya, YK
   Sharma, D
   Naik, AA
AF Dhuriya, Yogesh Kumar
   Sharma, Divakar
   Naik, Aijaz A.
TI Cellular demolition: Proteins as molecular players of programmed cell
   death
SO INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
LA English
DT Review
DE Apoptosis; Caspase; Phosphorylation; Ubiquitylation
ID BCL-2 FAMILY PROTEINS; MITOCHONDRIAL-MEMBRANE PERMEABILIZATION;
   ENDOPLASMIC-RETICULUM STRESS; DRUG-INDUCED APOPTOSIS; BH3 DOMAINS;
   GENE-EXPRESSION; GASTRIC-CANCER; BREAST-CANCER; IN-VITRO; PROAPOPTOTIC
   ACTIVITY
AB Apoptosis, a well-characterized and regulated cell death programme in eukaryotes plays a fundamental role in developing or later-life periods to dispose of unwanted cells to maintain typical tissue architecture, homeostasis in a spatiotemporal manner. This silent cellular death occurs without affecting any neighboring cells/tissue and avoids triggering of immunological response. Furthermore, diminished forms of apoptosis result in cancer and autoimmune diseases, whereas unregulated apoptosis may also lead to the development of a myriad of neurodegenerative diseases. Unraveling the mechanistic events in depth will provide new insights into understanding physiological control of apoptosis, pathological consequences of abnormal apoptosis and development of novel therapeutics for diseases. Here we provide a brief overview of molecular players of programmed cell death with discussion on the role of caspases, modifications, ubiquitylation in apoptosis, removal of the apoptotic body and its relevance to diseases. (C) 2019 Elsevier B.V. All rights reserved.
C1 [Dhuriya, Yogesh Kumar] CSIR, IITR, Syst Toxicol & Hlth Risk Assessment Grp, Dev Toxicol Lab, Vishvigyan Bhawan 31,Mahatma Gandhi Marg, Lucknow 226001, Uttar Pradesh, India.
   [Sharma, Divakar] Natl JALMA Inst Leprosy & Other Mycobacterial Dis, Dept Biochem, Agra, Uttar Pradesh, India.
   [Sharma, Divakar] Aligarh Muslim Univ, Interdisciplinary Biotechnol Unit, Aligarh 202002, Uttar Pradesh, India.
   [Naik, Aijaz A.] Univ Virginia, Sch Med, Neurol, Charlottesville, VA 22908 USA.
C3 Council of Scientific & Industrial Research (CSIR) - India; CSIR -
   Indian Institute of Toxicology Research (IITR); Indian Council of
   Medical Research (ICMR); ICMR - National JALMA Institute for Leprosy &
   Other Mycobacterial Diseases, Agra; Aligarh Muslim University;
   University of Virginia
RP Sharma, D (corresponding author), Natl JALMA Inst Leprosy & Other Mycobacterial Dis, Dept Biochem, Agra, Uttar Pradesh, India.
EM divakarsharma88@gmail.com
RI Naik, Aijaz/AAY-4852-2021; Sharma, Divakar/AFX-9466-2022
OI Sharma, Divakar/0000-0002-8735-5562
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NR 224
TC 22
Z9 25
U1 0
U2 10
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0141-8130
EI 1879-0003
J9 INT J BIOL MACROMOL
JI Int. J. Biol. Macromol.
PD OCT 1
PY 2019
VL 138
BP 492
EP 503
DI 10.1016/j.ijbiomac.2019.07.113
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Applied; Polymer Science
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry; Polymer Science
GA JA1HV
UT WOS:000487569000052
PM 31330212
DA 2025-06-01
ER

PT J
AU Pavlík, E
   Lukes, P
   Potuzníková, B
   Astl, J
   Hrdá, P
   Soucek, A
   Matucha, P
   Dosedèl, J
   Sterzl, I
AF Pavlik, E.
   Lukes, P.
   Potuznikova, B.
   Astl, J.
   Hrda, P.
   Soucek, A.
   Matucha, P.
   Dosedel, J.
   Sterzl, I.
TI Helicobacter pylori isolated from patients with tonsillar cancer
   or tonsillitis chronica could be of different genotype compared to
   isolates from gastrointestinal tract
SO FOLIA MICROBIOLOGICA
LA English
DT Article
ID ASSOCIATION
AB Helicobacter pylori from patients with different diseases, including so-called autoimmune thyroiditis, chronic tonsillitis and tonsillar cancer, was isolated and cultured. It was identified according to the genotype using labeled hybridization probes complementary to six sequences of cagA and vacA genes. Different types of strains were found in isolates from gastrointestinal tract and patients suffering from thyroiditis. Six out of seven genotyped isolates from patients in our Department of Othorhinolaryngology and Head and Neck Surgery exhibited the same genotype, differing from isolates obtained from other patients; the 7th isolate originated from a patient who had undergone surgery for deviatio septi nasi, at the same time suffering from autoimmune thyroiditis, having confirmed gastric infection by H. pylori from biopsy. This data made it possible to formulate the hypothesis on probable association of specific H. pylori genotype with chronic tonsillitis and tonsillar cancer. We assessed commercial transport media and improved nucleic acid isolation techniques and the RT-PCR-based tests, which allowed us to skip a culture step and to test directly The patients' samples; however, for full confirmation of our hypothesis and explanation of possible mechanisms of the contribution of Helicobacter sp. to the pathogenesis of the disease further data are to be collected and evaluated.
C1 Charles Univ Prague, Fac Med 1, Dept Immunol & Microbiol, Prague, Czech Republic.
   Charles Univ Prague, Fac Med 1, Dept Otorhinolaryngol Head & Neck Surg, Prague, Czech Republic.
   Charles Univ Prague, Teaching Hosp Motol, Prague, Czech Republic.
   Inst Endocrinol, Prague, Czech Republic.
   Hosp Sisters Order St Charles Boromeo, Prague, Czech Republic.
C3 Charles University Prague; Charles University Prague; Charles University
   Prague; Institute of Endocrinology - Prague; Charles University Prague
RP Pavlík, E (corresponding author), Charles Univ Prague, Fac Med 1, Dept Immunol & Microbiol, Prague, Czech Republic.
EM pavik.emil@seznam.cz
RI Astl, Jaromir/AAA-4810-2022; Lukes, Petr/G-3587-2017; PAVLIK,
   EMIL/J-6854-2017
OI Lukes, Petr/0000-0001-8007-8083; PAVLIK, EMIL/0000-0002-9132-163X
CR Akbayir N, 2005, EUR ARCH OTO-RHINO-L, V262, P170, DOI 10.1007/s00405-004-0794-0
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NR 11
TC 13
Z9 13
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0015-5632
EI 1874-9356
J9 FOLIA MICROBIOL
JI Folia Microbiol.
PY 2007
VL 52
IS 1
BP 91
EP 94
DI 10.1007/BF02932145
PG 4
WC Biotechnology & Applied Microbiology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biotechnology & Applied Microbiology; Microbiology
GA 160IN
UT WOS:000245934200015
PM 17571803
OA Bronze
DA 2025-06-01
ER

PT J
AU Rugge, M
   Genta, RM
   Malfertheiner, P
   Dinis-Ribeiro, M
   El-Serag, H
   Graham, DY
   Kuipers, EJ
   Leung, WK
   Park, JY
   Rokkas, T
   Schulz, C
   El-Omar, EM
AF Rugge, Massimo
   Genta, Robert M.
   Malfertheiner, Peter
   Dinis-Ribeiro, Mario
   El-Serag, Hashem
   Graham, David Y.
   Kuipers, Ernst J.
   Leung, Wai Keung
   Park, Jin Young
   Rokkas, Theodore
   Schulz, Christian
   El-Omar, Emad M.
TI RE.GA.IN.: the Real-world Gastritis Initiative-updating the updates
SO GUT
LA English
DT Review
DE HELICOBACTER PYLORI - GASTRITIS; GASTRIC CARCINOMA; GASTRIC PRE-CANCER;
   AUTOIMMUNITY; GASTROINTESTINAL PATHOLOGY
ID EPSTEIN-BARR-VIRUS; HELICOBACTER-PYLORI INFECTION; AUTOIMMUNE ATROPHIC
   GASTRITIS; PARIETAL-CELL AUTOANTIBODIES; IMMUNE CHECKPOINT INHIBITORS;
   HEALTHY LIFE-STYLE; INTESTINAL METAPLASIA; GASTROINTESTINAL-TRACT;
   PERNICIOUS-ANEMIA; CLINICAL-PRACTICE
AB At the end of the last century, a far-sighted 'working party' held in Sydney, Australia addressed the clinicopathological issues related to gastric inflammatory diseases. A few years later, an international conference held in Houston, Texas, USA critically updated the seminal Sydney classification. In line with these initiatives, Kyoto Global Consensus Report, flanked by the Maastricht-Florence conferences, added new clinical evidence to the gastritis clinicopathological puzzle.The most relevant topics related to the gastric inflammatory diseases have been addressed by the Real-world Gastritis Initiative (RE.GA.IN.), from disease definitions to the clinical diagnosis and prognosis. This paper reports the conclusions of the RE.GA.IN. consensus process, which culminated in Venice in November 2022 after more than 8 months of intense global scientific deliberations. A forum of gastritis scholars from five continents participated in the multidisciplinary RE.GA.IN. consensus. After lively debates on the most controversial aspects of the gastritis spectrum, the RE.GA.IN. Faculty amalgamated complementary knowledge to distil patient-centred, evidence-based statements to assist health professionals in their real-world clinical practice. The sections of this report focus on: the epidemiology of gastritis; Helicobacter pylori as dominant aetiology of environmental gastritis and as the most important determinant of the gastric oncogenetic field; the evolving knowledge on gastric autoimmunity; the clinicopathological relevance of gastric microbiota; the new diagnostic horizons of endoscopy; and the clinical priority of histologically reporting gastritis in terms of staging. The ultimate goal of RE.GA.IN. was and remains the promotion of further improvement in the clinical management of patients with gastritis.
C1 [Rugge, Massimo] Univ Padua, Dept Med DIMED, Padua, Italy.
   [Rugge, Massimo] Azienda Zero, Veneto Tumour Registry, Padua, Italy.
   [Genta, Robert M.] Inform Diagnost Res Inst, Gastrointestinal Pathol, Dallas, TX USA.
   [Genta, Robert M.] Baylor Coll Med, Pathol, Houston, TX USA.
   [Malfertheiner, Peter] Ludwig Maximilian Univ Klinikum Munchen, Med Klin & Poliklin 2, Munich, Germany.
   [Malfertheiner, Peter] Otto von Guericke Univ, Klin Gastroenterol Hepatol & Infektiol, Magdeburg, Germany.
   [Dinis-Ribeiro, Mario] Univ Porto, Porto Comprehens Canc Ctr & RISE CI IPO, Porto, Portugal.
   [Dinis-Ribeiro, Mario] Portuguese Inst Oncol Porto, Gastroenterol Dept, Porto, Portugal.
   [El-Serag, Hashem] Baylor Coll Med, Gastroenterol & Hepatol, Houston, TX USA.
   [El-Serag, Hashem] Michael E DeBakey VA Med Ctr, Houston VA Hlth Serv Res & Dev Ctr Excellence, Houston, TX USA.
   [Graham, David Y.] Michael E DeBakey VA Med Ctr, Dept Med, Houston, TX USA.
   [Kuipers, Ernst J.] Erasmus MC, Rotterdam, Netherlands.
   [Leung, Wai Keung] Univ Hong Kong, Med, Hong Kong, Peoples R China.
   [Park, Jin Young] Int Agcy Res Canc, Lyon, France.
   [Rokkas, Theodore] Henry Dunant Hosp Ctr, Gastroenterol, Athens, Greece.
   [Schulz, Christian] Ludwig Maximilians Univ Munchen, Dept Med 2, Munich, Germany.
   [El-Omar, Emad M.] Univ New South Wales, Microbiome Res Ctr, Sydney, NSW, Australia.
   [Rugge, Massimo] Univ Padua, Dept Med DIMED, I-35100 Padua, Italy.
C3 University of Padua; Azienda Zero; Baylor College of Medicine; Otto von
   Guericke University; Universidade do Porto; Universidade de Coimbra;
   Baylor College of Medicine; Baylor College of Medicine; Baylor College
   Medical Hospital; Baylor College of Medicine; Baylor College Medical
   Hospital; Erasmus University Rotterdam; Erasmus MC; University of Hong
   Kong; World Health Organization; International Agency for Research on
   Cancer (IARC); Henry Dunant Hospital; University of Munich; University
   of New South Wales Sydney; University of Padua
RP Rugge, M (corresponding author), Univ Padua, Dept Med DIMED, I-35100 Padua, Italy.
EM massimo.rugge@unipd.it
RI El-Omar, Emad/AAT-7780-2021; Kuipers, Ernst/KLZ-0923-2024; El-Serag,
   Hashem/AFR-4394-2022; Graham, David/AAL-2165-2021; Malfertheiner,
   Peter/AEZ-6553-2022; Leung, Wai Keung/B-8140-2011; schulz,
   christian/HOA-7122-2023; Fassan, Matteo/F-5152-2012
OI RUGGE, MASSIMO/0000-0002-0679-0563; Park, Jin Young/0000-0003-2491-5099;
   Fassan, Matteo/0000-0001-6515-5482; Kuipers, Ernst
   J./0000-0002-0633-3098; Genta, Robert/0000-0001-9482-4163
FU Menarini International Foundation
FX This study was supported by an unrestricted grant of Menarini
   International Foundation.
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AF Huang, An-Fang
   Su, Lin-Chong
   Jia, Hong
   Liu, Yi
   Xu, Wang-Dong
TI No association of single nucleotide polymorphisms within H19 and HOX
   transcript antisense RNA (HOTAIR) with genetic susceptibility to
   systemic lupus erythematosus, rheumatoid arthritis, and primary
   Sjogren's syndrome in a Chinese Han population
SO CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Autoimmune diseases; H19; HOTAIR; Polymorphism
ID LONG NONCODING RNA; RS920778 POLYMORPHISM; TURKISH POPULATION;
   BLADDER-CANCER; GASTRIC-CANCER; RISK; EXPRESSION; FEATURES; DISEASE;
   LOCI
AB The H19 (rs2839698, rs3741219) and HOTAIR (rs920778) polymorphisms were related to many kinds of cancers. However, these polymorphisms have been scarcely explored in different autoimmune diseases. Here, we aimed to examine the association of the polymorphisms with susceptibility to or protection against systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and primary Sjogren's syndrome (pSS) among Chinese Han patients. We conducted a case-control study including 800 patients (300 with SLE, 350 with RA, and 150 with pSS) and 350 healthy control individuals. The polymorphisms were specified from genomic DNA using TaqMan genotyping assay on a 7300 real-time reverse transcription polymerase chain reaction system. H19 rs2839698 was not associated with SLE susceptibility and was not associated with RA and pSS, respectively (P > 0.05). Similarly, we did not find significant differences of allele or genotype frequencies between SLE, RA, and pSS patients and healthy controls for H19 gene rs3741219 polymorphism (P > 0.05). In addition, no significant evidence was detected for the relationship of HOTAIR rs920778 polymorphism with risk of these diseases. Our results suggested that H19 rs2839698, rs3741219, and HOTAIR rs920778 polymorphisms may not be involved in the genetic background of SLE, RA, and pSS in Chinese.
C1 [Huang, An-Fang] Southwest Med Univ, Dept Rheumatol & Immunol, Affiliated Hosp, Luzhou, Sichuan, Peoples R China.
   [Su, Lin-Chong; Liu, Yi] Sichuan Univ, West China Hosp, Dept Rheumatol & Immunol, Chengdu, Sichuan, Peoples R China.
   [Su, Lin-Chong] Hubei Inst Nationalities, Dept Rheumatol & Immunol, Affiliated Minda Hosp, Enshi, Hubei, Peoples R China.
   [Jia, Hong; Xu, Wang-Dong] Southwest Med Univ, Sch Publ Hlth, 1 Xianglin Rd, Luzhou 646000, Sichuan, Peoples R China.
C3 Southwest Medical University; Sichuan University; Hubei Minzu
   University; Southwest Medical University
RP Xu, WD (corresponding author), Southwest Med Univ, Sch Publ Hlth, 1 Xianglin Rd, Luzhou 646000, Sichuan, Peoples R China.
EM loutch123@163.com
RI Lin, Lulu/JSL-6136-2023; , Hong/C-8795-2011
OI , Hong/0000-0001-7617-1146
FU National Natural Science Foundation of China [81701606]; Sichuan
   provincial health and Family Planning Commission [16PJ284]
FX This work was supported by grants from the National Natural Science
   Foundation of China (81701606) and Sichuan provincial health and Family
   Planning Commission (16PJ284).
CR [Anonymous], ONCOTARGET
   [Anonymous], ONCOTARGET
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NR 34
TC 15
Z9 16
U1 0
U2 11
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0770-3198
EI 1434-9949
J9 CLIN RHEUMATOL
JI Clin. Rheumatol.
PD NOV
PY 2017
VL 36
IS 11
BP 2447
EP 2453
DI 10.1007/s10067-017-3833-0
PG 7
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA FJ7PF
UT WOS:000412950500007
PM 28914367
DA 2025-06-01
ER

PT J
AU Lopes, V
   Machado, C
   Lages, AD
AF Lopes, Valentim
   Machado, Catarina
   Lages, Adriana De Sousa
TI Autoimmune hypothyroidism and trastuzumab therapy: a rare association
SO ENDOCRINOLOGY DIABETES AND METABOLISM CASE REPORTS
LA English
DT Article
DE Adult; Female; White; Portugal; Thyroid; Thyroid; Unusual effects of
   medical treatment; April; 2023
AB We report a case of a woman with a diagnosis of breast cancer who unintentionally started gaining weight, feeling tired, and constipated 44 weeks after the initiation of trastuzumab. Hypothyroidism secondary to an autoimmune thyroiditis associated with trastuzumab was diagnosed, the first case described in Portugal and the fourth case described worldwide. Our intention regarding the publication of this case report is to alert the clinicians treating people with trastuzumab that they should ask the patients about symptoms of hypothyroidism and should screen the thyroid function of the patients before, during, and after the initiation of trastuzumab. Learning points Trastuzumab is a humanized MAB used in HER2-positive breast and gastric cancer. Trastuzumab-associated autoimmune thyroid disease (AITD) is rare (incidence rate in an RCT of 0.3%). Manifestations of autoimmune thyroiditis associated with trastuzumab resemble those of hypothyroidism in other clinical contexts, but the presence of goiter is highlighted as a reason for medical evaluation. Biochemically, it is characterized by an increased thyroid-stimulating hormone (TSH) with or without a low FT4/FT3, and sonographically with a pattern of thyroiditis. The treatment consists of levothyroxine, in a dose of 1.6-1.8 & mu;g/kg/day, with re-evaluation of the thyroid function in 4-6 weeks. We report the first case of autoimmune thyroiditis secondary to trastuzumab in Portugal. It is important to evaluate the thyroid function before, during, and after the initiation of this therapeutic agent.
C1 [Lopes, Valentim; Machado, Catarina; Lages, Adriana De Sousa] Hosp Braga, EPE, Braga, Portugal.
   [Lages, Adriana De Sousa] Univ Coimbra, Fac Med, Coimbra, Portugal.
C3 Hospital de Braga; Universidade de Coimbra
RP Lopes, V (corresponding author), Hosp Braga, EPE, Braga, Portugal.
EM valentim.silva.lopes@hb.min-saude.pt
OI Lopes, Valentim/0000-0003-2835-7709; De Sousa Lages,
   Adriana/0000-0003-0499-9790
CR Alaniz L, 2009, CANCER LETT, V278, P9, DOI 10.1016/j.canlet.2008.12.029
   Min HK, 2016, KOREAN J INTERN MED, V31, P608, DOI 10.3904/kjim.2014.031
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NR 6
TC 1
Z9 1
U1 0
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA STARLING HOUSE, 1600 BRISTOL PARKWAY N, BRISTOL, ENGLAND
EI 2052-0573
J9 ENDOCR DIAB MET C R
JI Endocrinol. Diabetes Metab. Case Rep.
PD APR 1
PY 2023
VL 2023
IS 2
AR 220412
DI 10.1530/EDM-22-0412
PG 4
WC Endocrinology & Metabolism
WE Emerging Sources Citation Index (ESCI)
SC Endocrinology & Metabolism
GA O2QH0
UT WOS:001042311700001
PM 37096975
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Yokose, T
   Kodama, T
   Matsuno, Y
   Shimosato, Y
   Nishimura, M
   Mukai, K
AF Yokose, T
   Kodama, T
   Matsuno, Y
   Shimosato, Y
   Nishimura, M
   Mukai, K
TI Low-grade B cell lymphoma of mucosa-associated lymphoid tissue in the
   thymus of a patient with rheumatoid arthritis
SO PATHOLOGY INTERNATIONAL
LA English
DT Article
DE B cell lymphoma; centrocyte-like cell; gene rearrangement; low-grade
   malignant lymphoma; lymphoepithelial lesion; mucosa-associated lymphoid
   tissue; rheumatoid arthritis; thymus
ID EPSTEIN-BARR-VIRUS; POLYMERASE CHAIN-REACTION; MALIGNANT-LYMPHOMA; MALT
   LYMPHOMA; HELICOBACTER-PYLORI; GASTRIC LYMPHOMA; MYOEPITHELIAL
   SIALADENITIS; AUTOIMMUNE-DISEASE; SJOGRENS-SYNDROME; MONOCLONALITY
AB The majority of thymic lymphomas are either lymphoblastic lymphoma, large B cell lymphoma or Hodgkin's disease, and other types of non-Hodgkin lymphoma are rare. A case of low-grade B cell lymphoma of mucosa-associated lymphoid tissue (MALT) in the thymus is reported. A 55-year-old Japanese female with a history of rheumatoid arthritis (RA) complained of back pain. A mediastinal tumor was identified by computerized tomography and magnetic resonance imaging, and the thymus was resected through median sternotomy. The solid and nodular tumor had several small satellite extensions and was completely confined to within the thymus. Histologically, monotonous medium-sized centrocyte-like cells occupied the medulla of the thymus and infiltrated Hassall's corpuscles (lymphoepithelial lesions). Immunohistochemically, tumor cells were positive for CD20 and CD79a. IgA and kappa light chain restriction were also found in plasmacytoid cells in the tumor. Clonal rearrangement of the immunoglobulin heavy chain gene was demonstrated by polymerase chain reaction. This case was diagnosed as MALT-type low-grade B cell lymphoma in the thymus. This is the first report of low-grade B cell lymphoma in the thymus associated with RA. As autoimmune diseases are known to be associated with lymphoid neoplasms, it is suggested that the RA played an important role in the development of malignant lymphoma in this case.
C1 Natl Canc Ctr, Res Inst E, Div Pathol, Chiba 277, Japan.
   Natl Canc Ctr, Res Inst, Div Pathol, Chiba 277, Japan.
   Natl Canc Ctr Hosp, Clin Lab Div, Tokyo, Japan.
C3 National Cancer Center - Japan; National Cancer Center - Japan; National
   Cancer Center - Japan
RP Mukai, K (corresponding author), Natl Canc Ctr, Res Inst E, Div Pathol, Kashiwanoha 6-5-1, Chiba 277, Japan.
EM kmukai@east.ncc.go.jp
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NR 38
TC 23
Z9 26
U1 1
U2 3
PU BLACKWELL SCIENCE
PI CARLTON
PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA
SN 1320-5463
J9 PATHOL INT
JI Pathol. Int.
PD JAN
PY 1998
VL 48
IS 1
BP 74
EP 81
DI 10.1111/j.1440-1827.1998.tb03832.x
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA ZM228
UT WOS:000073517500013
PM 9589469
DA 2025-06-01
ER

PT J
AU Ecker, ME
   Weckauf, H
   Tebbe, S
   Schuppert, F
AF Ecker, Miriam Eva
   Weckauf, Helgard
   Tebbe, Sandra
   Schuppert, Frank
TI Immune-mediated Gastritis in a Patient with metastatic Lung Cancer due
   to Therapy with the immune Checkpoint Inhibitor Pembrolizumab -
   Differences and Similarities in Comparison to "endogenous" autoimmune
   Type A Gastritis and a review of literature
SO ZEITSCHRIFT FUR GASTROENTEROLOGIE
LA English
DT Review
DE immune-mediated gastritis; autoimmune gastritis; type A gastritis;
   non-small cell lung cancer; immune checkpoint inhibitor; pembrolizumab
ID ATROPHIC GASTRITIS
AB Immune checkpoint inhibitors are increasingly used in advanced malignant diseases and are well-known for their good results. With the blockade of immune checkpoints, the probability of immune-related adverse events is also increased.We present a 54-year-old female patient with advanced NSCLC. She was treated with pembrolizumab and developed a stable disease under therapy. After six cycles, she presented with massive epigastric pain to our emergency department. Gastroscopy showed severe erosive-fibrinous pangastritis without the involvement of the esophagus, duodenum, or other immune-related adverse effects. Histology showed the complete destruction of the gastric mucosa. We concluded an immune-mediated gastritis by pembrolizumab, after the exclusion of other differential diagnoses.Despite treatment with prednisolone and marked improvement of her symptoms, the mucosa was never fully reconstituted into a healthy mucosa.Furthermore, we collected published reports of similar cases and conducted a comparison with features of a typical, endogenous type A gastritis to highlight similarities and differences.
C1 [Ecker, Miriam Eva; Schuppert, Frank] Klinikum Kassel GmbH, Gastroenterol Endocrinol Diabetol & Gen Med, Kassel, Germany.
   [Weckauf, Helgard] Klinikum Kassel GmbH, Pathol, Kassel, Germany.
   [Tebbe, Sandra] Private Practice Haematol & Oncol, Kassel, Germany.
   [Ecker, Miriam Eva] Klinikum Kassel GmbH, Gastroenterol Endocrinol Diabetol & Gen Med, Monchebergstr 41-43, D-34125 Kassel, Germany.
C3 Klinikum Kassel; Klinikum Kassel; Klinikum Kassel
RP Ecker, ME (corresponding author), Klinikum Kassel GmbH, Gastroenterol Endocrinol Diabetol & Gen Med, Monchebergstr 41-43, D-34125 Kassel, Germany.
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NR 29
TC 4
Z9 4
U1 2
U2 4
PU GEORG THIEME VERLAG KG
PI STUTTGART
PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0044-2771
EI 1439-7803
J9 Z GASTROENTEROL
JI Z. Gastroent.
PD OCT
PY 2023
VL 61
IS 10
BP 1385
EP 1393
DI 10.1055/a-2000-5705
EA MAR 2023
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA U3LX1
UT WOS:000958476500001
PM 36963423
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU YUMOTO, N
   ARAKI, A
   SUMIDA, T
   SAITO, T
   TANIGUCHI, M
   MIKATA, A
AF YUMOTO, N
   ARAKI, A
   SUMIDA, T
   SAITO, T
   TANIGUCHI, M
   MIKATA, A
TI RESTRICTED V-BETA GENE USAGE OF TUMOR-INFILTRATING T-LYMPHOCYTES IN
   PRIMARY GASTRIC MALIGNANT B-CELL LYMPHOMA
SO VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY
LA English
DT Article
DE GASTRIC B CELL LYMPHOMA; T CELL RECEPTOR REPERTOIRE; TUMOR-INFILTRATING
   LYMPHOCYTE; T CELL RECEPTOR REARRANGEMENT; V-BETA USAGE
ID IMMUNOGLOBULIN HEAVY-CHAIN; LYMPHOPROLIFERATIVE DISORDERS; ANTIGEN
   RECEPTOR; GAMMA-CHAIN; AUTOIMMUNE ENCEPHALOMYELITIS; PREDOMINANT
   EXPRESSION; LIMITED HETEROGENEITY; VARIABLE-REGION; REARRANGEMENT;
   DISEASE
AB Ten cases of primary gastric malignant lymphoma (PGL) were investigated immunohistochemical and molecular genetic analysis. These cases were diagnosed histopathologically as follicular small cleaved cell type (1 case), diffuse small cleaved cell type (3 cases) and diffuse large cell type (6 cases) based on the WF (Working Formulation) classification. Seven cases classified as small cleaved or diffuse large cell type belong to low (4 cases) or high (3 cases) grade MALT lymphoma according to Isaacson's classification. All PGL belonged to B lineage cells according to immunohistochemical study and immunoglobulin rearrangements. Rearrangements of TCR beta chain genes were observed in four of the ten cases. The possibility that the TCR beta rearrangements were caused by tumour-infiltrating T-cells (TILs) was supported by the following observations: the tumours did not show T- and B-cell biphenotype, TCR beta exhibited functional VDJ rearrangement and V beta usage pattern was not a neoplastic type. Analysis of the repertoire of the TCR beta chain in TILs revealed a common usage of V beta 2 in the above four cases, and furthermore, predominant usage of a particular beta chain composed of V beta 2-D beta 2.1-J beta 2.3 was observed in one of the four cases. These results indicate that the TILs of PGL have a restricted TCR repertoire.
C1 CHIBA UNIV,SCH MED,DEPT INTERNAL MED 2,CHIBA 280,JAPAN.
   CHIBA UNIV,SCH MED,CTR BIOMED SCI,DIV MOLEC GENET,CHIBA 280,JAPAN.
   CHIBA UNIV,SCH MED,CTR BIOMED SCI,DIV MOLEC IMMUNOL,CHIBA 280,JAPAN.
C3 Chiba University; Chiba University; Chiba University
RP YUMOTO, N (corresponding author), CHIBA UNIV,SCH MED,DEPT PATHOL 1,CHUO KU,1-8-1 INOHANA,CHIBA 260,JAPAN.
RI Saito, Takashi/C-9684-2009
OI Saito, Takashi/0000-0001-9495-3547
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NR 42
TC 13
Z9 13
U1 0
U2 0
PU SPRINGER VERLAG
PI NEW YORK
PA 175 FIFTH AVE, NEW YORK, NY 10010
SN 0945-6317
J9 VIRCHOWS ARCH
JI Virchows Arch. Int. J. Pathol.
PD FEB
PY 1995
VL 426
IS 1
BP 11
EP 18
PG 8
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA QP647
UT WOS:A1995QP64700003
PM 7704319
DA 2025-06-01
ER

PT J
AU Azari, H
   Mousavi, P
   Karimi, E
   Sadri, F
   Zarei, M
   Rafat, M
   Shekari, M
AF Azari, Hanieh
   Mousavi, Pegah
   Karimi, Elham
   Sadri, Fatemeh
   Zarei, Mahboobeh
   Rafat, Milad
   Shekari, Mohammad
TI The expanding role of CDR1-AS in the regulation and development of
   cancer and human diseases
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Review
DE biogenesis; cancers; CDR1-AS; microvascular invasion; neurodegenerative
   disease; stem cells
ID CIRCULAR RNA; PROGNOSTIC BIOMARKER; THERAPEUTIC TARGET;
   COLORECTAL-CANCER; BLADDER-CANCER; GASTRIC-CANCER; OVARIAN-CANCER;
   EPIDEMIOLOGY; PROGRESSION; DIAGNOSIS
AB CircRNAs are a superabundant and highly conserved group of noncoding RNAs (ncRNAs) that are characterized by their high stability and integrity compared with linear forms of ncRNAs. Recently, their critical role in gene expression regulation has been shown; thus, it is not far-fetched to believe that their abnormal expression can be a cause of different kinds of diseases such as cancer, neurodegenerative, and autoimmune diseases. They can have a function in variety of biological processes such as microRNA (miRNA) sponging, interacting with RNA-binding proteins, or even an ability to translate to proteins. A huge challenge in finding diagnostic biomarkers is finding noninvasive biomarkers that can be detected in human fluids, especially blood samples. CircRNAs are becoming candidate biomarkers for diagnosis and prognosis of these diseases through their ability to transverse from the blood-brain barrier and their broad presence in circulating exosomes. The circRNA for miRNA-7 (ciRS-7) is newly recognized, and acknowledged to being related to human pathology and cancer progression. In this review, we first briefly summarize the latest studies about their characteristics, biogenesis, and their mechanisms of action in the regulation and development of human diseases. Finally, we provide a list of diseases that are linked to one member of this novel class of ncRNAs called ciRS-7.
C1 [Azari, Hanieh; Mousavi, Pegah; Karimi, Elham; Sadri, Fatemeh; Zarei, Mahboobeh; Rafat, Milad; Shekari, Mohammad] Hormozgan Univ Med Sci, Dept Med Genet, Fac Med, Bandar Abbas, Iran.
RP Shekari, M (corresponding author), Hormozgan Univ Med Sci, Dept Med Genet, Fac Med, Bandar Abbas, Iran.
EM mshekariomics@gmail.com
RI Mousavi, Pegah/JAN-6578-2023; Azari, Hanie/AAU-9230-2021; Mousavi,
   Pegah/K-9207-2018
OI Azari, Hanieh/0000-0002-2956-6222; Karimi, Elham/0000-0001-5864-5002;
   Mousavi, Pegah/0000-0002-5654-7561; Zarei, Mahboobeh/0000-0003-2101-1510
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NR 122
TC 15
Z9 15
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9541
EI 1097-4652
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD FEB
PY 2021
VL 236
IS 2
BP 771
EP 790
DI 10.1002/jcp.29950
EA JUL 2020
PG 20
WC Cell Biology; Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Physiology
GA OU0IY
UT WOS:000550898500001
PM 32697389
DA 2025-06-01
ER

PT J
AU Affandi, AJ
   Carvalheiro, T
   Ottria, A
   Broen, JCA
   Bossini-Castillo, L
   Tieland, RG
   van Bon, L
   Chouri, E
   Rossato, M
   Mertens, JS
   Garcia, S
   Pandit, A
   de Kroon, LMG
   Christmann, RB
   Martin, J
   van Roon, JAG
   Radstake, TRDJ
   Marut, W
AF Affandi, Alsya J.
   Carvalheiro, Tiago
   Ottria, Andrea
   Broen, Jasper C. A.
   Bossini-Castillo, Lara
   Tieland, Ralph G.
   van Bon, Lenny
   Chouri, Eleni
   Rossato, Marzia
   Mertens, Jorre S.
   Garcia, Samuel
   Pandit, Aridaman
   de Kroon, Laurie M. G.
   Christmann, Romy B.
   Martin, Javier
   van Roon, Joel A. G.
   Radstake, Timothy R. D. J.
   Marut, Wioleta
TI Low RUNX3 expression alters dendritic cell function in patients with
   systemic sclerosis and contributes to enhanced fibrosis
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Article
ID TUMOR-SUPPRESSOR RUNX3; TRANSCRIPTION FACTORS; GASTRIC-CANCER; T-CELLS;
   ACTIVATION; INTERFERON; ASSOCIATION; IMMUNITY; SKIN; HYPERMETHYLATION
AB Objectives Systemic sclerosis (SSc) is an autoimmune disease with unknown pathogenesis manifested by inflammation, vasculopathy and fibrosis in skin and internal organs. Type I interferon signature found in SSc propelled us to study plasmacytoid dendritic cells (pDCs) in this disease. We aimed to identify candidate pathways underlying pDC aberrancies in SSc and to validate its function on pDC biology.
   Methods In total, 1193 patients with SSc were compared with 1387 healthy donors and 8 patients with localised scleroderma. PCR-based transcription factor profiling and methylation status analyses, single nucleotide polymorphism genotyping by sequencing and flow cytometry analysis were performed in pDCs isolated from the circulation of healthy controls or patients with SSc. pDCs were also cultured under hypoxia, inhibitors of methylation and hypoxia-inducible factors and runt-related transcription factor 3 (RUNX3) levels were determined. To study Runx3 function, Itgax-Cre: Runx3(f/f) mice were used in in vitro functional assay and bleomycin-induced SSc skin inflammation and fibrosis model.
   Results Here, we show downregulation of transcription factor RUNX3 in SSc pDCs. A higher methylation status of the RUNX3 gene, which is associated with polymorphism rs6672420, correlates with lower RUNX3 expression and SSc susceptibility. Hypoxia is another factor that decreases RUNX3 level in pDC. Mouse pDCs deficient of Runx3 show enhanced maturation markers on CpG stimulation. In vivo, deletion of Runx3 in dendritic cell leads to spontaneous induction of skin fibrosis in untreated mice and increased severity of bleomycin-induced skin fibrosis.
   Conclusions We show at least two pathways potentially causing low RUNX3 level in SSc pDCs, and we demonstrate the detrimental effect of loss of Runx3 in SSc model further underscoring the role of pDCs in this disease.
C1 [Affandi, Alsya J.; Carvalheiro, Tiago; Ottria, Andrea; Broen, Jasper C. A.; Tieland, Ralph G.; van Bon, Lenny; Chouri, Eleni; Rossato, Marzia; Mertens, Jorre S.; Garcia, Samuel; Pandit, Aridaman; van Roon, Joel A. G.; Radstake, Timothy R. D. J.; Marut, Wioleta] Univ Utrecht, Univ Med Ctr Utrecht, Lab Translat Immunol, Utrecht, Netherlands.
   [Affandi, Alsya J.; Carvalheiro, Tiago; Ottria, Andrea; Broen, Jasper C. A.; Tieland, Ralph G.; van Bon, Lenny; Chouri, Eleni; Rossato, Marzia; Mertens, Jorre S.; Garcia, Samuel; Pandit, Aridaman; van Roon, Joel A. G.; Radstake, Timothy R. D. J.; Marut, Wioleta] Univ Utrecht, Univ Med Ctr Utrecht, Dept Rheumatol & Clin Immunol, Utrecht, Netherlands.
   [Affandi, Alsya J.; Broen, Jasper C. A.; van Bon, Lenny; de Kroon, Laurie M. G.; Christmann, Romy B.; Radstake, Timothy R. D. J.] Boston Univ, Sch Med, Dept Med, Rheumatol Sect, Boston, MA 02118 USA.
   [Bossini-Castillo, Lara; Martin, Javier] CSIC, IPBLN, Granada, Spain.
   [Bossini-Castillo, Lara] Wellcome Trust Sanger Inst, Dept Cellular Genet, Cambridge, England.
   [Rossato, Marzia] Univ Verona, Dept Biotechnol, Verona, Italy.
   [Mertens, Jorre S.] Radboud Univ Nijmegen, Med Ctr, Dept Dermatol, Nijmegen, Netherlands.
C3 Utrecht University; Utrecht University Medical Center; Utrecht
   University; Utrecht University Medical Center; Boston University;
   Consejo Superior de Investigaciones Cientificas (CSIC); CSIC - Instituto
   de Parasitologia y Biomedicina Lopez-Neyra (IPBLN); Wellcome Trust
   Sanger Institute; University of Verona; Radboud University Nijmegen
RP Marut, W (corresponding author), Univ Med Ctr Utrecht, Dept Rheumatol & Clin Immunol, Utrecht, Netherlands.; Radstake, TRDJ (corresponding author), Univ Utrecht, Univ Med Ctr Utrecht, Lab Translat Immunol, Utrecht, Netherlands.; Radstake, TRDJ (corresponding author), Univ Utrecht, Univ Med Ctr Utrecht, Dept Rheumatol & Clin Immunol, Utrecht, Netherlands.; Radstake, TRDJ (corresponding author), Boston Univ, Sch Med, Dept Med, Rheumatol Sect, Boston, MA 02118 USA.
EM R.D.J.Radstake@umcutrecht.nl; w.k.marut@umcutrecht.nl
RI Mertens, Jorre/P-5078-2015; Rossato, Marzia/AAB-7827-2019; Pandit,
   Aridaman/ABH-1221-2021; Martin, Javier/B-8141-2008; Bossini-Castillo,
   Lara/G-1234-2016; Garcia Perez, Samuel/I-4729-2015
OI Ottria, Andrea/0000-0001-8722-3968; Martin, Javier/0000-0002-2202-0622;
   Bossini-Castillo, Lara/0000-0002-5471-5824; Pandit,
   Aridaman/0000-0003-2057-9737; ROSSATO, Marzia/0000-0002-6101-1550;
   Affandi, Alsya/0000-0003-0859-2322; Carvalheiro,
   Tiago/0000-0002-3187-2288; Garcia Perez, Samuel/0000-0002-5902-2699
FU Dutch Arthritis Association (Reumafonds grant) [NR-10-1-301];
   Netherlands Organisation for Scientific Research (Mosaic grant)
   [017.008.014]; Portuguese national funding agency for science, research
   and technology: Fundacao para a Ciencia e a Tecnologia
   [SFRH/BD/93526/2013]; VENI Award from the Netherlands Organisation for
   Scientific Research (NWO) [91614041]; Marie Curie Intra-European
   Fellowship [624871]; NWO VENI [91919149]; ERC Starting Grant
   (ERC-2011-StG, Circumvent); Fundação para a Ciência e a Tecnologia
   [SFRH/BD/93526/2013] Funding Source: FCT
FX AJA was supported by the Dutch Arthritis Association (Reumafonds grant
   NR-10-1-301) and the Netherlands Organisation for Scientific Research
   (Mosaic grant 017.008.014). TC is supported by a grant from the
   Portuguese national funding agency for science, research and technology:
   Fundacao para a Ciencia e a Tecnologia [SFRH/BD/93526/2013]. JCAB is
   supported by a VENI Award from the Netherlands Organisation for
   Scientific Research (NWO project number 91614041). WM obtained funding
   from Marie Curie Intra-European Fellowship (Proposal number: 624871) and
   from the NWO VENI (grant number 91919149). TRDJR and JAGvR received
   funding from ERC Starting Grant (ERC-2011-StG, Circumvent). We thanked
   Kei Yasuda, Mike DiMarzio (Boston University), Chiara Angiolilli, Aniek
   Meijers, Ana P Lopes, M Ines Ramos (UMC Utrecht), and Mascha
   Schijvenaars (Radboud University Nijmegen) for their advice and
   technical expertise.
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NR 67
TC 23
Z9 25
U1 0
U2 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
EI 1468-2060
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD SEP
PY 2019
VL 78
IS 9
BP 1249
EP 1259
DI 10.1136/annrheumdis-2018-214991
PG 11
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA IX8OJ
UT WOS:000485946700029
PM 31126957
DA 2025-06-01
ER

PT J
AU Mohammadi, M
   Attar, A
   Mohammadbeigi, M
   Peymani, A
   Bolori, S
   Fardsanei, F
AF Mohammadi, Mahnaz
   Attar, Adeleh
   Mohammadbeigi, Maryam
   Peymani, Amir
   Bolori, Shahin
   Fardsanei, Fatemeh
TI The possible role of Helicobacter pylori in liver diseases
SO ARCHIVES OF MICROBIOLOGY
LA English
DT Review
DE Helicobacter pylori; Liver diseases; HPV; And HCV
ID UNIDENTIFIED CURVED BACILLI; HEPATIC STELLATE CELLS;
   HEPATOCELLULAR-CARCINOMA; FIBROSIS STAGE; INFECTION; DIAGNOSIS;
   ASSOCIATION; CIRRHOSIS; SEROPREVALENCE; EPIDEMIOLOGY
AB According to previous studies, Helicobacter pylori infection is associated with liver disease. In order to better understand the risk of acquiring various liver diseases, we reviewed current knowledge on the impact of H. pylori on the onset, intensification, and progression of various liver diseases caused by the infection of H. pylori. It has been estimated that between 50 and 90% of people worldwide have been infected with H. pylori. The bacterium is mostly responsible for inflamed gastric mucosa, ulcers, and cancers associated with the gastric mucosa. Through the active antioxidant system in H. pylori, the bacteria can neutralize free radicals by synthesizing VacA, a toxin that causes cell damage and apoptosis. Furthermore, there is a possibility that CagA genes may play a role in cancer development. People who have been infected with H. pylori are likely to develop lesions in the skin, the circulation system, and the pancreas. Moreover, transferring blood from the stomach may allow H. pylori to colonize the liver. The bacterium worsened liver function during autoimmune inflammation, toxic injury, chronic HCV infection, chronic HBV infection, and liver cirrhosis. Increasing portal pressure, hyperammonemia, and esophageal varices may be associated with H pylori infection. As a result, it is crucial to diagnose and treat this infection in patients with H. pylori.
C1 [Mohammadi, Mahnaz; Attar, Adeleh; Mohammadbeigi, Maryam; Peymani, Amir; Bolori, Shahin; Fardsanei, Fatemeh] Qazvin Univ Med Sci, Med Microbiol Res Ctr, Qazvin, Iran.
C3 Qazvin University of Medical Sciences (QUMS)
RP Fardsanei, F (corresponding author), Qazvin Univ Med Sci, Med Microbiol Res Ctr, Qazvin, Iran.
EM Atefeh_fardsanei@yahoo.com
RI fardsanei, fatemeh/AAZ-7223-2021; Attar, Adeleh/JVD-7902-2023
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NR 147
TC 5
Z9 5
U1 1
U2 12
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 0302-8933
EI 1432-072X
J9 ARCH MICROBIOL
JI Arch. Microbiol.
PD AUG
PY 2023
VL 205
IS 8
AR 281
DI 10.1007/s00203-023-03602-z
PG 14
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA L4PU3
UT WOS:001023109400001
PM 37430019
DA 2025-06-01
ER

PT J
AU Setti, G
   Pezzi, ME
   Viani, MV
   Pertinhez, TA
   Cassi, D
   Magnoni, C
   Bellini, P
   Musolino, A
   Vescovi, P
   Meleti, M
AF Setti, Giacomo
   Pezzi, Margherita E.
   Viani, Maria Vittoria
   Pertinhez, Thelma A.
   Cassi, Diana
   Magnoni, Cristina
   Bellini, Pierantonio
   Musolino, Antonino
   Vescovi, Paolo
   Meleti, Marco
TI Salivary MicroRNA for Diagnosis of Cancer and Systemic Diseases: A
   Systematic Review
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE saliva; biomarkers; miRNA; cancer; diagnosis
ID CLINICAL UTILITY; CROHNS-DISEASE; EXPRESSION; BIOMARKERS; SERUM;
   PROTEINS; EXOSOMES; MIR-204; RNA
AB Background: The aberrant expression of microRNAs (miRNAs) has been associated with several diseases, including cancer, inflammatory, and autoimmune conditions. Interest in salivary miRNAs as non-invasive tools for the diagnosis of malignancies and systemic diseases is rapidly increasing. The present systematic review was developed for answering the question: "Are salivary microRNAs reliable biomarkers for diagnosis of cancer and systemic diseases?" Methods: The application of inclusion and exclusion criteria led to the selection of 11 papers. Critical appraisals and quality assessments of the selected studies were performed through the National Institute of Health "Study Quality Assessment Tool" and the classification of the Oxford Center for Evidence-Based Medicine. Results: Seven studies reported statistically significant correlations between one or more salivary miRNAs and the investigated disease. The critical analysis allowed us to classify only two studies (18.2%) as having "good" quality, the rest being scored as "intermediate" (8; 73%) and "poor" (1; 9%). Evidence exists that salivary miR-940 and miR-3679-5p are reliable markers for pancreatic cancer and that miR140-5p and miR301a are promising molecules for the salivary diagnosis of gastric cancer. Conclusions: Further studies, possibly avoiding the risk of bias highlighted here, are necessary to consolidate these findings and to identify new reliable salivary biomarkers.
C1 [Setti, Giacomo] Univ Parma, Mol Med PhD Sch, Dept Med & Surg, I-43125 Parma, Italy.
   [Setti, Giacomo; Bellini, Pierantonio] Univ Modena & Reggio Emilia, Dept Surg Med Dent & Morphol Sci Interest Transpl, Dent & Oral & Maxillofacial Surg, Largo Pozzo 71, I-41125 Modena, Italy.
   [Pezzi, Margherita E.; Viani, Maria Vittoria; Cassi, Diana; Vescovi, Paolo; Meleti, Marco] Univ Parma, Ctr Univ Odontoiatria, Via Gramsci 14, I-43126 Parma, Italy.
   [Pertinhez, Thelma A.] Dept Med & Surg, Via Volturno 39, I-43125 Parma, Italy.
   [Pertinhez, Thelma A.] IRCCS Reggio Emilia, Azienda USL, Transfus Med Unit, Viale Umberto 1,50, I-42123 Reggio Emilia, Italy.
   [Magnoni, Cristina] Univ Modena & Reggio Emilia, Dept Surg Med Dent & Morphol Sci Interest Transpl, Dermatol, Largo Pozzo 71, I-41125 Modena, Italy.
   [Musolino, Antonino] Univ Hosp Parma, Med Oncol & Breast Unit, Via Gramsci 14, I-43125 Parma, Italy.
C3 University of Parma; Universita di Modena e Reggio Emilia; University of
   Parma; University Hospital of Parma; Universita di Modena e Reggio
   Emilia; University of Parma; University Hospital of Parma
RP Setti, G (corresponding author), Univ Parma, Mol Med PhD Sch, Dept Med & Surg, I-43125 Parma, Italy.; Setti, G (corresponding author), Univ Modena & Reggio Emilia, Dept Surg Med Dent & Morphol Sci Interest Transpl, Dent & Oral & Maxillofacial Surg, Largo Pozzo 71, I-41125 Modena, Italy.
EM giacomo.setti@unipr.it; margherita.pezzi@gmail.com;
   mariavittoriaviani@gmail.com; thelma.pertinhez@unipr.it;
   diana.cassi@unipr.it; magnoni.cristina@gmail.com;
   pierantonio.bellini@unimore.it; amusolino@ao.pr.it;
   paolo.vescovi@unipr.it; marco.meleti@unipr.it
RI Bellini, Pierantonio/B-1939-2017; Cassi, Diana/HCH-6383-2022; Setti,
   Giacomo/HCH-2535-2022; Musolino, Antonino/M-6904-2016
OI MELETI, Marco/0000-0002-9111-3224; Musolino,
   Antonino/0000-0002-7979-6261; Setti, Giacomo/0000-0002-2933-8174
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NR 72
TC 57
Z9 62
U1 0
U2 10
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD FEB
PY 2020
VL 21
IS 3
AR 907
DI 10.3390/ijms21030907
PG 22
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA KY4PQ
UT WOS:000522551604004
PM 32019170
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Franceschi, F
   Zuccalà, G
   Roccarina, D
   Gasbarrini, A
AF Franceschi, Francesco
   Zuccala, Giuseppe
   Roccarina, Davide
   Gasbarrini, Antonio
TI Clinical effects of Helicobacter pylori outside the stomach
SO NATURE REVIEWS GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
ID IDIOPATHIC THROMBOCYTOPENIC PURPURA; IRON-DEFICIENCY ANEMIA;
   COLORECTAL-CANCER RISK; CORONARY-HEART-DISEASE; PRIMARY OPEN-ANGLE; ABO
   BLOOD-GROUP; PANCREATIC-CANCER; AUTOIMMUNE PANCREATITIS; HIGH
   PREVALENCE; EXTRAGASTRIC MANIFESTATIONS
AB The discovery of Helicobacter pylori infection in the stomach could be considered as one of the most important events of modern gastroenterology. Understanding of the natural history of many disorders of the upper gastrointestinal tract, including chronic gastritis, peptic ulcer disease, gastric cancer and MALT lymphoma, was altered by this discovery. Interestingly, epidemiological studies have also revealed a correlation between H. pylori infection and some diseases localized outside the stomach, especially those characterized by persistent and low-grade systemic inflammation. Of note, H. pylori has an important role in iron deficiency anaemia, idiopathic thrombocytopenic purpura and vitamin B-12 deficiency. Moreover, the association of this bacterial pathogen with many other diseases, including hepatobiliary, pancreatic, cardiovascular and neurodegenerative disorders is currently under investigation. In this Review, we summarize the results of the most important studies performed to date surrounding the association of H. pylori infection with extragastric diseases, as well as the strength of the evidence. We also provide information concerning bacterial-host interactions and the mechanisms implicated in the pathogenesis of each of these extragastric diseases.
C1 [Franceschi, Francesco; Zuccala, Giuseppe; Roccarina, Davide] Univ Cattolica Sacro Cuore, Policlin A Gemelli, Inst Internal Med, I-00168 Rome, Italy.
   [Gasbarrini, Antonio] Univ Cattolica Sacro Cuore, Policlin A Gemelli, I-00168 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli;
   Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Franceschi, F (corresponding author), Univ Cattolica Sacro Cuore, Policlin A Gemelli, Inst Internal Med, Largo A Gemelli 8, I-00168 Rome, Italy.
EM francesco.franceschi@rm.unicatt.it
RI Zuccalà, Giuseppe/AAC-4677-2022; Gasbarrini, Antonio/AAB-8487-2019;
   Roccarina, Davide/AAO-2854-2020; Franceschi, Francesco/AAB-3458-2019
OI Gasbarrini, Antonio/0000-0003-4863-6924; Zuccala,
   Giuseppe/0000-0002-2567-2220; Franceschi, Francesco/0000-0002-9090-8244;
   Roccarina, Davide/0000-0002-1224-5502; Gasbarrini,
   Antonio/0000-0002-6230-1779
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NR 117
TC 117
Z9 124
U1 1
U2 41
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5045
EI 1759-5053
J9 NAT REV GASTRO HEPAT
JI Nat. Rev. Gastroenterol. Hepatol.
PD APR
PY 2014
VL 11
IS 4
BP 234
EP 242
DI 10.1038/nrgastro.2013.243
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AE5XZ
UT WOS:000334063900006
PM 24345888
DA 2025-06-01
ER

PT J
AU Afzal, H
   Shaukat, A
   Ul Haq, MZ
   Khaliq, N
   Zahid, M
   Shakeel, L
   Zuberi, MAW
   Akilimali, A
AF Afzal, Hadiya
   Shaukat, Ayesha
   Ul Haq, Muhammad Zain
   Khaliq, Nawal
   Zahid, Maha
   Shakeel, Laiba
   Zuberi, Muhammad Abdul Wasay
   Akilimali, Aymar
TI Serum metabolic profiling analysis of chronic gastritis and gastric
   cancer by untargeted metabolomics
SO ANNALS OF MEDICINE AND SURGERY
LA English
DT Article
DE atrophic gastritis; biomarkers; chronic gastritis; gastric cancer;
   Helicobacter pylori; metabolomics
ID HELICOBACTER-PYLORI INFECTION; CHRONIC ATROPHIC GASTRITIS;
   DIAGNOSTIC-APPROACH; BIOMARKERS; ASSOCIATION; MICROBIOME; METAANALYSIS;
   ERADICATION; MECHANISMS; STRATEGIES
AB Chronic gastritis (CG), particularly when associated with Helicobacter pylori (H. pylori) infection, is a significant precursor to gastric cancer (GC), a leading cause of cancer-related deaths worldwide. The persistent inflammation in CG, driven by factors such as H. pylori, induces oxidative stress and DNA damage in gastric epithelial cells, which can lead to malignant transformation. Atrophic gastritis, a form of CG, can be categorized into autoimmune and H. pylori-associated types, both of which increase the risk of GC development, particularly when compounded by external factors like smoking and dietary habits. This manuscript explores the pathophysiological mechanisms underlying CG and its progression to GC, highlighting the critical role of metabolomics in advancing our understanding of these processes. Metabolomics, the comprehensive study of metabolites, offers a novel approach to identifying biomarkers that could facilitate early detection and improve the accuracy of GC diagnosis and prognosis. The analysis of metabolic alterations, particularly in glucose, lipid, and amino acid metabolism, reveals distinct biochemical pathways associated with the progression from benign gastritis to malignancy. Integrating metabolomic profiling with traditional diagnostic methods can revolutionize GC management, enabling more personalized treatment strategies and improving clinical outcomes. However, significant challenges remain, including the need to validate biomarkers across diverse populations and standardize metabolomic techniques. Future research should address these challenges to fully realize the potential of metabolomics in early GC detection and treatment, ultimately aiming to reduce the global burden of this deadly disease.
C1 [Afzal, Hadiya; Shaukat, Ayesha; Ul Haq, Muhammad Zain; Khaliq, Nawal; Zahid, Maha; Shakeel, Laiba; Zuberi, Muhammad Abdul Wasay] Dow Univ Hlth Sci, Dept Internal Med, Karachi, Pakistan.
   [Akilimali, Aymar] Med Res Circle MedReC, Dept Res, Goma, DEM REP CONGO.
C3 Dow University of Health Sciences
RP Akilimali, A (corresponding author), Dept Res, Postal Code 73 Gisenyi, Goma, DEM REP CONGO.
EM hadiyadhanani@gmail.com; ayeshaa.skt@gmail.com; zainulhaq550@gmail.com;
   nawmkm@gmail.com; maha.zahid.098@gmail.com; laibashrr@gmail.com;
   abdulwasayasad@gmail.com; aymarakilimali@gmail.com
RI Khaliq, Nawal/JNE-1756-2023
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TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 2049-0801
J9 ANN MED SURG
JI Ann. Med. Surg.
PD FEB
PY 2025
VL 87
IS 2
BP 583
EP 597
DI 10.1097/MS9.0000000000002977
PG 15
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA X3M6U
UT WOS:001424436500032
PM 40110261
OA gold
DA 2025-06-01
ER

PT J
AU Tang, LP
   Lu, CJ
   Zheng, GJ
   Burgering, BMT
AF Tang, Lipeng
   Lu, Chuanjian
   Zheng, Guangjuan
   Burgering, Boudewijn M. T.
TI Emerging insights on the role of gasdermins in infection and
   inflammatory diseases
SO CLINICAL & TRANSLATIONAL IMMUNOLOGY
LA English
DT Review
DE Gasdermins; inflammatory bowel disease; multiple sclerosis; NETosis;
   pyroptosis; rheumatoid arthritis
ID GENOME-WIDE ASSOCIATION; NEUTROPHIL EXTRACELLULAR TRAPS; GASTRIC-CANCER;
   PYROPTOSIS; GSDMD; EXPRESSION; MUTATION; LOCI; PORE; GENE
AB The gasdermins, family of pore-forming proteins, are emerging key regulators of infection, autoinflammation and antitumor immunity. Multiple studies have recently characterised their crucial roles in driving pyroptosis, a lytic pro-inflammatory type of cell death. Additionally, gasdermins also act as key effectors of NETosis, secondary necrosis and apoptosis. In this review, we will address current understanding of the mechanisms of gasdermin activation and further describe the protective and detrimental roles of gasdermins in host defence and autoinflammatory diseases. These data suggest that gasdermins play a prominent role in innate immunity and autoinflammatory disorders, thereby providing potential new therapeutic avenues for the treatment of infection and autoimmune disease.
C1 [Tang, Lipeng; Zheng, Guangjuan] Guangzhou Univ Chinese Med, Dept Pharmacol Tradit Chinese Med, Affiliated Hosp 2, Guangzhou, Peoples R China.
   [Tang, Lipeng; Burgering, Boudewijn M. T.] Univ Med Ctr Utrecht, Ctr Mol Med, Dept Mol Canc Res, Univ Weg 100, NL-3584 CG Utrecht, Netherlands.
   [Lu, Chuanjian] Guangzhou Univ Chinese Med, Dept Dermatol, Affiliated Hosp 2, 111 Dade Rd, Guangzhou 510120, Peoples R China.
   [Zheng, Guangjuan] Guangzhou Univ Chinese Med, Dept Pathol, Affiliated Hosp 2, Guangzhou, Peoples R China.
C3 Guangzhou University of Chinese Medicine; Utrecht University; Utrecht
   University Medical Center; Guangzhou University of Chinese Medicine;
   Guangzhou University of Chinese Medicine
RP Burgering, BMT (corresponding author), Univ Med Ctr Utrecht, Ctr Mol Med, Dept Mol Canc Res, Univ Weg 100, NL-3584 CG Utrecht, Netherlands.; Lu, CJ (corresponding author), Guangzhou Univ Chinese Med, Dept Dermatol, Affiliated Hosp 2, 111 Dade Rd, Guangzhou 510120, Peoples R China.; Zheng, GJ (corresponding author), Guangzhou Univ Chinese Med, Dept Pharmacol Tradit Chinese Med & Pathol, Affiliated Hosp 2, 111 Dade Rd, Guangzhou 510120, Peoples R China.
EM lcj@gzucm.edu.cn; zhengguangjuan@gzucm.edu.cn;
   b.m.t.burgering@umcutrecht.nl
RI Zheng, Guangjuan/ABB-6496-2020; Tang, Lipeng/ABB-6481-2020
FU Innovative and Enhancement Research Program of Guangdong Province
   [2019KTSCX025]; Specific Research Fund for TCM Science and Technology of
   Guangdong Provincial Hospital of Chinese Medicine [YN2018QJ03]; Natural
   Science Foundation of Guangdong Province [2017A030313639]; Medical
   Scientific Research Foundation of Guangdong Province [A2017277]
FX This study was supported by Innovative and Enhancement Research Program
   of Guangdong Province (No. 2019KTSCX025); the Specific Research Fund for
   TCM Science and Technology of Guangdong Provincial Hospital of Chinese
   Medicine (YN2018QJ03); the Natural Science Foundation of Guangdong
   Province (No. 2017A030313639); and Medical Scientific Research
   Foundation of Guangdong Province (No. A2017277). We thank Tao Shi and
   Tianshu Gui for assistances in paper submission and modification.
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NR 110
TC 28
Z9 33
U1 2
U2 25
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2050-0068
J9 CLIN TRANSL IMMUNOL
JI Clin. Transl. Immunol.
PY 2020
VL 9
IS 10
AR e1186
DI 10.1002/cti2.1186
PG 18
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA OU2QB
UT WOS:000591377000002
PM 33033617
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Iwamuro, M
   Tanaka, T
   Otsuka, M
AF Iwamuro, Masaya
   Tanaka, Takehiro
   Otsuka, Motoyuki
TI Update in Molecular Aspects and Diagnosis of Autoimmune Gastritis
SO CURRENT ISSUES IN MOLECULAR BIOLOGY
LA English
DT Review
DE autoimmune gastritis; esophagogastroduodenoscopy; genetic
   predisposition; lymphocyte; oxidative stress
ID ATROPHIC GASTRITIS; T-CELLS; HELICOBACTER-PYLORI; AUTOANTIBODIES;
   PEPSINOGEN; TARGET; TH1
AB Recent studies have advanced our understanding of the pathophysiology of autoimmune gastritis, particularly its molecular aspects. The most noteworthy recent advancement lies in the identification of several candidate genes implicated in the pathogenesis of pernicious anemia through genome-wide association studies. These genes include PTPN22, PNPT1, HLA-DQB1, and IL2RA. Recent studies have also directed attention towards other genes such as ATP4A, ATP4B, AIRE, SLC26A7, SLC26A9, and BACH2 polymorphism. In-depth investigations have been conducted on lymphocytes and cytokines, including T helper 17 cells, interleukin (IL)-17A, IL-17E, IL-17F, IL-21, IL-19, tumor necrosis factor-& alpha;, IL-15, transforming growth factor-& beta;1, IL-13, and diminished levels of IL-27. Animal studies have explored the involvement of roseolovirus and H. pylori in relation to the onset of the disease and the process of carcinogenesis, respectively. Recent studies have comprehensively examined the involvement of autoantibodies, serum pepsinogen, and esophagogastroduodenoscopy in the diagnosis of autoimmune gastritis. The current focus lies on individuals demonstrating atypical presentations of the disease, including those diagnosed in childhood, those yielding negative results for autoantibodies, and those lacking the typical endoscopic characteristics of mucosal atrophy. Here, we discuss the recent developments in this field, focusing on genetic predisposition, epigenetic modifications, lymphocytes, cytokines, oxidative stress, infectious agents, proteins, microRNAs, autoantibodies, serum pepsinogen, gastrin, esophagogastroduodenoscopy and microscopic findings, and the risk of gastric neoplasm.
C1 [Iwamuro, Masaya; Otsuka, Motoyuki] Okayama Univ, Dept Gastroenterol & Hepatol, Dent & Pharmaceut Sci, Grad Sch Med, Okayama 7008558, Japan.
   [Tanaka, Takehiro] Okayama Univ, Dept Pathol, Dent & Pharmaceut Sci, Grad Sch Med, Okayama 7008558, Japan.
C3 Okayama University; Okayama University
RP Iwamuro, M (corresponding author), Okayama Univ, Dept Gastroenterol & Hepatol, Dent & Pharmaceut Sci, Grad Sch Med, Okayama 7008558, Japan.
EM iwamuromasaya@yahoo.co.jp
RI Otsuka, Motoyuki/H-9067-2019; Iwamuro, Masaya/AFL-1666-2022
OI Iwamuro, Masaya/0000-0002-1757-5754
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NR 67
TC 7
Z9 8
U1 3
U2 15
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1467-3037
EI 1467-3045
J9 CURR ISSUES MOL BIOL
JI Curr. Issues Mol. Biol.
PD JUL
PY 2023
VL 45
IS 7
BP 5263
EP 5275
DI 10.3390/cimb45070334
PG 13
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA N2BO0
UT WOS:001035130200001
PM 37504250
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Cai, TT
   Zhang, J
   Wang, X
   Song, RH
   Qin, Q
   Muhali, FS
   Zhou, JZ
   Xu, J
   Zhang, JA
AF Cai, Tian-tian
   Zhang, Jian
   Wang, Xuan
   Song, Rong-hua
   Qin, Qiu
   Muhali, Fatuma-said
   Zhou, Jiao-zhen
   Xu, Jian
   Zhang, Jin-an
TI Gene-gene and gene-sex epistatic interactions of DNMT1,
   DNMT3A and DNMT3B in autoimmune thyroid disease
SO ENDOCRINE JOURNAL
LA English
DT Article
DE DNA methyltransferases (DNMTs); Autoimmune thyroid diseases; Graves'
   disease; Hashimoto's thyroiditis; Single nucleotide polymorphism (SNP)
ID GLOBAL DNA METHYLATION; SINGLE NUCLEOTIDE POLYMORPHISM;
   SYSTEMIC-LUPUS-ERYTHEMATOSUS; MULTIFACTOR DIMENSIONALITY REDUCTION;
   RHEUMATOID-ARTHRITIS; GASTRIC-CANCER; ENVIRONMENT INTERACTIONS;
   SUSCEPTIBILITY LOCI; RISK; ASSOCIATION
AB The aim of this study was to investigate the associations of DNA methyltransferases (DNMTs) polymorphisms with susceptibility to autoimmune thyroid diseases (AITDs) and to test gene gene/gene-sex epistasis interactions. Eight single-nucleotide polymorphisms (SNPs) in DNMTI, DNMT3A and DNMT3B were selected and genotyped by multiplex polymerase chain reaction combined with ligase detection reaction method (PCR-LDR). A total of 685 Graves' disease (GD) patients, 353 Hashimoto's thyroiditis (HT) patients and 909 healthy controls were included in the final analysis. Epistasis was tested by additive model, multiplicative model and general multifactor dimensionality reduction (general MDR). Rs2424913 (DNMT3B) and rs2228611 (DNMT1) were associated with susceptibility to AITD and GD in the dominant and overdominant model, respectively (rs2424913: P=0.009 for AITD, P=0.0041 for GD; rs2228611: P=0.035 for AITD, P=0.043 for GD). Multiplicative and multiple high dimensional gene-gene or gene-sex interactions were also observed in this study. We have found evidence for a potential role of rs2424913 (DNMT3B) and rs2228611 (DNMT1) in AITD susceptibility and identified novel gene gene/gene-sex interactions in AITD. Our study may highlight sex and genes of DNMTs family as contributors to the pathogenesis of AITD.
C1 [Cai, Tian-tian; Wang, Xuan; Song, Rong-hua; Qin, Qiu; Muhali, Fatuma-said; Zhou, Jiao-zhen; Xu, Jian; Zhang, Jin-an] Fudan Univ, Dept Endocrinol, Jinshan Hosp, 1508 Longhang Rd, Shanghai 201508, Peoples R China.
   [Zhang, Jian] Fudan Univ, Jinshan Hosp, Clin Lab, Shanghai 201508, Peoples R China.
C3 Fudan University; Fudan University
RP Zhang, JA (corresponding author), Fudan Univ, Dept Endocrinol, Jinshan Hosp, 1508 Longhang Rd, Shanghai 201508, Peoples R China.
EM zhangjinan@hotmail.com
RI Song, Ronghua/D-4539-2012
OI Song, Ronghua/0000-0002-6779-4576; Song, Ronghua/0000-0003-1466-5428;
   Zhang, Jin-an/0000-0002-1700-4695
FU National Natural Science Foundation of China [81471004]; Key Disciplines
   Development of Shanghai Jinshan District [2012-23]
FX This work was supportm the National Natural Science Foundation of China
   (81471004) and the Key Disciplines Development of Shanghai Jinshan
   District (No. 2012-23). The authors would like to thank all of the
   participants who took part in the studies.
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NR 41
TC 18
Z9 19
U1 0
U2 6
PU JAPAN ENDOCRINE SOC
PI KYOTO
PA 75  YANAGINOBANBA NISHIIRU-MASUYA-CHO, SANJOU-DORI, NAKAGYOU-KU, KYOTO,
   604-8111, JAPAN
SN 0918-8959
EI 1348-4540
J9 ENDOCR J
JI Endocr. J.
PD JUL 20
PY 2016
VL 63
IS 7
BP 643
EP 653
PG 11
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA DV3CC
UT WOS:000382797600007
PM 27237591
DA 2025-06-01
ER

PT J
AU MELICHAR, B
   MALIROVA, E
   BURES, J
   KOMARKOVA, O
   KOLESAR, J
   REJCHRT, S
   FIXA, B
AF MELICHAR, B
   MALIROVA, E
   BURES, J
   KOMARKOVA, O
   KOLESAR, J
   REJCHRT, S
   FIXA, B
TI GASTRIC-JUICE NEOPTERIN IN HELICOBACTER-PYLORI INFECTION
SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
LA English
DT Article; Proceedings Paper
CT Pathogenesis and Host Response in Helicobacter pylori Infection Meeting
CY JUN 21-24, 1994
CL HELSINGOR, DENMARK
SP European Study Grp Immunol Helicobacter Infect
DE GASTRIC JUICE; HELICOBACTER PYLORI; NEOPTERIN
ID ALLOGRAFT RECIPIENTS; IMMUNE-RESPONSE; EXCRETION; DISEASES; MARKER;
   SALIVA
AB Neopterin, a pteridine compound produced by macrophages activated by interferon-gamma, is widely used to assess the activation of cellular immunity. An elevation in serum or urinary neopterin reflects immune activation in many different disorders, including viral infections, cancer, autoimmune diseases or acute myocardial infarction, but less attention has been paid to neopterin concentration in other biological fluids. The aim of the present study was to examine neopterin concentration in gastric juice. An association with the presence of Helicobacter pylori, a bacterium linked to the most common disorders of upper digestive tract, was also investigated. Gastric juice was obtained at endoscopy from 61 patients. Neopterin was determined by a radioimmunoassay and the presence of H. pylori was examined by urease test. The macroscopic finding of bile in gastric juice was associated with significantly higher neopterin levels compared to patients where no bile was noted (15.5 +/- 15.6 vs. 2.1 +/- 3.0 nmol/l, P < 0.001). However, similar concentrations were observed in the H. pylori positive and H. pylori negative patients (7.6 +/- 12.0 vs. 11.1 +/- 14.9 nmol/l). Even in the absence of macroscopic bile contamination, no significant difference could be found between the infected and uninfected patients (2.3 +/- 3.2 vs. 1.3 +/- 1.9 nmol/l), and the patients with duodenal ulcer and normal findings (3.8 +/- 4.6 vs 1.6 +/- 1.9 nmol/l). The contamination of gastric juice with bile represents the limitation for the use of neopterin as a marker of immune activation in the gastric mucosa. Rather than an index of immune activation, gastric juice neopterin concentration represents a marker of duodenogastric reflux.
C1 CHARLES UNIV, SCH MED, DEPT NUCL MED, HRADEC KRALOVE, CZECH REPUBLIC.
C3 Charles University Prague
RP CHARLES UNIV, SCH MED, DEPT INTERNAL MED 2, POSPISILOVA 365, CR-50036 HRADEC KRALOVE, CZECH REPUBLIC.
RI Rejchrt, Stanislav/W-3456-2017; Bures, Jan/E-5116-2017
OI Rejchrt, Stanislav/0000-0001-5166-9503; Bures, Jan/0000-0003-0326-117X
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NR 22
TC 2
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0928-8244
EI 1574-695X
J9 FEMS IMMUNOL MED MIC
JI FEMS Immunol. Med. Microbiol.
PD FEB
PY 1995
VL 10
IS 3-4
BP 335
EP 338
DI 10.1016/0928-8244(94)00100-8
PG 4
WC Immunology; Infectious Diseases; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED); Conference Proceedings Citation Index - Science (CPCI-S)
SC Immunology; Infectious Diseases; Microbiology
GA QK370
UT WOS:A1995QK37000022
PM 7773251
OA Bronze
DA 2025-06-01
ER

PT J
AU Oertli, M
   Sundquist, M
   Hitzler, I
   Engler, DB
   Arnold, IC
   Reuter, S
   Maxeiner, J
   Hansson, M
   Taube, C
   Quiding-Järbrink, M
   Müller, A
AF Oertli, Mathias
   Sundquist, Malin
   Hitzler, Iris
   Engler, Daniela B.
   Arnold, Isabelle C.
   Reuter, Sebastian
   Maxeiner, Joachim
   Hansson, Malin
   Taube, Christian
   Quiding-Jaerbrink, Marianne
   Mueller, Anne
TI DC-derived IL-18 drives Treg differentiation, murine Helicobacter
   pylori-specific immune tolerance, and asthma protection
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID REGULATORY T-CELLS; DENDRITIC CELLS; GASTRIC-CANCER; PEYERS-PATCHES;
   INFECTION; DISEASE; SIGN; LIPOPOLYSACCHARIDES; COLONIZATION; POPULATION
AB Persistent colonization with the gastric bacterial pathogen Helicobacter pylori causes gastritis and predisposes infected individuals to gastric cancer. Conversely, it is also linked to protection from allergic, chronic inflammatory, and autoimmune diseases. We demonstrate here that H. pylori inhibits LPS-induced maturation of DCs and reprograms DCs toward a tolerance-promoting phenotype. Our results showed that DCs exposed to H. pylori in vitro or in vivo failed to induce T cell effector functions. Instead, they efficiently induced expression of the forkhead transcription factor FoxP3, the master regulator of Tregs, in naive T cells. Depletion of DCs in mice infected with H. pylori during the neonatal period was sufficient to break H. pylori-specific tolerance. DC depletion resulted in improved control of the infection but also aggravated T cell-driven immunopathology. Consistent with the mouse data, DCs infiltrating the gastric mucosa of human H. pylori carriers exhibited a semimature DC-SIGN(+)HLA(-)DR(hi)CD80(lo)CD86(lo) phenotype. Mechanistically, the tolerogenic activity of H. pylori-experienced DCs was shown to require IL-18 in vitro and in vivo; DC-derived IL-18 acted directly on T cells to drive their conversion to Tregs. CD4(+)CD25(+) Tregs from infected wild-type mice but not Il18(-/-) or Il18r1(-/-) mice prevented airway inflammation and hyperresponsiveness in an experimental model of asthma. Taken together, our results indicate that tolerogenic reprogramming of DCs ensures the persistence of H. pylori and protects against allergic asthma in a process that requires IL-18.
C1 [Oertli, Mathias; Hitzler, Iris; Engler, Daniela B.; Arnold, Isabelle C.; Mueller, Anne] Univ Zurich, Inst Mol Canc Res, CH-8057 Zurich, Switzerland.
   [Sundquist, Malin; Hansson, Malin; Quiding-Jaerbrink, Marianne] Univ Gothenburg, Sahlgrenska Acad, Dept Microbiol & Immunol, Gothenburg, Sweden.
   [Reuter, Sebastian; Maxeiner, Joachim; Taube, Christian] Johannes Gutenberg Univ Mainz, Med Clin 3, Mainz, Germany.
   [Taube, Christian] Leiden Univ, Med Ctr, Dept Pulm Med, Leiden, Netherlands.
C3 University of Zurich; University of Gothenburg; Johannes Gutenberg
   University of Mainz; Leiden University - Excl LUMC; Leiden University;
   Leiden University Medical Center (LUMC)
RP Müller, A (corresponding author), Univ Zurich, Inst Mol Canc Res, Winterthurerstr 190, CH-8057 Zurich, Switzerland.
EM mueller@imcr.uzh.ch
RI Arnold, Isabelle/JMB-4984-2023; Quiding-Järbrink,
   Marianne/AAU-5746-2021; Reuter, Sebastian/L-1804-2013
OI Arnold, Isabelle C./0000-0001-8679-9666; Muller,
   Anne/0000-0002-1368-8276; Reuter, Sebastian/0000-0002-1784-0124
FU Swiss National Science Foundation; Zurich University; Deutsche
   Forschungsgemeinschaft; Research Center for Immunology of the University
   of Mainz; Swedish Science Council; Foundation for Strategic Research
   through the MIVAC centre of excellence
FX We thank all volunteers and patients for their participation in the
   study. This study was supported by the Swiss National Science Foundation
   and the Zurich University Research Priority Program in Systems Biology
   (to A. Muller), the Deutsche Forschungsgemeinschaft and Research Center
   for Immunology of the University of Mainz (to C. Taube), and the Swedish
   Science Council and Foundation for Strategic Research through the MIVAC
   centre of excellence (to M. Quiding-Jarbrink). We are grateful to
   Burkhard Becher, Wolf-Dietrich Hardt, and Tim Sparwasser for providing
   mouse strains.
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NR 44
TC 250
Z9 272
U1 0
U2 18
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
J9 J CLIN INVEST
JI J. Clin. Invest.
PD MAR
PY 2012
VL 122
IS 3
BP 1082
EP 1096
DI 10.1172/JCI61029
PG 15
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 902EN
UT WOS:000301021500031
PM 22307326
OA Green Published, Bronze
DA 2025-06-01
ER

PT J
AU Milota, T
   Smetanova, J
   Klojdova, I
AF Milota, Tomas
   Smetanova, Jitka
   Klojdova, Iveta
TI Gastrointestinal Involvement in Primary Antibody Deficiencies
SO GASTROINTESTINAL DISORDERS
LA English
DT Review
DE selective immunoglobulin A deficiency; common variable immunodeficiency;
   X-linked agammaglobulinemia; gastrointestinal tract; microbiome; celiac
   disease; inflammatory bowel disease; gastric cancer; lymphoma
ID COMMON VARIABLE IMMUNODEFICIENCY; SELECTIVE IGA DEFICIENCY; X-LINKED
   AGAMMAGLOBULINEMIA; IMMUNOGLOBULIN-A DEFICIENCY; CHRONIC NOROVIRUS
   INFECTION; INFLAMMATORY-BOWEL-DISEASE; CELL-ACTIVATING FACTOR;
   REGULATORY T-CELLS; B-CELLS; CROHNS-DISEASE
AB Primary antibody deficiencies (PADs) are the most frequent group of inborn errors of immunity. Impaired B-cell development, reduced production of immunoglobulins (mainly IgG and IgA), and specific antibodies resulting in recurrent infections are their hallmarks. Infections typically affect the respiratory tract; however, gastrointestinal involvement is also common. These include infection with Helicobacter pylori, Salmonella, Campylobacter species, Giardia, and noroviruses. Impaired IgA production also contributes to dysbiosis and thereby an increase in abundance of species with proinflammatory properties, resulting in immune system dysregulation. Dysregulation of the immune system results in a broad spectrum of non-infectious manifestations, including autoimmune, lymphoproliferative, and granulomatous complications. Additionally, it increases the risk of malignancy, which may be present in more than half of patients with PADs. Higher prevalence is often seen in monogenic causes, and gastrointestinal involvement may clinically mimic various conditions including inflammatory bowel diseases and celiac disease but possess different immunological features and response to standard treatment, which make diagnosis and therapy challenging. The spectrum of malignancies includes gastric cancer and lymphoma. Thus, non-infectious manifestations significantly affect mortality and morbidity. In this overview, we provide a comprehensive insight into the epidemiology, genetic background, pathophysiology, and clinical manifestations of infectious and non-infectious complications.
C1 [Milota, Tomas; Smetanova, Jitka] Charles Univ Prague, Fac Med 2, Dept Immunol, Prague 15006, Czech Republic.
   [Milota, Tomas; Smetanova, Jitka] Motol Univ Hosp, Prague 15006, Czech Republic.
   [Klojdova, Iveta] Czech Univ Life Sci, Fac Agrobiol Food & Nat Resources, DRIFT FOOD, Prague 15006, Czech Republic.
C3 Motol University Hospital; Charles University Prague; Motol University
   Hospital; Czech University of Life Sciences Prague
RP Milota, T (corresponding author), Charles Univ Prague, Fac Med 2, Dept Immunol, Prague 15006, Czech Republic.; Milota, T (corresponding author), Motol Univ Hosp, Prague 15006, Czech Republic.
EM tomas.milota@fnmotol.cz
RI Milota, Tomas/N-5853-2017; Klojdová, Iveta/AFO-3135-2022
OI Milota, Tomas/0000-0003-2105-3462; , Iveta/0000-0002-6524-0916
FU Czech Health Research Council [NU22-05-00402]; European Union's Horizon
   2020 Research and Innovation Program [952594]
FX This work was supported by the grant of the Czech Health Research
   Council (project no. NU22-05-00402) and European Union's Horizon 2020
   Research and Innovation Program (grant agreement no. 952594, ERA Chair
   project DRIFT-FOOD).
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NR 133
TC 0
Z9 0
U1 2
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2624-5647
J9 GASTROINTEST DISORD
JI Gastrointest. Disord.
PD MAR
PY 2023
VL 5
IS 1
BP 52
EP 67
DI 10.3390/gidisord5010006
PG 16
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA C0IF0
UT WOS:000958853000001
OA gold
DA 2025-06-01
ER

PT J
AU Ochoa, ER
   Harris, NL
   Pilch, BZ
AF Ochoa, ER
   Harris, NL
   Pilch, BZ
TI Marginal zone B-cell lymphoma of the salivary gland arising in chronic
   sclerosing sialadenitis (Kuttner tumor)
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE extranodal marginal zone B-cell lymphoma; MALT lymphoma; chronic
   sclerosing sialadenitis; Kuttner tumor; lymphoepithelial sialadenitis;
   salivary gland
ID MYOEPITHELIAL SIALADENITIS; HELICOBACTER-PYLORI; MALIGNANT-LYMPHOMA;
   GASTRIC LYMPHOMA; TISSUE
AB We report a case of extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) type of the salivary gland arising in a background of chronic sclerosing sialadenitis. Chronic sclerosing sialadenitis is a common fibrosing chronic inflammatory lesion of the submandibular gland, which is thought to be the result of sialolithiasis, and is not associated with a systemic autoimmune disease. Salivary MALT lymphomas are typically associated with lymphoepithelial sialadenitis (LESA) in a patient with or without Sjogren's syndrome. Our case of salivary MALT lymphoma was neither preceded by Sjogren's syndrome nor accompanied by LESA. This case suggests that chronic inflammatory processes other than Sjogren's syndrome may provide a substrate for the development of MALT lymphoma.
C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
C3 Harvard University; Harvard Medical School; Harvard University Medical
   Affiliates; Massachusetts General Hospital
RP Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Pathol, Warren 2,14 Fruit St, Boston, MA 02114 USA.
EM pilch.ben@mgh.harvard.edu
CR Digiuseppe Joseph A., 1996, Current Opinion in Oncology, V8, P232
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NR 15
TC 50
Z9 54
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD DEC
PY 2001
VL 25
IS 12
BP 1546
EP 1550
DI 10.1097/00000478-200112000-00012
PG 5
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA 496ZU
UT WOS:000172428900012
PM 11717546
DA 2025-06-01
ER

PT J
AU Nagahara, A
   Shiotani, A
   Iijima, K
   Kamada, T
   Fujiwara, Y
   Kasugai, K
   Kato, M
   Higuchi, K
AF Nagahara, Akihito
   Shiotani, Akiko
   Iijima, Katsunori
   Kamada, Tomoari
   Fujiwara, Yasuhiro
   Kasugai, Kunio
   Kato, Mototsugu
   Higuchi, Kazuhide
TI The role of advanced endoscopy in the management of inflammatory
   digestive diseases (upper gastrointestinal tract)
SO DIGESTIVE ENDOSCOPY
LA English
DT Review
DE autoimmune gastritis; eosinophilic gastritis; gastroesophageal reflux
   disease; Helicobacter pylori; Kyoto Classification of Gastritis
AB The Japan Gastroenterological Endoscopy Society held four serial symposia between 2019 and 2020 on the state-of-the-art of issues related to upper GI inflammatory diseases. This review discusses some of the topics addressed in these symposia. The papers regarding nonerosive reflux disease, recent improvements in intraesophageal pH-impedance monitoring and endoscopic diagnosis using image-enhanced endoscopy have been published. Many publications have addressed its usefulness in endoscopic treatment of gastroesophageal reflux disease such as anti-reflux mucosectomy. In the management of eosinophilic esophagitis, since the symptoms are subjective, objective indicators have been sought, and ultrasonography and high-resolution manometry may be useful tools for evaluation. The natural course of this condition, especially of asymptomatic cases, is not well clarified. Some newly developed anti-acid or anti-inflammatory medicines are now under investigation. With regard to autoimmune gastritis, because of widespread medical examinations, diagnosis of asymptomatic cases has been increasing. Recently, its endoscopic characteristics have become clear and the natural history of these conditions is being elucidated. The Kyoto Classification of Gastritis has been reported to be useful not only for Helicobacter pylori diagnosis but also for identification of risks of gastric cancer. Its usefulness is now recognized in Asia and Europe.
C1 [Nagahara, Akihito] Juntendo Univ, Sch Med, Dept Gastroenterol, Tokyo, Japan.
   [Shiotani, Akiko] Kawasaki Med Sch, Dept Internal Med, Div Gastroenterol, Okayama, Japan.
   [Kamada, Tomoari] Kawasaki Med Sch, Dept Hlth Care Med, Okayama, Japan.
   [Iijima, Katsunori] Akita Univ, Sch Med, Dept Gastroenterol, Akita, Japan.
   [Fujiwara, Yasuhiro] Osaka City Univ, Dept Gastroenterol, Grad Sch Med, Osaka, Japan.
   [Higuchi, Kazuhide] Osaka Med Coll, Dept Internal Med 2, Osaka, Japan.
   [Kasugai, Kunio] Aichi Med Univ, Dept Gastroenterol, Nagakute, Aichi, Japan.
   [Kato, Mototsugu] Natl Hosp Org Hakodate Natl Hosp, Dept Gastroenterol, Hakodate, Hokkaido, Japan.
C3 Juntendo University; Kawasaki Medical School; Kawasaki Medical School;
   Akita University; Osaka Metropolitan University; Osaka Medical &
   Pharmaceutical University; Aichi Medical University
RP Nagahara, A (corresponding author), Juntendo Univ, Sch Med, Dept Gastroenterol, Bunkyo Ku, 2-1-1 Hongo, Tokyo 1138421, Japan.
EM nagahara@juntendo.ac.jp
RI Nagahara, Akihito/L-4010-2016; Fujiwara, Yasuhiro/AAM-5504-2020
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NR 88
TC 4
Z9 5
U1 1
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0915-5635
EI 1443-1661
J9 DIGEST ENDOSC
JI Dig. Endosc.
PD JAN
PY 2022
VL 34
IS 1
BP 63
EP 72
DI 10.1111/den.13982
EA APR 2021
PG 10
WC Gastroenterology & Hepatology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Surgery
GA YE4NK
UT WOS:000642137500001
PM 33772880
OA Bronze
DA 2025-06-01
ER

PT J
AU Ibrahim, DB
   Ibrahim, SK
   Jasim, SA
AF Ibrahim, Dania Bahaulddin
   Ibrahim, Suhaib Khalid
   Jasim, Sarah Anwer
TI DETERMINATION THE ASSOCIATION BETWEEN KERATOCONJUNCTIVITIS SICCA AND
   HELICOBACTER PYLORI INFECTIONS IN MIDDLE AGED ADULTS: CROSS SECTIONAL
   STUDY
SO GOMAL JOURNAL OF MEDICAL SCIENCES
LA English
DT Article
DE Conjunctivitis; Dry eye disease; Gastritis; Helicobacter pylori
ID DIAGNOSIS
AB Background: H. pylori can lead to chronic gastritis, peptic ulcers, and gastric adenocarcinoma along with several extra gastric manifestations, such as glaucoma, other dry eye illnesses, and several autoimmune diseases. The purpose of this was to determine the association of patients' clinical aspects with dry eye disease along with Helicobacter pylori (H. pylori) using serology IgG antibody & urea breath test, which is a non-invasive to find out the relationship of Keratoconjunctivitis sicca and H. pylori chronic gastritis. Materials & Methods: This cross-sectional, observational study was conducted at Baghdad Teaching Hospital and other medical city hospitals in Baghdad, Iraq, from October to December 2022. One hundred eyes from 50 patients were examined using physical assessments and modern techniques to detect various dry eye diseases based on the severity of sicca stages (0-3). Blood samples were collected from all patients to determine serological IgG antibody levels for chronic gastritis diagnosis, along with more specific urea breath tests for H. pylori detection. Results: patients diagnosed with H. pylori-induced chronic gastritis were positive for serology IgG antibody & urea breath test IN 30 (60%) cases and negative for both tests in 20 (40%) cases from a total of 50 patients. Patients were aged between (40-60) years old with mean age 50, most patients 20(40%) belong to sicca stage 3 suffered from severe dry eye diseases along with most prevalent investigated 14(28%) positive chronic gastritis caused by H. pylori. Conclusions: There is a strong relationship between the frequency of dry eye diseases in patients suffering from chronic gastritis caused by the H. pylori bacterium.
C1 [Ibrahim, Dania Bahaulddin] Ibn Sina Univ Med & Pharmaceut Sci, Dent Coll, Minist Higher Educ & Sci Res, Baghdad, Iraq.
   [Ibrahim, Suhaib Khalid] Middle Tech Univ, Coll Hlth & Med Tech, Minist Higher Educ & Sci Res, Baghdad, Iraq.
   [Jasim, Sarah Anwer] Al Suwaira Gen Hosp, Minist Hlth, Baghdad, Iraq.
C3 Ibn Sina University for Medical & Pharmaceutical Sciences; Middle
   Technical University; Ministry of Health Iraq
RP Ibrahim, DB (corresponding author), Ibn Sina Univ Med & Pharmaceut Sci, Dent Coll, Minist Higher Educ & Sci Res, Baghdad, Iraq.
EM danoo.baha@ibnsina.edu.iq
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NR 18
TC 0
Z9 0
U1 0
U2 0
PU GOMAL MEDICAL COLL
PI DERA ISMAIL KHAN
PA NORTH CIRCULAR RD, DERA ISMAIL KHAN, 00000, PAKISTAN
SN 1819-7973
EI 1997-2067
J9 GOMAL J MED SCI
JI Gomal J. Med. Sci.
PD JAN-MAR
PY 2025
VL 23
IS 1
BP 146
EP 150
DI 10.46903/gjms/23.1.Special.1846
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA 2VK1J
UT WOS:001492234000012
DA 2025-06-01
ER

PT J
AU Lee, HE
   Mounajjed, T
   Erickson, LA
   Wu, TT
AF Lee, Hee Eun
   Mounajjed, Taofic
   Erickson, Lori A.
   Wu, Tsung-Teh
TI Sporadic Gastric Well-Differentiated Neuroendocrine Tumors Have a Higher
   Ki-67 Proliferative Index
SO ENDOCRINE PATHOLOGY
LA English
DT Article
DE Gastric neoplasm; Well-differentiated neuroendocrine tumor; Ki-67
   proliferative index; Survival analysis
ID MULTIPLE ENDOCRINE NEOPLASIA; CARCINOID-TUMORS; PROGNOSTIC EVALUATION;
   CELL TUMOR; HIGH-GRADE; STOMACH; SYSTEM; HYPERGASTRINEMIA;
   CLASSIFICATION; PATHOGENESIS
AB Well-differentiated neuroendocrine tumor (WDNET) of the stomach can arise in three distinct clinical settings: (1) in association with autoimmune atrophic gastritis, (2) in association with multiple neuroendocrine neoplasia type I (MEN I) or Zollinger-Ellison syndrome (ZES), or (3) sporadic. The Ki-67 proliferative index (PI) in gastric WDNETs in these three distinct clinical settings has not been evaluated in detail. Forty-five gastric WNETs underwent polypectomy (n = 4), endoscopic mucosal resection (n = 12), and surgical resection (n = 29) between 1994 and 2015 were included. H&E slides from each case were reviewed, and Ki-67 immunostain was performed on one representative tumor block. Ki-67 PI was determined by quantitative Aperio image analysis software in areas of strongest nuclear labeling ("hot spots"), and correlated with underlying clinical and pathological features. Twenty-one patients were male and 24 female with a median age of 57 years (range, 30-80 years). Tumors were classified as type I (n = 17), type II (n = 6), and type III (n = 22) WDNETs. Types II and III showed more advanced TNM stage compared to type I (p = 0.02, overall). WHO grade based on Ki-67 PI was higher in type III WDNETs [grade 1 (G1), n = 3; grade 2 (G2), n = 15; and grade 3 (G3), n = 4] than in type I WDNETs [G1, n = 5; G2, n = 12] and in type II WDNETs [G1, n = 2; G2, n = 4] (p = 0.050, overall). Ki-67 PI was significantly higher in type III WDNETs (mean +/- SD = 13.0 +/- 13.3 %) than in non-sporadic (type I and II) WDNETs (mean +/- SD = 5.3 +/- 3.3 %; p = 0.015). There was no difference in Ki-67 PI between type I WDNETs (mean +/- SD = 5.2 +/- 3.5 %) and type II WDNETs (mean +/- SD = 5.6 +/- 3.1%; p = 0.817). Higher Ki-67 PI was associated with higher tumor T stage (p = 0.003) and also tended to be associated with lymph node metastasis (p = 0.071). In the Kaplan-Meier survival analysis, type I was associated with a significantly longer disease-free survival (DFS) time compared to type II (p = 0.018) or III (0.010). Also, the WHO G3 group had a significantly shorter DFS time than the WHO G1 (p = 0.020) or G2 (p = 0.007) group. Gastric WDNET is a heterogeneous disease entity encompassing three clinical subtypes-type I, type II, and type III-having their own distinct clinicopathologic characteristics and prognosis. Our results showed that sporadic (type III) WDNET had a significantly higher Ki-67 PI than non-sporadic cases (type I or II); increased PI was associated with higher tumor stage. We also described four type III cases of morphologically WD gastric NET with WHO grade 3 on the basis of Ki-67 PI.
C1 [Lee, Hee Eun; Mounajjed, Taofic; Erickson, Lori A.; Wu, Tsung-Teh] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
C3 Mayo Clinic
RP Wu, TT (corresponding author), Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
EM Wu.TsungTeh@mayo.edu
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NR 31
TC 15
Z9 17
U1 0
U2 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1046-3976
EI 1559-0097
J9 ENDOCR PATHOL
JI Endocr. Pathol.
PD SEP
PY 2016
VL 27
IS 3
BP 259
EP 267
DI 10.1007/s12022-016-9443-6
PG 9
WC Endocrinology & Metabolism; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Pathology
GA DT6LD
UT WOS:000381594800011
PM 27306997
DA 2025-06-01
ER

PT J
AU Huitron, LHM
   Cruz-Holguin, VJ
   Ulloa-Aguilar, JM
   De Jesús-González, LA
   Osuna-Ramos, JF
   Guzmán-Huerta, M
   de León-Bautista, MP
   León-Reyes, G
   García-Cordero, J
   Cedillo-Barrón, L
   Cerna-Cortes, JF
   León-Juárez, M
AF Herrera-Moro Huitron, Luis
   Cruz-Holguin, Victor Javier
   Ulloa-Aguilar, Jose Manuel
   De Jesus-Gonzalez, Luis Adrian
   Osuna-Ramos, Juan Fidel
   Guzman-Huerta, Mario
   de Leon-Bautista, Mercedes Piedad
   Leon-Reyes, Guadalupe
   Garcia-Cordero, Julio
   Cedillo-Barron, Leticia
   Cerna-Cortes, Jorge Francisco
   Leon-Juarez, Moises
TI Beyond Infection: The Role of Secreted Viral Proteins in Pathogenesis,
   Disease Severity and Diagnostic Applications
SO CELLS
LA English
DT Review
DE secretion of viral proteins; pathogenesis; diagnostic; biomarkers of
   severity and immune system evasion
ID RSV G-PROTEIN; NASOPHARYNGEAL CARCINOMA; GASTRIC-CANCER; G GLYCOPROTEIN;
   HIV-1 TAT; IN-VITRO; VIRUS; NS1; PEPTIDE; BARF1
AB Secreted viral proteins are crucial in virus-host interactions, as they modify the host microenvironment to promote infection. These secreted proteins could alter immune and inflammatory responses, allowing viruses to evade defense mechanisms such as cytotoxic T cell activation and antibody neutralization. Some secreted proteins mimic host molecules to suppress antiviral responses, making them valuable targets for antivirals and diagnostics. Notable examples include BARF1 from Epstein-Barr virus, associated with gastric cancer; vIL-10 from Epstein-Barr virus, which regulates immune responses and contributes to autoimmune diseases; NS1 from dengue virus, associated with vascular permeability and early diagnosis; and NSP4 from rotavirus as an enterotoxin, among others. The study of these proteins improves our understanding of viral pathogenesis and helps to develop innovative treatments for infectious and non-infectious diseases, taking advantage of the evolutionary adaptations of viruses. This review explores their impact on the infection cycle, disease progression, and key processes, such as cell cycle regulation, apoptosis, and cell signaling. Research on these proteins deepens our basic knowledge of virology and generates alternative methods for detecting biomarkers and creating more effective therapies, as well as implementing some emerging technologies, such as biosensors and plasmon resonance, for the diagnosis of viral diseases.
C1 [Herrera-Moro Huitron, Luis; Cruz-Holguin, Victor Javier; Ulloa-Aguilar, Jose Manuel; Leon-Juarez, Moises] Inst Nacl Perinatol, Lab Virol Perinatal & Diseno Mol Antigenos & Bioma, Dept Inmunobioquim, Mexico City 11000, Mexico.
   [Herrera-Moro Huitron, Luis; Cerna-Cortes, Jorge Francisco] Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Dept Microbiol, Lab Microbiol Mol, Mexico City 11340, Mexico.
   [De Jesus-Gonzalez, Luis Adrian] Inst Mexicano Seguro Social, Unidad Invest Biomed Zacatecas, Zacatecas 98000, Mexico.
   [Osuna-Ramos, Juan Fidel] Univ Autonoma Sinaloa, Fac Med, Culiacan 80019, Mexico.
   [Guzman-Huerta, Mario] Inst Nacl Perinatol, Dept Med Traslac, Mexico City 11000, Mexico.
   [de Leon-Bautista, Mercedes Piedad] Univ Vasco Quiroga, Escuela Med, Morelia 58090, Mexico.
   [de Leon-Bautista, Mercedes Piedad] INEX LAB, Lab Enfermedades Infecciosas & Genom, Morelia 58280, Mexico.
   [Leon-Reyes, Guadalupe] Inst Nacl Med Genomica INMEGEN, Lab Nutrigenet & Nutrigen, Mexico City 14610, Mexico.
   [Garcia-Cordero, Julio; Cedillo-Barron, Leticia] Inst Politecn Nacl CINVESTAV IPN, Ctr Invest & Estudios Avanzados, Dept Biomed Mol, Mexico City 07360, Mexico.
C3 Universidad Nacional Autonoma de Mexico; Instituto Politecnico Nacional
   - Mexico; Instituto Mexicano del Seguro Social; Universidad Autonoma de
   Sinaloa; Universidad Nacional Autonoma de Mexico; CINVESTAV - Centro de
   Investigacion y de Estudios Avanzados del Instituto Politecnico Nacional
RP León-Juárez, M (corresponding author), Inst Nacl Perinatol, Lab Virol Perinatal & Diseno Mol Antigenos & Bioma, Dept Inmunobioquim, Mexico City 11000, Mexico.
EM luis_5m5@hotmail.com; vic_cruise@hotmail.com; josemanuel7111@gmail.com;
   luis.dejesus@cinvestav.mx; osunajuanfidel.fm@uas.edu.mx;
   mguzmanhuerta@yahoo.com.mx; dramercedespiedad@gmail.com;
   greyes@inmegen.gob.mx; jugarcia@cinvestav.mx; lcedillo@cinvestav.mx;
   jorgecerna1008@gmail.com; moisesleoninper@gmail.com
RI Osuna-Ramos, Juan/AAV-7653-2020; De Jesús González, Luis
   Adrián/ACY-1642-2022; Juarez, Moises/AAI-1958-2019
FU Instituto Nacional de Perinatologa Isidro Espinosa de los Reyes
   [2017-2-81]
FX This research was funded by a grant from Instituto Nacional de
   Perinatologia Isidro Espinosa de los Reyes 2017-2-81 to M.L.-J.
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NR 119
TC 0
Z9 0
U1 0
U2 0
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2073-4409
J9 CELLS-BASEL
JI Cells
PD APR 22
PY 2025
VL 14
IS 9
AR 624
DI 10.3390/cells14090624
PG 21
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 2MF3R
UT WOS:001485985800001
PM 40358148
DA 2025-06-01
ER

PT J
AU Sakabe, H
   Bamba, M
   Nomura, K
   Kitamura, S
   Segawa, H
   Yasui, H
   Inoue, T
   Taniwaki, M
   Fujiyama, Y
   Bamba, T
AF Sakabe, H
   Bamba, M
   Nomura, K
   Kitamura, S
   Segawa, H
   Yasui, H
   Inoue, T
   Taniwaki, M
   Fujiyama, Y
   Bamba, T
TI MALT lymphoma at the base of the tongue developing without any
   background of immunodeficiency or autoimmune disease
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE MALT lymphoma; tongue; Helicobacter pylori; t(11;18) (q21;21); trisomy 3
ID IN-SITU HYBRIDIZATION; NON-HODGKINS-LYMPHOMA; EPSTEIN-BARR-VIRUS; B-CELL
   LYMPHOMA; TISSUE TYPE; HELICOBACTER-PYLORI; GASTRIC LYMPHOMA;
   T(11/18)(Q21,Q21); REGRESSION; GENE
AB We report a very rare case of a mucosa-associated lymphoid tissue (MALT) lymphoma of the base of the tongue. A 61-year-old woman was admitted to our hospital for further examination of a 12 mm x 15 mm x 5 mm tongue tumor. Histological examination of the tumor revealed a marked lymphoepithelial lesion. Lymphoma cells expressed CD5(-), CD10(-), CD19(+), CD20(+) on the surface of the cells by fluorescence activated cell sorter, and the genotypic analysis of the tumor cells revealed the presence of immunoglobulin heavy chain rearrangement and the absence of BCL-2 gene rearrangement by southern blot hybridization. Furthermore, neither the t(11; 18) (q21; q21) translocation nor trisomy 3 was detected in lymphoma cells by fluorescence in situ hybridization method. The tongue tumor was completely resected and no recurrence has been noted in the 13 months to date.
C1 Kohka Publ Hosp, Dept Internal Med, Shiga 5280014, Japan.
   Shiga Univ Med Sci, Dept Pathol 1, Shiga, Japan.
   Kyoto Prefectural Univ Med, Dept Internal Med 3, Kyoto 602, Japan.
   Shiga Univ Med Sci, Dept Internal Med 2, Shiga, Japan.
C3 Shiga University of Medical Science; Kyoto Prefectural University of
   Medicine; Shiga University of Medical Science
RP Kohka Publ Hosp, Dept Internal Med, Rokusin 3-39, Shiga 5280014, Japan.
EM hidesa@waltz.plala.or.jp
RI Bamba, Takeshi/KOD-6144-2024
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NR 22
TC 13
Z9 13
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1042-8194
EI 1029-2403
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PY 2003
VL 44
IS 5
BP 875
EP 878
DI 10.1080/1042819031000063390
PG 4
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA 646VY
UT WOS:000181057300021
PM 12802929
DA 2025-06-01
ER

PT J
AU Yamamoto, A
   Ito, A
   Nakamura, S
   Higuchi, T
   Harigai, M
   Shinohara, A
   Yamamoto, T
   Nagashima, Y
   Tokushige, K
AF Yamamoto, Ayako
   Ito, Ayumi
   Nakamura, Shinichi
   Higuchi, Tomoaki
   Harigai, Masayoshi
   Shinohara, Akihito
   Yamamoto, Tomoko
   Nagashima, Yoji
   Tokushige, Katsutoshi
TI A case of gastric/duodenal diffuse large B cell lymphoma observed during
   the administration of tacrolimus/azathioprine for dermatomyositis
SO CLINICAL JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune disease; Tacrolimus; Azathioprine; Gastrointestinal
   lymphoproliferative disorder; DLBCL
ID EPSTEIN-BARR-VIRUS; RHEUMATOID-ARTHRITIS; LYMPHOPROLIFERATIVE DISORDERS;
   MALIGNANCY; PATIENT; DISEASE
AB The patient was diagnosed with amyopathic dermatomyositis complicated with interstitial pneumonia (IP) at age 35. She had been treated with prednisolone and maintained on tacrolimus (TAC) + azathioprine (AZA). Eight years later, she experienced epigastric pain, and esophagogastroduodenoscopy (EGD) led to a diagnosis of duodenal ulcer. The pain did not improve, so she visited our hospital, where she presented with malaise, anemia, and weight loss. An EGD revealed submucosal tumor-like protrusions in the anterior and posterior walls of the gastric antrum and punched-out ulcers with auricle-like marginal swelling on the inside of the protrusions. Irregular-shaped punched-out ulcers were also observed in the duodenal bulb. Lymphoma was suspected, and biopsy was performed. Histopathology showed diffuse large, atypical lymphocytes with enlarged nuclei, and immunohistochemical staining revealed CD20-positive cells. Diffuse large B cell lymphoma (DLBCL) was diagnosed, which was considered as lymphomas arising in immune deficiency/dysregulation. After discontinuing TAC + AZA for three months, the gastrointestinal symptoms improved, and on EGD, the duodenal lesions had disappeared, with only a shallow depression covered with regenerated epithelium remaining in the posterior wall of the gastric antrum. Seven months later, the patient underwent follow-up EGD, and the disappearance of lymphoma cells was confirmed histopathologically by biopsy. Repeated and detailed endoscopic examination should be considered in an immunosuppressed patient with treatment-resistant gastric or duodenal ulcers.
C1 [Yamamoto, Ayako; Ito, Ayumi; Nakamura, Shinichi; Tokushige, Katsutoshi] Tokyo Womens Med Univ, Dept Internal Med, Div Gastroenterol, 8-1 Kawada Cho,Shinjuku, Tokyo 1628666, Japan.
   [Higuchi, Tomoaki; Harigai, Masayoshi] Tokyo Womens Med Univ, Div Rheumatol, Dept Internal Med, Tokyo, Japan.
   [Shinohara, Akihito] Tokyo Womens Med Univ, Dept Internal Med, Div Hematol, Tokyo, Japan.
   [Yamamoto, Tomoko; Nagashima, Yoji] Tokyo Womens Med Univ, Dept Surg Pathol, Tokyo, Japan.
C3 Tokyo Women's Medical University; Tokyo Women's Medical University;
   Tokyo Women's Medical University; Tokyo Women's Medical University
RP Yamamoto, A; Ito, A (corresponding author), Tokyo Womens Med Univ, Dept Internal Med, Div Gastroenterol, 8-1 Kawada Cho,Shinjuku, Tokyo 1628666, Japan.
EM yamamoto.ayako@twmu.ac.jp; ito.ayumi@twmu.ac.jp
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NR 25
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 1865-7257
EI 1865-7265
J9 CLIN J GASTROENTEROL
JI Clin. J. Gastroenterol.
PD FEB
PY 2025
VL 18
IS 1
BP 67
EP 73
DI 10.1007/s12328-024-02077-9
EA DEC 2024
PG 7
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA U2X7D
UT WOS:001370710800001
PM 39638937
DA 2025-06-01
ER

PT J
AU Zhao, YS
   Zhao, JN
   Ma, HY
   Han, Y
   Xu, WC
   Wang, J
   Cai, YR
   Jia, XM
   Jia, QZ
   Yang, Q
AF Zhao, Yashuo
   Zhao, Jianing
   Ma, Hongyu
   Han, Yan
   Xu, Weichao
   Wang, Jie
   Cai, Yanru
   Jia, Xuemei
   Jia, Qingzhong
   Yang, Qian
TI High Hepcidin Levels Promote Abnormal Iron Metabolism and Ferroptosis in
   Chronic Atrophic Gastritis
SO BIOMEDICINES
LA English
DT Article
DE hepcidin; chronic atrophic gastritis; ferroptosis; iron; IL-6/STAT3
   signaling pathway
ID HELICOBACTER; DEFICIENCY; EXPRESSION; AUTOIMMUNE
AB Background: Chronic atrophic gastritis (CAG) is a chronic inflammatory disease and premalignant lesion of gastric cancer. As an antimicrobial peptide, hepcidin can maintain iron metabolic balance and is susceptible to inflammation. Objectives: The objective of this study was to clarify whether hepcidin is involved in abnormal iron metabolism and ferroptosis during CAG pathogenesis. Methods: Non-atrophic gastritis (NAG) and chronic atrophic gastritis (CAG) patient pathology slides were collected, and related protein expression was detected by immunohistochemical staining. The CAG rat model was established using MNNG combined with an irregular diet. Results: CAG patients and rats exhibited iron deposition in gastric tissue. CAG-induced ferroptosis in the stomach was characterized by decreased GPX4 and FTH levels and increased 4-HNE levels. Hepcidin, which is mainly located in parietal cells, was elevated in CAG gastric tissue. The high gastric level of hepcidin inhibited iron absorption in the duodenum by decreasing the protein expression of DMT1 and FPN1. In addition, the IL-6/STAT3 signaling pathway induced hepcidin production in gastric tissue. Conclusion: Our results showed that the high level of gastric hepcidin induced ferroptosis in the stomach but also inhibited iron absorption in the intestines. Inhibiting hepcidin might be a new strategy for the prevention of CAG in the future.
C1 [Zhao, Yashuo; Zhao, Jianing; Ma, Hongyu; Han, Yan; Xu, Weichao; Wang, Jie; Cai, Yanru; Jia, Xuemei; Yang, Qian] Hebei Univ Chinese Med, Affiliated Hosp 1, Shijiazhuang 050013, Peoples R China.
   [Zhao, Yashuo; Zhao, Jianing; Ma, Hongyu; Han, Yan; Xu, Weichao; Wang, Jie; Cai, Yanru; Jia, Xuemei; Yang, Qian] Hebei Prov Hosp Chinese Med, Dept Gastroenterol, Shijiazhuang 050013, Peoples R China.
   [Zhao, Yashuo] Hebei Univ Chinese Med, Hebei Technol Innovat Ctr TCM Combined Hydrogen Me, Shijiazhuang 050200, Peoples R China.
   [Jia, Qingzhong] Hebei Med Univ, Sch Pharm, Shijiazhuang 050017, Peoples R China.
C3 Hebei University of Chinese Medicine; Hebei University of Chinese
   Medicine; Hebei University of Chinese Medicine; Hebei Medical University
RP Yang, Q (corresponding author), Hebei Univ Chinese Med, Affiliated Hosp 1, Shijiazhuang 050013, Peoples R China.; Yang, Q (corresponding author), Hebei Prov Hosp Chinese Med, Dept Gastroenterol, Shijiazhuang 050013, Peoples R China.; Jia, QZ (corresponding author), Hebei Med Univ, Sch Pharm, Shijiazhuang 050017, Peoples R China.
EM qizhjia@hebmu.edu.cn; yang0311qian@126.com
RI Zhao, Jianing/JRY-2106-2023; Hongyu, Ma/AAG-8510-2020; Zhao,
   Yashuo/JBR-7939-2023
OI Zhao, Yashuo/0000-0002-5793-5574
FU China Postdoctoral Science Foundation [2022M711000]; Natural Science
   Foundation of Hebei Province [H2023423001]
FX This research was funded by the China Postdoctoral Science Foundation
   (grant number 2022M711000) and the Natural Science Foundation of Hebei
   Province (grant number H2023423001).
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NR 53
TC 12
Z9 15
U1 3
U2 28
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD SEP
PY 2023
VL 11
IS 9
AR 2338
DI 10.3390/biomedicines11092338
PG 15
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA T3XH8
UT WOS:001077345000001
PM 37760781
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Ebert, A
   König, J
   Frommer, L
   Schuppan, D
   Kahaly, GJ
AF Ebert, Antonia
   Koenig, Jochem
   Frommer, Lara
   Schuppan, Detlef
   Kahaly, George J.
TI Chromogranin Serves as Novel Biomarker of Endocrine and Gastric
   Autoimmunity
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
DE chromogranin; type 1 diabetes; autoimmune polyendocrinopathy; thyroid
   autoimmunity; autoimmune gastritis; celiac disease
ID ATROPHIC GASTRITIS; ATHEROSCLEROSIS; PATHOGENESIS; ANTIGENS; DISEASES;
   MARKERS; MICE
AB Context: The glycoprotein chromogranin A (CgA) is expressed by endocrine and neuroendocrine cells. High levels of serum CgA serve as markers of neuroendocrine tumors (NET), but its role in autoimmunity has not been assessed.
   Objective: To investigate CgA utility as a marker of endocrine autoimmunity.
   Methods: CgA serum levels were evaluated in 807 consecutive unselected participants (cross-sectional study) with the time-resolved amplified cryptate emission technology.
   Results: Serum CgA concentrations were increased in 66%, 39%, 38%, and 24% of patients with NET, type 1 diabetes (T1D), autoimmune gastritis (AG) and autoimmune polyendocrinopathy (AP), respectively. Compared with healthy participant controls (C), the odds of positive CgA measurement were up to 28 times higher in the disease groups. In detail, the odds ratios (ORs) for positive CgA levels were 27.98, 15.22, 7.32 (all P < 0.0001) and 3.89 (P = 0.0073) in patients with NET, T1D, AG, and AP, respectively. In AG, CgA and serum gastrin correlated positively (r = 0.55; P < 0.0001). The area under the receiver operating characteristic curve to predict AG was higher for parietal cell antibody (PCA) positivity than for CgA (0.84 vs 0.67; P < 0.0001). However, in combination with PCA and intrinsic factor autoantibodies, CgA independently improved prediction of AG (OR 6.5; P = 0.031). An impact of age on CgA positivity and on CgA value was detected (P < 0.0001) while current smoking significantly increased CgA serum levels by 25% (P = 0.0080).
   Conclusion: CgA qualifies as a novel biomarker for T1D, AP, and AG.
C1 [Ebert, Antonia; Frommer, Lara; Kahaly, George J.] Johannes Gutenberg Univ JGU, Dept Med 1, Med Ctr, D-55101 Mainz, Germany.
   [Koenig, Jochem] Johannes Gutenberg Univ Mainz, Med Ctr, Inst Med Biostat Epidemiol & Informat IMBEI, D-55101 Mainz, Germany.
   [Schuppan, Detlef] Johannes Gutenberg Univ Mainz, Inst Translat Immunol, Med Ctr, D-55101 Mainz, Germany.
   [Schuppan, Detlef] Johannes Gutenberg Univ Mainz, Res Ctr Immunotherapy FZI, Med Ctr, D-55101 Mainz, Germany.
   [Schuppan, Detlef] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Gastroenterol, Boston, MA 02215 USA.
C3 Johannes Gutenberg University of Mainz; Johannes Gutenberg University of
   Mainz; Johannes Gutenberg University of Mainz; Johannes Gutenberg
   University of Mainz; Harvard University; Harvard University Medical
   Affiliates; Beth Israel Deaconess Medical Center; Harvard Medical School
RP Kahaly, GJ (corresponding author), Johannes Gutenberg Univ JGU, Dept Med 1, Med Ctr, D-55101 Mainz, Germany.
EM george.kahaly@unimedizin-mainz.de
RI Schuppan, Detlef/AER-9743-2022; König, Jochem/T-3500-2019
FU ThermoFisher Scientific, Henningsdorf, Germany; German Research
   Foundation DFG [Schu 646/20-1]; German Research Foundation DFG
   Collaborative Research Center [SFB128 A08]
FX ThermoFisher Scientific, Henningsdorf, Germany, funded this research in
   parts. The work by D.S. was supported by research grants from the German
   Research Foundation DFG Schu 646/20-1 (Allergy) and the Collaborative
   Research Center SFB128 A08 (Multiple sclerosis).
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NR 54
TC 7
Z9 8
U1 0
U2 2
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD AUG
PY 2020
VL 105
IS 8
BP 2606
EP 2615
DI 10.1210/clinem/dgaa288
PG 10
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA NJ3DE
UT WOS:000565927300072
PM 32436949
DA 2025-06-01
ER

PT J
AU Snyder, BL
   Blackshear, PJ
AF Snyder, Brittany L.
   Blackshear, Perry J.
TI Clinical implications of tristetraprolin (TTP) modulation in the
   treatment of inflammatory diseases
SO PHARMACOLOGY & THERAPEUTICS
LA English
DT Review
DE RNA-binding protein; Tristetraprolin (TTP); Zfp36; Cytokines;
   Inflammation; Tumor necrosis factor
ID MESSENGER-RNA STABILITY; AU-RICH ELEMENT; EXPERIMENTAL AUTOIMMUNE
   UVEORETINITIS; POLYPEPTIDE-EXPRESSING METAPLASIA; CCR4-NOT DEADENYLASE
   COMPLEX; COLONY-STIMULATING FACTOR; ZINC-FINGER PROTEIN;
   RHEUMATOID-ARTHRITIS; GASTRIC METAPLASIA; BINDING PROTEINS
AB Abnormal regulation of pro-inflammatory cytokine and chemokine mediators can contribute to the excess inflammation characteristic of many autoimmune diseases, such as rheumatoid arthritis, psoriasis, Crohn's disease, type 1 diabetes, and many others. The tristetraprolin (TTP) family consists of a small group of related RNA binding proteins that bind to preferred AU-rich binding sites within the 3 '-untranslated regions of specific mRNAs to promote mRNA deadenylation and decay. TTP deficient mice develop a severe systemic inflammatory syndrome consisting of arthritis, myeloid hyperplasia, dermatitis, autoimmunity and cachexia, due at least in part to the excess accumulation of proinflammatory chemokine and cytokine mRNAs and their encoded proteins. To investigate the possibility that increased TTP expression or activity might have a beneficial effect on inflammatory diseases, at least two mouse models have been developed that provide proof of principle that increasing TTP activity can promote the decay of pro-inflammatory and other relevant transcripts, and decrease the severity of mouse models of inflammatory disease. Animal studies of this type are summarized here, and we briefly review the prospects for harnessing these insights for the development of TTP-based anti-inflammatory treatments in humans. Published by Elsevier Inc.
C1 [Snyder, Brittany L.; Blackshear, Perry J.] Natl Inst Environm Hlth Sci, NIH, Signal Transduct Lab, Res Triangle Pk, NC 27709 USA.
   [Blackshear, Perry J.] Duke Univ Med Ctr, Dept Med, Durham, NC 27710 USA.
   [Snyder, Brittany L.; Blackshear, Perry J.] Duke Univ Med Ctr, Dept Biochem, Durham, NC 27710 USA.
   [Blackshear, Perry J.] Natl Inst Environm Hlth Sci, Signal Transduct Lab, Box F1-13,Room F187,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Institute of
   Environmental Health Sciences (NIEHS); Duke University; Duke University;
   National Institutes of Health (NIH) - USA; NIH National Institute of
   Environmental Health Sciences (NIEHS)
RP Blackshear, PJ (corresponding author), Natl Inst Environm Hlth Sci, Signal Transduct Lab, Box F1-13,Room F187,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM Black009@niehs.nih.gov
RI Blackshear, Perry/C-6206-2019
OI Snyder, Brittany/0000-0002-3356-2603
FU Intramural Program of the National Institute of Environmental Health
   Sciences, National Institutes of Health; National Institute of
   Environmental Health Sciences [ZIAES090080] Funding Source: NIH RePORTER
FX We are grateful to the members of the Blackshear laboratory for many
   useful discussions. This work was supported by the Intramural Program of
   the National Institute of Environmental Health Sciences, Na-tional
   Institutes of Health.
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NR 151
TC 10
Z9 11
U1 0
U2 20
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0163-7258
EI 1879-016X
J9 PHARMACOL THERAPEUT
JI Pharmacol. Ther.
PD NOV
PY 2022
VL 239
AR 108198
DI 10.1016/j.pharmthera.2022.108198
EA MAY 2022
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 1U1KX
UT WOS:000805178800002
PM 35525391
OA Green Accepted, Bronze
DA 2025-06-01
ER

PT J
AU Cebe, KM
   Swanson, PE
   Upton, MP
   Westerhoff, M
AF Cebe, Katherine M.
   Swanson, Paul E.
   Upton, Melissa P.
   Westerhoff, Maria
TI Increased IgG4+ Cells in Duodenal Biopsies Are Not Specific for
   Autoimmune Pancreatitis
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE Serum IgG4 concentration; Autoimmune pancreatitis type I; Ampullary
   biopsy
ID IMMUNOGLOBULIN G4; DISEASE; DIAGNOSIS
AB Endoscopic ampullary biopsies showing increased immunoglobulin (Ig) G4+ plasma cells have been reported as an alternative to pancreatic biopsy in diagnosing auto immune pancreatitis (AIP). This study assessed whether increased IgG4+ cells can be seen outside the context of AIP. Fifty-four cases (45 duodenal or ampullary biopsies, 9 ampullae from pancreatic resections) were selected, and all specimens were AIP for IgG4 and IgG. Duodenal or ampullary biopsies containing normal duodenal mucosa (n = 6) and increased intraepithelial lymphocytes without villous blunting (n = 7) were negative for IgG4. Increased IgG4+ cells (>10 per high-power field) were found in 7 cases of 18 serologically confirmed celiac disease patients and in 3 of 14 patients with duodenitis or gastric heterotopias. Two of 6 ampullae from patients with pancreatic cancer showed increased IgG4+ cells. In summary, 12 of 51 patients without AIP had duodenal biopsies or ampullae showing increased IgG4+ plasma cells. The finding of increased IgG4+ cells in duodenal biopsies is not specific for AIP without the correct clinical context.
C1 [Cebe, Katherine M.] San Antonio Mil Med Ctr, Ft Sam Houston, TX USA.
   [Swanson, Paul E.; Upton, Melissa P.; Westerhoff, Maria] Univ Washington, Med Ctr, Seattle, WA 98195 USA.
C3 San Antonio Military Medical Center; University of Washington;
   University of Washington Seattle
RP Westerhoff, M (corresponding author), 1959 NE Pacific St,Box 356100, Seattle, WA 98195 USA.
EM mwest2@uw.edu
FU University of Washington Department of Pathology Resident Research Fund
FX Supported by the University of Washington Department of Pathology
   Resident Research Fund.
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NR 15
TC 16
Z9 16
U1 0
U2 0
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
EI 1943-7722
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD MAR
PY 2013
VL 139
IS 3
BP 323
EP 329
DI 10.1309/AJCPT00NHQHXAHDS
PG 7
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 099GC
UT WOS:000315608500008
PM 23429368
DA 2025-06-01
ER

PT J
AU Prades, E
   Alobid, I
   Alós, L
   Guilemany, JM
   Bernal-Sprekelsen, M
   Mullol, J
AF Prades, E
   Alobid, I
   Alós, L
   Guilemany, JM
   Bernal-Sprekelsen, M
   Mullol, J
TI Extranodal lymphoma originating from mucosa-associated lymphoid tissue
   of the nasopharynx
SO ACTA OTO-LARYNGOLOGICA
LA English
DT Article
DE chemotherapy; lymphoma; mucosa-associated lymphoid tissue; nasopharynx
ID B-CELL LYMPHOMA; EPSTEIN-BARR-VIRUS; HELICOBACTER-PYLORI; MALT LYMPHOMA
AB Non-Hodgkin's lymphoma originating from mucosa-associated lymphoid tissue has been connected with autoimmune disease. These tumours often arise in gastric mucosa and are extremely rare in airway mucosa. Three cases of mucosa-associated lymphoid tissue lymphoma in the cavum have been reported in the literature. A 52-year-old mate with rheumatoid arthritis presented with an 8-month history of nasal obstruction and recurrent nasal blood discharge. On physical examination a bulky mass was observed in the nasopharynx. CT demonstrated a soft tissue lesion in the nasopharynx. without bone destruction. MRI showed a contrast-enhanced mass with extension to the left pterygoid muscle. Biopsy revealed a low-grade B-cell lymphoid tumour of the marginal zone. The patient received six cycles of cyclophosphamide, vincristine and prednisone with adriamycin treatment, together with intracranial methrotrexate as a prophylactic measure. After 48 months of follow-up there was no evidence of disease and a control MRI scan was normal. The prognosis of this type of tumour is unpredictable and there are too few cases to enable definitive conclusions to be drawn.
C1 Hosp Clin Barcelona, Dept Otorhinolaryngol, Rhinol Unit, ES-08036 Barcelona, Spain.
   Hosp Clin Barcelona, Dept Pathol, Barcelona, Spain.
C3 University of Barcelona; Hospital Clinic de Barcelona; University of
   Barcelona; Hospital Clinic de Barcelona
RP Hosp Clin Barcelona, Dept Otorhinolaryngol, Rhinol Unit, C Villarroel 170, ES-08036 Barcelona, Spain.
EM 32874iao@comb.es
RI Bernal-Sprekelsen, Manuel/AAG-4299-2021; Prades, Eduardo/AAF-1608-2021
OI Bernal-Sprekelsen, Manuel/0000-0001-8191-9833; GUILEMANY, JOSEP
   MARIA/0000-0002-3393-0947
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NR 21
TC 4
Z9 5
U1 0
U2 0
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 0001-6489
EI 1651-2251
J9 ACTA OTO-LARYNGOL
JI Acta Oto-Laryngol.
PD DEC
PY 2003
VL 123
IS 9
BP 1098
EP 1101
DI 10.1080/00016480310014868
PG 4
WC Otorhinolaryngology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Otorhinolaryngology
GA 757FQ
UT WOS:000187550600016
PM 14710915
DA 2025-06-01
ER

PT J
AU Liu, X
   Xia, SY
   Zhang, ZB
   Wu, H
   Lieberman, J
AF Liu, Xing
   Xia, Shiyu
   Zhang, Zhibin
   Wu, Hao
   Lieberman, Judy
TI Channelling inflammation: gasdermins in physiology and disease
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Review
ID NONSYNDROMIC HEARING IMPAIRMENT; NEUTROPHIL EXTRACELLULAR TRAPS; DFNA5
   GENE; GASTRIC-CANCER; HAIR FOLLICLE; GASTROINTESTINAL-TRACT; PROMOTER
   METHYLATION; MACROPHAGE APOPTOSIS; IL-1-BETA RELEASE; CELL-DEATH
AB Gasdermins were recently identified as the mediators of pyroptosis - inflammatory cell death triggered by cytosolic sensing of invasive infection and danger signals. Upon activation, gasdermins form cell membrane pores, which release pro-inflammatory cytokines and alarmins and damage the integrity of the cell membrane. Roles for gasdermins in autoimmune and inflammatory diseases, infectious diseases, deafness and cancer are emerging, revealing potential novel therapeutic avenues. Here, we review current knowledge of the family of gasdermins, focusing on their mechanisms of action and roles in normal physiology and disease. Efforts to develop drugs to modulate gasdermin activity to reduce inflammation or activate more potent immune responses are highlighted.
   Gasdermins (GSDMs) are a recently characterized protein family that mediate a programmed inflammatory cell death termed pyroptosis. Here, Lieberman and colleagues review current understanding of the expression, activation and regulation of GSDMs, highlighting their roles in cell death, cytokine secretion and inflammation. Emerging opportunities to develop GSDM-targeted drugs and the associated challenges are highlighted.
C1 [Liu, Xing] Chinese Acad Sci, Ctr Microbes Dev & Hlth, Inst Pasteur Shanghai, Key Lab Mol Virol & Immunol, Shanghai, Peoples R China.
   [Xia, Shiyu; Zhang, Zhibin; Wu, Hao; Lieberman, Judy] Boston Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.
   [Xia, Shiyu; Wu, Hao] Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
   [Zhang, Zhibin; Lieberman, Judy] Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA.
C3 Chinese Academy of Sciences; Shanghai Institute of Immunity and
   Infection, CAS; Pasteur Network; Harvard University; Harvard University
   Medical Affiliates; Boston Children's Hospital; Program in Cellular &
   Molecular Medicine (PCMM); Harvard University; Harvard Medical School;
   Harvard University; Harvard Medical School
RP Liu, X (corresponding author), Chinese Acad Sci, Ctr Microbes Dev & Hlth, Inst Pasteur Shanghai, Key Lab Mol Virol & Immunol, Shanghai, Peoples R China.; Wu, H; Lieberman, J (corresponding author), Boston Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA.; Wu, H (corresponding author), Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.; Lieberman, J (corresponding author), Harvard Med Sch, Dept Pediat, Boston, MA 02115 USA.
EM xingliu@ips.ac.cn; wu@crystal.harvard.edu;
   judy.lieberman@childrens.harvard.edu
RI Wu, Hao/ACI-6411-2022; Xia, Shiyu/P-8621-2019
OI Xia, Shiyu/0000-0001-9024-0689; , Hao/0000-0002-7281-8579; Zhang,
   Zhibin/0000-0003-1349-2713; Liu, Xing/0000-0002-6277-3856
FU NIH [R01AI139914, R01CA240955]; Key Research Program of the Chinese
   Academy of Sciences [ZDBS-LY-SM008]; National Key R&D Program of China
   [2020YFA0509600]; National Natural Science Foundation of China
   [31972897]; Strategic Priority Research Program of Chinese Academy of
   Sciences [XDB29030300]; Shanghai Municipal Science and Technology Major
   Project [2019SHZDZX02]
FX This work was supported by NIH R01AI139914 (H.W.), R01CA240955 (J.L.),
   Key Research Program of the Chinese Academy of Sciences (ZDBS-LY-SM008),
   National Key R&D Program of China (2020YFA0509600), National Natural
   Science Foundation of China (31972897), Strategic Priority Research
   Program of Chinese Academy of Sciences (XDB29030300) and Shanghai
   Municipal Science and Technology Major Project (2019SHZDZX02) (X.L.).
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   Butte, MJ
   Freeman, GJ
   Sharpel, AH
AF Keir, Mary E.
   Butte, Manish J.
   Freeman, Gordon J.
   Sharpel, Arlene H.
TI PD-1 and its ligands in tolerance and immunity
SO ANNUAL REVIEW OF IMMUNOLOGY
SE Annual Review of Immunology
LA English
DT Review; Book Chapter
DE costimulation; T cell; autoimmunity; infectious disease; tumor
ID T-CELL-ACTIVATION; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
   SYSTEMIC-LUPUS-ERYTHEMATOSUS; PROGRAMMED DEATH-1 PATHWAY;
   GAMMA-DEPENDENT MECHANISM; GASTRIC EPITHELIAL-CELLS; CROSS-LINKING
   ANTIBODY; CHRONIC HEPATITIS-B; RESPONSES IN-VIVO; DENDRITIC CELLS
AB Programmed death 1 (PD-1) and its ligands, PD-L1 and PD-L2, deliver inhibitory signals that regulate the balance between T cell activation, tolerance, and immunopathology. Immune responses to foreign and self-antigens require specific and balanced responses to clear pathogens and tumors and yet maintain tolerance. Induction and maintenance of T cell tolerance requires PD-1, and its ligand PD-L1 on nonhematopoietic cells can limit effector T cell responses and protect tissues from immune-mediated tissue damage. The PD-1:PD-L pathway also has been usurped by microorganisms and tumors to attenuate antimicrobial or tumor immunity and facilitate chronic infection and tumor survival. The identification of B7-1 as an additional binding partner for PD-L1, together with the discovery of an inhibitory bidirectional interaction between PD-L1 and B7-1, reveals new ways the B7:CD28 family regulates T cell activation and tolerance. In this review, we discuss current understanding of the immunoregulatory functions of PD-1 and its ligands and their therapeutic potential.
C1 [Keir, Mary E.; Butte, Manish J.; Sharpel, Arlene H.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
   [Keir, Mary E.; Butte, Manish J.; Sharpel, Arlene H.] Brigham & Womens Hosp, Boston, MA 02115 USA.
   [Freeman, Gordon J.] Harvard Univ, Sch Med, Dept Med, Dana Farber Canc Inst,Dept Med Oncol, Boston, MA 02115 USA.
C3 Harvard University; Harvard Medical School; Harvard University; Harvard
   University Medical Affiliates; Brigham & Women's Hospital; Harvard
   University; Harvard University Medical Affiliates; Dana-Farber Cancer
   Institute; Harvard Medical School
RP Keir, ME (corresponding author), Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
EM arlene_sharpe@hms.harvard.edu
RI Butte, Manish/T-8860-2019; , Gordon/ADF-6477-2022
OI Butte, Manish/0000-0002-4490-5595
FU NIAID NIH HHS [R01 AI038310, P01 AI056299] Funding Source: Medline
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NR 152
TC 4257
Z9 5035
U1 25
U2 897
PU ANNUAL REVIEWS
PI PALO ALTO
PA 4139 EL CAMINO WAY, PO BOX 10139, PALO ALTO, CA 94303-0139 USA
SN 0732-0582
EI 1545-3278
J9 ANNU REV IMMUNOL
JI Annu. Rev. Immunol.
PY 2008
VL 26
BP 677
EP 704
DI 10.1146/annurev.immunol.26.021607.090331
PG 28
WC Immunology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 293QH
UT WOS:000255349300022
PM 18173375
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Trop-Steinberg, S
   Azar, Y
AF Trop-Steinberg, Shivtia
   Azar, Yehudit
TI AP-1 Expression and its Clinical Relevance in Immune Disorders and
   Cancer
SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES
LA English
DT Review
DE AP-1; Immune disorders; Hematopoietic stem cell transplantation;
   Carcinomas; Hematological malignancies
ID N-TERMINAL KINASE; ACTIVATOR PROTEIN-1 AP-1; UROKINASE-RECEPTOR GENE;
   T-CELL-ACTIVATION; C-FOS; RHEUMATOID-ARTHRITIS; BREAST-CANCER;
   MESSENGER-RNA; ENDOMETRIAL CANCER; MYELOID-LEUKEMIA
AB The inflammatory response is known to have a significant role in certain autoimmune diseases and malignancies. We review current knowledge regarding the functions of activator protein 1 (AP-1) as an important modulator in several immune disorders and carcinomas. AP-1 is overexpressed in rheumatoid arthritis and in long-term allogeneic hematopoietic stem cell transplantation survivors; however, decreased expression of AP-1 has been observed in psoriasis, systematic lupus erythematosus and in patients who do not survive after hematopoietic stem cell transplantation. AP-1 also is implicated in the control of various cancer cells. Higher levels of AP-1 components are present in breast and endometrial carcinomas, colorectal cancer and in acute myeloid leukemia, Hodgkin's lymphoma and anaplastic large cell lymphoma, with downregulation in ovarian and gastric carcinomas and in patients with chronic myelogenous leukemia. AP-1 may enable the development of helpful markers to identify early-stage disease or to predict severity.
C1 [Trop-Steinberg, Shivtia] JCT Lev Acad Inst, Fac Life & Hlth Sci, 11 Beit Hadfus St, Jerusalem, Israel.
   [Azar, Yehudit] Hadassah Hebrew Univ, Med Ctr, Dept Bone Marrow Transplantat, Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hadassah University Medical Center
RP Trop-Steinberg, S (corresponding author), JCT Lev Acad Inst, Fac Life & Hlth Sci, 11 Beit Hadfus St, Jerusalem, Israel.
EM shivtia@g.jct.ac.il
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NR 108
TC 93
Z9 110
U1 1
U2 31
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0002-9629
EI 1538-2990
J9 AM J MED SCI
JI Am. J. Med. Sci.
PD MAY
PY 2017
VL 353
IS 5
BP 474
EP 483
DI 10.1016/j.amjms.2017.01.019
PG 10
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA EY1XL
UT WOS:000403761400011
PM 28502334
DA 2025-06-01
ER

PT J
AU Notohara, K
   Kamisawa, T
   Uchida, K
   Zen, Y
   Kawano, M
   Kasashima, S
   Sato, Y
   Shiokawa, M
   Uehara, T
   Yoshifuji, H
   Hayashi, H
   Inoue, K
   Iwasaki, K
   Kawano, H
   Matsubayashi, H
   Moritani, Y
   Murakawa, K
   Oka, Y
   Tateno, M
   Okazaki, K
   Chiba, T
AF Notohara, Kenji
   Kamisawa, Terumi
   Uchida, Kazushige
   Zen, Yoh
   Kawano, Mitsuhiro
   Kasashima, Satomi
   Sato, Yasuharu
   Shiokawa, Masahiro
   Uehara, Takeshi
   Yoshifuji, Hajime
   Hayashi, Hiroko
   Inoue, Koichi
   Iwasaki, Keisuke
   Kawano, Hiroo
   Matsubayashi, Hiroyuki
   Moritani, Yukitoshi
   Murakawa, Katsuhiko
   Oka, Yoshio
   Tateno, Masatoshi
   Okazaki, Kazuichi
   Chiba, Tsutomu
TI Gastrointestinal manifestation of immunoglobulin G4-related disease:
   clarification through a multicenter survey
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE IgG4-related disease; Gastrointestinal tract; Inflammatory pseudotumor;
   Pathology; IgG4
ID IGG4-RELATED SCLEROSING DISEASE; PLASMA-CELL INFILTRATION; ENTEROCOLIC
   LYMPHOCYTIC PHLEBITIS; NODULAR FIBROUS PSEUDOTUMOR; AUTOIMMUNE
   PANCREATITIS; DIAGNOSTIC-CRITERIA; GASTRIC-ULCER; RETROPERITONEAL
   FIBROSIS; INFLAMMATORY PSEUDOTUMOR; TRACT
AB Several reports on immunoglobulin (Ig)G4-related disease (IgG4-RD) with gastrointestinal involvement (IgG4-related gastrointestinal disease; IgG4-GID) have been published, although this entity has not been fully established clinicopathologically. Thus, we carried out a multicenter survey.
   Patients with possible IgG4-GID who underwent resection were collected. Histologic slides were reevaluated, and eight cases with diffuse lymphoplasmacytic infiltration but without numerous neutrophils, granulations or epithelioid granulomas were further analyzed.
   Overall, the IgG4 counts (87-345/high-power field) and IgG4/IgG-positive ratio were high (44-115%). The demographic findings included advanced age among the patients (55-80 years) and male preponderance (six cases). Six lesions (five gastric, one esophageal), consisting of lymphoplasmacytic infiltration with neural involvement in the muscularis propria and/or bottom-heavy plasmacytosis in the gastric mucosa, were histologically regarded as highly suggestive of IgG4-RD. Storiform fibrosis and obliterative phlebitis were found in two cases, and the former gave rise to a 7-cm-sized inflammatory pseudotumor (IPT) in one case. Ulceration and carcinoma co-existed in three and two lesions, respectively. All the patients had other organ involvement (OOI), and serum IgG4 levels were markedly elevated (four of five patients). The remaining two cases with gastric IPTs featuring reactive nodular fibrous pseudotumor or nodular lymphoid hyperplasia were regarded as possible cases of IgG4-RD because of the histologic findings and lack of OOI.
   IgG4-GID is found in the setting of IgG4-RD, often with ulceration or cancer. Characteristic histologic findings are observed in the muscularis propria and gastric mucosa. Cases with IPT may be heterogeneous, and there may be mimickers of IgG4-GID.
C1 [Notohara, Kenji] Kurashiki Cent Hosp, Dept Anat Pathol, Kurashiki, Okayama, Japan.
   [Kamisawa, Terumi] Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Tokyo, Japan.
   [Uchida, Kazushige; Okazaki, Kazuichi] Kansai Med Univ, Dept Gastroenterol & Hepatol, Hirakata, Osaka, Japan.
   [Zen, Yoh] Kobe Univ, Dept Diagnost Pathol, Grad Sch Med, Kobe, Hyogo, Japan.
   [Kawano, Mitsuhiro] Kanazawa Univ, Div Rheumatol, Dept Internal Med, Grad Sch Med, Kanazawa, Ishikawa, Japan.
   [Kasashima, Satomi] Natl Hosp Org, Kanazawa Med Ctr, Dept Pathol, Kanazawa, Ishikawa, Japan.
   [Sato, Yasuharu] Okayama Univ, Dept Pathol, Grad Sch Med Dent & Pharmaceut Sci, Okayama, Japan.
   [Shiokawa, Masahiro; Chiba, Tsutomu] Kyoto Univ, Grad Sch Med, Dept Gastroenterol & Hepatol, Kyoto, Japan.
   [Uehara, Takeshi] Shinshu Univ, Dept Lab Med, Sch Med, Matsumoto, Nagano, Japan.
   [Yoshifuji, Hajime] Kyoto Univ, Grad Sch Med, Dept Rheumatol & Clin Immunol, Kyoto, Japan.
   [Hayashi, Hiroko] Nagasaki Univ, Dept Pathol, Grad Sch Biomed Sci, Nagasaki, Japan.
   [Inoue, Koichi] Yamachika Mem Hosp, Div Surg, Odawara, Kanagawa, Japan.
   [Iwasaki, Keisuke] Sasebo City Gen Hosp, Dept Pathol, Sasebo, Japan.
   [Kawano, Hiroo] Yamaguchi Univ, Dept Lab Sci, Grad Sch Med, Fac Hlth Sci, Ube, Yamaguchi, Japan.
   [Matsubayashi, Hiroyuki] Shizuoka Canc Ctr, Div Endoscopy, Shizuoka, Japan.
   [Moritani, Yukitoshi] Moritani Surg Clin, Okayama, Japan.
   [Murakawa, Katsuhiko] Obihiro Kosei Gen Hosp, Dept Surg, Obihiro, Hokkaido, Japan.
   [Oka, Yoshio] Nishinomiya Municipal Cent Hosp, Dept Surg, Nishinomiya, Hyogo, Japan.
   [Tateno, Masatoshi] Kushiro Red Cross Hosp, Dept Pathol, Kushiro, Hokkaido, Japan.
C3 Kurashiki Central Hospital; Tokyo Metropolitan Cancer & Infectious
   Diseases Center Komagome Hospital; Kansai Medical University; Kobe
   University; Kanazawa University; Okayama University; Kyoto University;
   Shinshu University; Kyoto University; Nagasaki University; Yamaguchi
   University; Shizuoka Cancer Center
RP Kamisawa, T (corresponding author), Tokyo Metropolitan Komagome Hosp, Dept Internal Med, Tokyo, Japan.
EM kamisawa@cick.jp
RI Yoshifuji, Hajime/AAZ-1657-2020; Uchida, Kazushige/AAD-4966-2020;
   Kasashima, Satomi/W-1863-2019
OI Yoshifuji, Hajime/0000-0001-7082-4900; Uchida,
   Kazushige/0000-0002-3160-3184
FU Health and Labour Sciences Research Grants (Intractable Diseases) from
   Japan's Ministry of Health, Labour and Welfare; Grants-in-Aid for
   Scientific Research [16K08666, 15K08345] Funding Source: KAKEN
FX This work was supported by Health and Labour Sciences Research Grants
   (Intractable Diseases) from Japan's Ministry of Health, Labour and
   Welfare.
CR [Anonymous], ISRN GASTROENTEROL
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NR 62
TC 38
Z9 39
U1 0
U2 2
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD JUL
PY 2018
VL 53
IS 7
BP 845
EP 853
DI 10.1007/s00535-017-1420-4
PG 9
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GJ7XF
UT WOS:000435602800005
PM 29222587
DA 2025-06-01
ER

PT J
AU Nam, H
   Lim, DH
   Kim, JJ
   Lee, JH
   Min, BH
   Lee, H
AF Nam, Heerim
   Lim, Do Hoon
   Kim, Jae J.
   Lee, Jun Haeng
   Min, Byung-Hoon
   Lee, Hyuk
TI Long-Term Clinical Outcome and Predictive Factors for Relapse after
   Radiation Therapy in 145 Patients with Stage I Gastric B-Cell Lymphoma
   of Mucosa-Associated Lymphoid Tissue Type
SO CANCERS
LA English
DT Article
DE gastric MALT lymphoma; radiotherapy; long-term outcome; tumor location
ID HELICOBACTER-PYLORI ERADICATION; MARGINAL ZONE LYMPHOMA; MALT-LYMPHOMA;
   VARIABLE FREQUENCIES; T(11/18)(Q21,Q21); RADIOTHERAPY; FEATURES; GENE
AB Simple Summary
   Helicobacter pylori-associated gastric low-grade B-cell lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma) constitutes >80% of gastric MALT lymphoma. Eradication therapy has been accepted as a standard approach for initial treatment. However, in patients who present without evidence of infection or who fail to respond to eradication therapy, a solid consensus for treatment is not available. Furthermore, few studies have evaluated the predictive factors for response or relapse after radiation therapy (RT) as heterogeneous, relatively small study populations have been treated with RT, and only a small number of events have been reported after treatment. In this study, we report the long-term clinical outcome of stage I gastric MALT lymphoma treated with RT. We also identified that the tumor's dominant location in the stomach is a predictive factor for relapse after RT.
   This study aimed to evaluate the clinical outcomes of radiation therapy (RT) for stage I gastric mucosa-associated lymphoid tissue (MALT) lymphoma and find predictive factors for relapse after RT. This retrospective study included 145 patients without a prior history of treatment, except Helicobacter pylori eradication therapy, who were irradiated for stage I gastric MALT lymphoma. The gastric body was the most commonly involved location of the dominant lesion (66.9%), and H. pylori infection at first diagnosis was detected in 61 (42.1%) patients. The median RT dose was 30 Gy (range, 24-40). Seven patients had an autoimmune disease. All patients except one achieved a complete remission at post-treatment endoscopic biopsy after a median of 2 months (range, 1-36). During the median follow-up at 51 months (range, 2-146), 11 patients experienced relapses: in the stomach (n = 5), in a distant site (n = 4), and in both (n = 2). The five-year overall, local relapse-free, distant relapse-free, and relapse-free survival (RFS) rates were 98.6%, 94.0%, 97.1%, and 92.3%, respectively. In multivariate analysis for RFS, the location of MALT lymphoma other than in the gastric body was significantly associated with an increased risk of relapse (hazard ratio 5.85 (95% CI 1.49-22.9), p = 0.011). RT results in favorable clinical outcomes in patients with stage I gastric MALT lymphoma. Tumor location could be a predictive factor for relapse after RT.
C1 [Nam, Heerim] Sungkyunkwan Univ, Kangbuk Samsung Hosp, Dept Radiat Oncol, Sch Med, Seoul 03181, South Korea.
   [Lim, Do Hoon] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Radiat Oncol, Seoul 06351, South Korea.
   [Kim, Jae J.; Lee, Jun Haeng; Min, Byung-Hoon; Lee, Hyuk] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med, Seoul 06351, South Korea.
C3 Sungkyunkwan University (SKKU); Sungkyunkwan University (SKKU); Samsung
   Medical Center; Sungkyunkwan University (SKKU); Samsung Medical Center
RP Lim, DH (corresponding author), Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Radiat Oncol, Seoul 06351, South Korea.
EM heerim.nam@gmail.com; dh8lim@skku.edu; jjkim@skku.edu;
   stomachlee@gmail.com; jason1080.min@samsung.com; leehyuk@skku.edu
RI Kim, Ji/AAU-5043-2020; Lee, Hyuk-Joon/J-2782-2012; LEE,
   KYUNG-HAN/HPD-9299-2023
OI Lee, Hyuk/0000-0003-4271-7205; nam, heerim/0000-0002-1118-8200
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NR 36
TC 5
Z9 5
U1 0
U2 0
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD JAN
PY 2021
VL 13
IS 2
AR 169
DI 10.3390/cancers13020169
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA PX1UX
UT WOS:000611149100001
PM 33418965
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Koivurova, OP
   Karhukorpi, JMJ
   Joensuu, ET
   Koistinen, PO
   Valtonen, JM
   Karttunen, TJ
   Niemelä, SE
   Karttunen, RA
AF Koivurova, OP
   Karhukorpi, JMJ
   Joensuu, ET
   Koistinen, PO
   Valtonen, JM
   Karttunen, TJ
   Niemelä, SE
   Karttunen, RA
TI IL-1 RN 2/2 genotype and simultaneous carriage of genotypes IL-1 RN 2/2
   and IL-1β-511 T/T associated with oesophagitis in Helicobacter
   pylori-negative patients
SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE genetic polymorphisms; Helicobacter pylori; interleukin-1 receptor
   antagonist; interleukin-1 beta; oesophagitis
ID RECEPTOR ANTAGONIST GENE; SYMPTOMATIC GASTROESOPHAGEAL REFLUX;
   BARRETTS-ESOPHAGUS; INTERLEUKIN-1 POLYMORPHISMS; FAMILIAL AGGREGATION;
   ULCER RECURRENCE; ACID-SECRETION; ADENOCARCINOMA; INFECTION; DISEASE
AB Background: Interleukin-1 receptor antagonist genotype 2/2 is associated with a prolonged and enhanced inflammatory response. It is suspected of being a risk factor for atrophic gastritis and gastric cancer and for some autoimmune diseases. No specific genetic risk factors for oesophagitis have been identified so far and there are no reports of IL-1 polymorphism in relation to oesophageal disease. Methods: We studied the IL-1RN, IL-1beta-511 and IL-1beta + 3953 polymorphisms in an unselected series of 142 adult patients scheduled for gastrointestinal endoscopy because of dyspepsia. The control group consisted of university staff and students (n = 179). Helicobacter pylori status was determined by antibody testing and bacterial detection. Results: Endoscopic oesophagitis was noted in 40 patients. The IL-1RN 2/2 genotype was significantly more prevalent in the patients with H. pylori-negative oesophagitis than in the control subjects (27% versus 9%; OR 3.574, CI 1.23 - 10.35, P = 0.034) or in the dyspeptic patients (27% versus 7%; OR 5.089, CI 1.51 - 17.11, P = 0.009). IL-1beta-511 T/T genotype tended to be more frequent in the H. pylori-negative patients with oesophagitis than in the control subjects ( P = 0.071). The strongest association was between the simultaneous carriage of genotypes IL-1RN 2/2 and IL-1beta - 511 T/T and H. pylori-negative oesophagitis, where the combined genotype was more prevalent than in the control subjects (23% versus 6%; OR 4.492, CI 1.40 - 14.46, P = 0.012) or the dyspeptic patients without oesophagitis ( 23% versus 3%; OR 9.706, CI 2.12 - 44.42, P = 0.003). Conclusion: The results indicate that the IL-1RN 2/2 genotype and the carriage of combined genotypes IL-1RN 2/2 + IL-1beta-511 T/T are associated with H. pylori-negative oesophagitis. This is the first report on the association between IL-1 gene polymorphism and oesophagitis.
C1 Oulu City Hosp, FIN-90220 Oulu, Finland.
   Oulu Univ Hosp, Dept Internal Med, Oulu, Finland.
   Univ Oulu, Dept Med Microbiol, Oulu, Finland.
   Univ Oulu, Dept Pathol, Oulu, Finland.
   Deaconess Inst Oulu, Oulu, Finland.
C3 University of Oulu; University of Oulu; University of Oulu
RP Koivurova, OP (corresponding author), Oulu City Hosp, Kiviharjuntie 5, FIN-90220 Oulu, Finland.
OI Karttunen, Tuomo/0000-0002-8843-7957
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NR 42
TC 19
Z9 19
U1 0
U2 2
PU TAYLOR & FRANCIS AS
PI OSLO
PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY
SN 0036-5521
J9 SCAND J GASTROENTERO
JI Scand. J. Gastroenterol.
PD DEC
PY 2003
VL 38
IS 12
BP 1217
EP 1222
DI 10.1080/00365520310006504
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 754XL
UT WOS:000187358600005
PM 14750640
DA 2025-06-01
ER

PT J
AU den Hollander, WJ
   Kuipers, EJ
AF den Hollander, Wouter J.
   Kuipers, Ernst J.
TI Current pharmacotherapy options for gastritis
SO EXPERT OPINION ON PHARMACOTHERAPY
LA English
DT Review
DE gastritis; gastropathy; Helicobacter pylori; pharmacotherapy
ID HELICOBACTER-PYLORI ERADICATION; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
   PROTON-PUMP INHIBITOR; 10-DAY SEQUENTIAL THERAPY; RANDOMIZED
   CLINICAL-TRIAL; TRIPLE THERAPY; ANTIBIOTIC-RESISTANCE; DOUBLE-BLIND;
   EOSINOPHILIC GASTROENTERITIS; LYMPHOCYTIC GASTRITIS
AB Introduction: Gastritis is a broad term, which is used for different conditions by clinicians, endoscopists and pathologists. Classification strategies have led to more congruence between specialists. The histological evaluation of the gastric mucosa is mandatory for diagnosing and classifying gastritis. Main aetiologic factor is infection with Helicobacter pylori. The clinical importance of gastritis lays in the fact that it predisposes to more pronounced damage to the gastric mucosa, in particular peptic ulcer disease, and eventually atrophic gastritis, intestinal metaplasia and gastric malignancy, both adenocarcinoma and MALT lymphoma.
   Areas covered: This review covers the current pharmacotherapy options for different forms of gastritis. The main focus is on H. pylori induced gastritis. Thereafter, other forms of gastritis like autoimmune gastritis and non-steroidal anti-inflammatory drug (NSAID)-related gastropathy are covered
   Expert opinion: The emerging problem of antibiotic resistance requires an accurate knowledge of local eradication rates. Standard triple therapy should be abandoned in regions with high clarithromycin resistance. In these areas, sequential or quadruple therapy is best initial treatment. Further research should focus on non-invasive and effective techniques of susceptibility testing, making a tailored and cost-effective approach. Primary prevention of NSAID-related gastropathy can be enhanced by better education for clinicians and patients, so that both right prescription of gastroprotective agents as therapy adherence will improve.
C1 [den Hollander, Wouter J.; Kuipers, Ernst J.] Erasmus MC Univ Med Ctr, Dept Gastroenterol, NL-3000 CA Rotterdam, Netherlands.
   [den Hollander, Wouter J.; Kuipers, Ernst J.] Erasmus MC Univ Med Ctr, Dept Hepatol, NL-3000 CA Rotterdam, Netherlands.
C3 Erasmus University Rotterdam; Erasmus MC; Erasmus University Rotterdam;
   Erasmus MC
RP den Hollander, WJ (corresponding author), Erasmus MC Univ Med Ctr, Dept Gastroenterol, POB 2040, NL-3000 CA Rotterdam, Netherlands.
EM w.denhollander@erasmusmc.nl
RI Kuipers, Ernst/H-3293-2019; den Hollander, Wouter/P-5451-2014
OI den Hollander, Wouter/0000-0003-2503-5632
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NR 108
TC 33
Z9 34
U1 3
U2 22
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1465-6566
EI 1744-7666
J9 EXPERT OPIN PHARMACO
JI Expert Opin. Pharmacother.
PD DEC
PY 2012
VL 13
IS 18
BP 2625
EP 2636
DI 10.1517/14656566.2012.747510
PG 12
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 059KH
UT WOS:000312703500005
PM 23167300
DA 2025-06-01
ER

PT J
AU Xiao, SB
   Huang, Q
   Ren, H
   Yang, M
AF Xiao, Shibai
   Huang, Qin
   Ren, Hao
   Yang, Min
TI The mechanism and function of super enhancer RNA
SO GENESIS
LA English
DT Review
DE autoimmune disease; cancer; embryonic stem cell; super enhancer; super
   enhancer RNA
ID LONG NONCODING RNA; CELL LUNG-CANCER; TRANSCRIPTION FACTORS;
   GASTRIC-CANCER; PROMOTES; GENE; EXPRESSION; MYC; IDENTITY; DRIVES
AB Super enhancer (SE) is a cluster of enhancers that has a stronger ability to promote transcription compared to the typical enhancer (TE). Similar to TE, which can transcribe enhancer RNA (eRNA), SE produces super enhancer RNA (seRNA). The activation of SE is cell and tissue-specific, and the SE-associated genes are mostly linked to the cell fate. This is demonstrated by the important role-played by SE in the embryonic stem cell (ESC) and multiple cancer development. SeRNA regulates transcription in both cis and trans configuration, and those located in the cytoplasm mediates various cell activities. However, the functions of seRNAs are unclear, and most of them have a synergistic effect with SE and SE-associated genes. In this mini review, we summarized the mechanisms of seRNA and functions of both SE and seRNA.
C1 [Xiao, Shibai; Huang, Qin; Ren, Hao; Yang, Min] Southern Med Univ, Nanfang Hosp, Dept Rheumatol & Immunol, 1838 North Guangzhou Ave, Guangzhou 510515, Peoples R China.
C3 Southern Medical University - China
RP Yang, M (corresponding author), Southern Med Univ, Nanfang Hosp, Dept Rheumatol & Immunol, 1838 North Guangzhou Ave, Guangzhou 510515, Peoples R China.
EM minyanggz@163.com
RI Xiao, Shibai/JXN-4113-2024
FU National Natural Science Foundation of China [81771747]; Natural Science
   Foundation of Guangdong Province [2017A030313475]
FX National Natural Science Foundation of China, Grant/Award Number:
   81771747; Natural Science Foundation of Guangdong Province, Grant/Award
   Number: 2017A030313475
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NR 70
TC 22
Z9 22
U1 0
U2 21
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1526-954X
EI 1526-968X
J9 GENESIS
JI Genesis
PD JUN
PY 2021
VL 59
IS 5-6
AR e23422
DI 10.1002/dvg.23422
EA MAY 2021
PG 10
WC Developmental Biology; Genetics & Heredity
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Developmental Biology; Genetics & Heredity
GA SS1XL
UT WOS:000653198700001
PM 34028961
DA 2025-06-01
ER

PT J
AU Lin, F
   Luo, XR
   Tsun, A
   Li, ZY
   Li, D
   Li, B
AF Lin, Fang
   Luo, Xuerui
   Tsun, Andy
   Li, Zhiyuan
   Li, Dan
   Li, Bin
TI Kaempferol enhances the suppressive function of Treg cells by inhibiting
   FOXP3 phosphorylation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Kaempferol; Treg cells; FOXP3 phosphorylation; PIM1; Autoimmune disease
ID TRANSCRIPTION FACTOR FOXP3; DIETARY FLAVONOID INTAKE; CANCER; PROTEIN;
   ENTEROPATHY; KINASE; RISK
AB Kaempferol is a natural flavonoid found in many vegetables and fruits. Epidemiologic studies have described that Kaempferol intake could reduce risk of cancer, especially lung, gastric, pancreatic and ovarian cancers. Recent studies have shown that Kaempferol could also be beneficial to the body to defend against inflammation, and infection by bacteria and viruses; however, the molecular mechanism of its immunoregulatory function remains largely unknown. Through screening a small molecule library of traditional Chinese medicine (TCM), we identified that Kaempferol could enhance the suppressive function of regulatory T cells (Tregs). Kaempferol was found to increase FOXP3 expression level in Treg cells and prevent pathological symptoms of collagen-induced arthritis in a rat animal model. Kaempferol could also reduce PIM1-mediated FOXP3 phosphotylation at S422. Our study reveals a molecular mechanism that underlies the anti-inflammatory action of Kaempferol for the prevention and treatment of inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis. (C) 2015 Elsevier B.V. All rights reserved.
C1 [Lin, Fang; Luo, Xuerui; Tsun, Andy; Li, Zhiyuan; Li, Dan; Li, Bin] Chinese Acad Sci, Inst Pasteur Shanghai, Unit Mol Immunol, Key Lab Mol Virol & Immunol, Shanghai 200031, Peoples R China.
C3 Pasteur Network; Chinese Academy of Sciences; Shanghai Institute of
   Immunity and Infection, CAS
RP Li, B (corresponding author), Chinese Acad Sci, Inst Pasteur Shanghai, Unit Mol Immunol, Shanghai 200031, Peoples R China.
EM binli@sibs.ac.cn
RI Li, Dan/J-7581-2016; li, zhiyuan/M-5096-2015; Li, Bin/AAR-4966-2021
OI , li bin/0000-0002-7640-8884
FU National Basic Research Program of China (973 Program) [2014CB541803,
   2014CB541903, NSFC 81330072, 31370863, 31170825, 81271835, 31200646,
   81302532, 31300711, SMCST 14JC1406100]
FX The study is supported by National Basic Research Program of China (973
   Program) 2014CB541803, 2014CB541903, NSFC 81330072, 31370863, 31170825,
   81271835, 31200646, 81302532, 31300711, and SMCST 14JC1406100.
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NR 22
TC 71
Z9 84
U1 2
U2 43
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD OCT
PY 2015
VL 28
IS 2
SI SI
BP 859
EP 865
DI 10.1016/j.intimp.2015.03.044
PG 7
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA CT5NT
UT WOS:000362857800009
PM 25870037
DA 2025-06-01
ER

PT J
AU Chetty, R
   Serra, S
   Gauchotte, G
   Märkl, B
   Agaimy, A
AF Chetty, Runjan
   Serra, Stefano
   Gauchotte, Guillaume
   Maerkl, Bruno
   Agaimy, Abbas
TI Sclerosing nodular lesions of the gastrointestinal tract containing
   large numbers of IgG4 plasma cells
SO PATHOLOGY
LA English
DT Article
DE Fibrous nodules; reactive nodular pseudotumour; IgG4 plasma cells;
   polyps; gastrointestinal tract
ID FIBROUS PSEUDOTUMOR; AUTOIMMUNE PANCREATITIS; DISEASE; MESENTERY;
   SPECTRUM; ENTITY
AB Background: Hyalinised fibrous nodules have been encountered within the gastrointestinal tract (GIT) and been labelled as reactive nodular fibrous tumours. Several have a history of abdominal surgery and/or sepsis that acts as a precipitating cause for the fibrosis. Recently, much attention has been focused on IgG4 related fibrosing lesions that are typically associated with a high population of IgG4 positive plasma cells and tissue fibrosis. There may be attendant elevated serum IgG4 levels and associated autoimmune disease.
   Methods: We present four patients with well-circumscribed fibrous nodular lesions occurring in the GIT. Tissue was formalin fixed after microwave antigen retrieval and H&E stains and immunohistochemistry were performed. IgG4/IgG ratios were calculated from the three high power fields containing the densest concentration of positive plasma cells.
   Results: The patients were two females (45 and 56 years) and two males (47 and 60 years) who presented with gastric (2 cases), caecal and sigmoid flexure involvement. One case had four lesions while the other three cases were solitary nodules. Two patients had coexistent autoimmune disease. All lesions were nodular and composed of paucicellular, hyalinised fibrous tissue associated with chronic inflammation. In all lesions the plasma cell population was strongly IgG4 positive.
   Conclusions: This paper describes unique, well-circumscribed sclerosing nodules containing IgG4 positive plasma cells within the bowel wall that may cause mucosal polypoid lesions. It is possible that these lesions may be related to the spectrum of IgG4 related sclerosing disease or belong to a separate subset of inflammatory reactive conditions that are rich in IgG4 plasma cells.
C1 [Chetty, Runjan] Univ Glasgow, Dept Pathol, Glasgow G12 8QQ, Lanark, Scotland.
   [Serra, Stefano] Univ Hlth Network, Dept Pathol, Toronto, ON, Canada.
   [Serra, Stefano] Univ Toronto, Toronto, ON, Canada.
   [Gauchotte, Guillaume] Ctr Hosp Reg Univ, Dept Pathol, Nancy, France.
   [Maerkl, Bruno] Klinikum Augsburg, Inst Pathol, Augsburg, Germany.
   [Agaimy, Abbas] Univ Hosp, Inst Pathol, Erlangen, Germany.
C3 University of Glasgow; University of Toronto; University Health Network
   Toronto; University of Toronto; CHU de Nancy; Klinikum Augsburg;
   University of Erlangen Nuremberg
RP Chetty, R (corresponding author), Western Infirm & Associated Hosp, Dept Pathol & Gene Regulat, McGregor Bldg,Dumbarton Rd, Glasgow G11 6NT, Lanark, Scotland.
EM r.chetty@clinmed.gla.ac.uk
RI Märkl, Bruno/AAT-5038-2020
OI Markl, Bruno/0000-0002-7704-850X; serra, stefano/0000-0002-3258-2637
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NR 17
TC 53
Z9 55
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0031-3025
J9 PATHOLOGY
JI Pathology
PD JAN
PY 2011
VL 43
IS 1
BP 31
EP 35
DI 10.1097/PAT.0b013e328340e450
PG 5
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 704HA
UT WOS:000286040500005
PM 21240062
DA 2025-06-01
ER

PT J
AU Chu, HJ
   Cao, WK
   Chen, W
   Pan, SD
   Xiao, Y
   Liu, Y
   Gu, HY
   Guo, W
   Xu, L
   Hu, ZB
   Shen, H
AF Chu, Hongjun
   Cao, Weike
   Chen, Wei
   Pan, Shandong
   Xiao, Yong
   Liu, Yao
   Gu, Haiyong
   Guo, Wei
   Xu, Lin
   Hu, Zhibin
   Shen, Hongbing
TI Potentially functional polymorphisms in IL-23 receptor and risk of
   esophageal cancer in a Chinese population
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE IL-23R; polymorphism; esophageal cancer
ID GASTRIC-CANCER; INTERLEUKIN-23 RECEPTOR; ASSOCIATION; GENES; IL23R;
   IDENTIFICATION; VARIANTS; MULTIPLE; GROWTH
AB Interleukin-23 (IL-23)/IL-23 receptor (IL-23R) is essential for Th17 cell-mediated immune response, involved in autoimmune diseases and cancer pathogenesis. Two potentially functional genetic single nucleotide polymorphisms (SNPs; IL-23R rs6682925 T>C and rs1884444 T>G) were found to contribute to cancer susceptibility. In our study, we conducted a casecontrol study including 1,645 patients with esophageal cancer and 1,694 cancer-free controls in a Chinese population to assess the association between the two SNPs and the risk of esophageal cancer. We found that IL-23R rs6682925 TC/CC and rs1884444 TG/GG variant genotypes were associated with significantly increased risk of esophageal cancer [rs1884444: adjusted odds ratio (OR) = 1.16, 95% confidence intervals (CIs) =1.011.33; rs6682925: adjusted OR = 1.23, 95% CIs = 1.071.42], compared to their corresponding wild-type homozygotes. Furthermore, the increased risks associated with the two SNPs were independent from smoking and alcohol drinking status. These findings indicated that genetic variants in IL-23R may contribute to esophageal cancer risk in our Chinese population.
C1 [Chu, Hongjun; Cao, Weike; Guo, Wei; Hu, Zhibin; Shen, Hongbing] Nanjing Med Univ, Ctr Canc, Clin Epidemiol Sect, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Peoples R China.
   [Chu, Hongjun; Xiao, Yong] First Peoples Hosp HuaiAn, Dept Thorac Surg, Huaian, Peoples R China.
   [Cao, Weike] First Peoples Hosp HuaiAn, Dept Lab Diag, Huaian, Peoples R China.
   [Chen, Wei; Pan, Shandong; Liu, Yao; Hu, Zhibin; Shen, Hongbing] Nanjing Med Univ, Dept Epidemiol & Biostat, Sch Publ Hlth, Nanjing, Peoples R China.
   [Chen, Wei; Pan, Shandong; Liu, Yao; Hu, Zhibin; Shen, Hongbing] Nanjing Med Univ, Minist Educ, Key Lab Modern Toxicol, Sch Publ Hlth, Nanjing, Peoples R China.
   [Gu, Haiyong] Jiangsu Univ, Affiliated Peoples Hosp, Dept Thorac Surg, Zhenjiang, Peoples R China.
   [Xu, Lin] Jiangsu Canc Hosp, Dept Thorac Surg, Nanjing, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University; Ministry of
   Education - China; Nanjing Medical University; Jiangsu University;
   Nanjing Medical University
RP Shen, H (corresponding author), Nanjing Med Univ, Ctr Canc, Clin Epidemiol Sect, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Nanjing, Peoples R China.
EM zhibin_hu@njmu.edu.cn; hbshen@njmu.edu.cn
RI XU, Lin/HZL-5726-2023
FU National High Technology Research and Development Program of China
   [2009AA022706]
FX Grant sponsor: National High Technology Research and Development Program
   of China; Grant number: 2009AA022706
CR Cargill M, 2007, AM J HUM GENET, V80, P273, DOI 10.1086/511051
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NR 20
TC 34
Z9 34
U1 1
U2 75
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0020-7136
EI 1097-0215
J9 INT J CANCER
JI Int. J. Cancer
PD MAR 1
PY 2012
VL 130
IS 5
BP 1093
EP 1097
DI 10.1002/ijc.26130
PG 5
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 869MF
UT WOS:000298601500011
PM 21484795
OA Bronze
DA 2025-06-01
ER

PT J
AU Belkovets, AV
   Ozhiganova, NV
   Kruchinina, MV
   Polonskaya, YV
   Shcherbakova, LV
AF Belkovets, A. V.
   Ozhiganova, N. V.
   Kruchinina, M. V.
   Polonskaya, Ya. V.
   Shcherbakova, L. V.
TI Analyzing serological screening of the functional state of gastric
   mucosa in clinical practice
SO BYULLETEN SIBIRSKOY MEDITSINY
LA English
DT Article
DE pepsinogens; GastroPanel; GastroScreen-3; Helicobacterpylori; fundus
   atrophy; autoimmune gastritis
ID ATROPHIC GASTRITIS; BIOMARKERS; DIAGNOSIS; CANCER; PEPSINOGENS;
   POPULATION; ANTIBODIES
AB Aim. To analyze the results of the GastroPanel and GastroScreen-3 tests over a 15-year follow-up and determine the incidence of autoimmune gastritis (AIG) in clinical practice and in a random sample of Novosibirsk residents. Materials and methods. Biomarkers were analyzed in two groups: 1,742 people, average age of 50.0 +/- 13.53 years (GastroPanel test, Biohit Oy, Finland), and 170 people, average age of 53.8 +/- 12.89 years (GastroScreen-3 test, Vector-Best, Russia), from 2007 to 2022. The AIG incidence was calculated in current clinical practice and in a random sample of Novosibirsk residents aged 45-69 years. The PGI level of 160 mu g / l was taken as the upper limit of normal, PGI of 31-50 mu g / l indicated moderate atrophy, PGI < 30 <mu>g / l and the PGI / PGII ratio <= 3 indicated severe gastric fundus atrophy. AIG was considered at PGI <= 10.1 mu g / l, the PGI / PGI ratio <= 1.3, and gastrin-17 >= 42.4 pmol / l (GastroPanel) and at PGI <= 16.8 mu g / l and the PGI / PGII ratio <= 1.5 (GastroScreen-3). The H. pylori IgG level > 42 EIU was considered to be positive. Antibodies to CagA protein were determined using the HelicoBest Antibody test (Vector-Best, Novosibirsk). Results. Serological signs of severe and moderate gastric fundus atrophy were detected in 10 and 9.4% (GastroPanel test) and in 13.3 and 7% (GastroScreen-3 test) of those examined, respectively. Signs of multifocal atrophy were found in 0.7% of cases. Antibodies to H. pylori were detected in 57.7%, CagA+ strain - in 56.1% of cases. Peptic ulcer disease (PGI >= 160 mu g / l) was found in 15.3% (GastroPanel test) and 10% (GastroScreen-3 test) of the examined. According to the GastroPanel and GastroScreen-3 tests, the incidence of AIG was 1.6% in a random sample and 2.6 and 3.5% in current clinical practice, respectively. Conclusion. Twenty percent of the examined persons were at risk of developing gastric cancer and 10-15% had peptic ulcer disease, which requires further examination. The incidence of AIG in different study groups based on serological screening was 1.6-3.5%.
C1 [Belkovets, A. V.; Ozhiganova, N. V.; Kruchinina, M. V.; Polonskaya, Ya. V.; Shcherbakova, L. V.] Russian Acad Sci, Res Inst Internal & Prevent Med, Branch Inst Cytol & Genet, Siberian Branch, 175-1 B Bogatkova Str, Novosibirsk 630089, Russia.
   [Belkovets, A. V.; Kruchinina, M. V.] Novosibirsk State Med Univ, Dept Introduct Internal Dis, 52 Krasny Prospect, Novosibirsk 630091, Russia.
C3 Russian Academy of Sciences; Siberian Branch of the Russian Academy of
   Sciences; Novosibirsk State Medical University
RP Ozhiganova, NV (corresponding author), Russian Acad Sci, Res Inst Internal & Prevent Med, Branch Inst Cytol & Genet, Siberian Branch, 175-1 B Bogatkova Str, Novosibirsk 630089, Russia.
EM belkovets@gmx.de; natalya.safyanova@mail.ru; kruchmargo@yandex.ru;
   yana-polonskaya@yandex.ru; 9584792@mail.ru
RI Kruchinina, Margarita/A-7750-2014; Kashtanova, Elena/J-4675-2016;
   Polonskaa, Ana/H-4397-2016
OI Polonskaa, Ana/0000-0002-3538-0280; Serbakova, Lilia/0000-0001-9270-9188
CR Agréus L, 2012, SCAND J GASTROENTERO, V47, P136, DOI 10.3109/00365521.2011.645501
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   Biohit HealthCare, GastroPanel
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NR 23
TC 0
Z9 0
U1 0
U2 0
PU SIBERIAN STATE MEDICAL UNIV
PI TOMSK
PA UL LENINA 107, TOMSK, 63405, RUSSIA
SN 1682-0363
EI 1819-3684
J9 BYULLETEN SIB MED
JI BYULLETEN SIB. MED.
PY 2024
VL 23
IS 2
DI 10.20538/1682-0363-2024-2-21-27
PG 202
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA J7T2G
UT WOS:001339042100003
OA gold
DA 2025-06-01
ER

PT J
AU Renzullo, A
   Accardo, G
   Esposito, D
   De Bellis, A
   Bizzarro, A
   Romano, M
   Federico, A
   Gravina, AG
   Conzo, G
   Pannone, G
   Faggiano, A
   Colao, A
   Pasquali, D
AF Renzullo, A.
   Accardo, G.
   Esposito, D.
   De Bellis, A.
   Bizzarro, A.
   Romano, M.
   Federico, A.
   Gravina, A. G.
   Conzo, G.
   Pannone, G.
   Faggiano, A.
   Colao, A.
   Pasquali, D.
TI HASHIMOTO'S THYROIDITIS AND ENTERO-CHROMAFFIN-LIKE CELL HYPERPLASIA:
   EARLY DETECTION AND SOMATOSTATIN ANALOGUE TREATMENT
SO EUROPEAN JOURNAL OF INFLAMMATION
LA English
DT Article
DE Hashimoto's thyroiditis; chronic atrophic gastritis; hypergastrinemia;
   entero-chromaffin-like cells; somatostatin analogs
ID ATROPHIC BODY GASTRITIS; NEUROENDOCRINE TUMORS; EPIDEMIOLOGY
AB Type IIIb polyglandular autoimmune disease comprises autoimmune thyroid disease (HT) and chronic atrophic gastritis (AIG). Hypergastrinemia, secondary to AIG, predisposes to gastric enterochromaffin-like cell (ECL) hyperplasia, a preneoplastic condition. We evaluated the prevalence of AIG, hypergastrinemia and ECL hyperplasia in HT patients. A secondary end-point was to assess the efficacy of treatment with a somatostatin analogue in HT patient with ECL hyperplasia. From 2009 to 2011, 146 HT patients were enrolled in a prospective study. All cases underwent hormonal profile, and parietal cell antibody (PCA), gastrin, and chromogranin A (CgA) serum level assays. Selected patients with elevated gastrin and CgA levels underwent gastro esophageal endoscopy (EGDS). Patients positive for ECL hyperplasia received Octreotide LAR 30 mg/28 days for 12 months. Gastrin and CgA assays were repeated every three months and EGDS after one year. The results show that gastrin and CgA were significantly higher than normal in 17/115 (14.7%) patients. Seven more HT had isolated PCA positivity and in the 17 PCA positive patients histology diagnosed AIG, corpus prevalent, with mild to moderate atrophy. Diffuse ECL hyperplasia of the gastric body was present in three subjects, one of them presenting a type-1 carcinoid. Gastrin and CgA levels were significantly reduced (p<0.01) after 3 months of therapy with a somatostatin analogue and returned to normal after 1 year. ECL hyperplasia regressed in all three patients. We suggest that selected HT patients may need a more accurate surveillance for early signs of gastric EC risk. In the case of altered values of gastrin and in the presence of PCA positivity, EGDS and histology should be performed for an early diagnosis of AIG and treatment of ECL hyperplasia.
C1 [Renzullo, A.; Accardo, G.; Esposito, D.; De Bellis, A.; Bizzarro, A.; Pasquali, D.] Univ Naples 2, Dept Cardiothorac & Resp Sci, Endocrine Unit, I-80131 Naples, Italy.
   [Romano, M.; Federico, A.; Gravina, A. G.; Conzo, G.] Univ Naples 2, Dept Magrassi Lanzara, Gastroenterol Unit, I-80131 Naples, Italy.
   [Pannone, G.] Univ Foggia, Sect Biomorphol Stomatol & Reconstruct Sci, Dept Clin & Sperimental Med, Foggia, Italy.
   [Faggiano, A.; Colao, A.] Univ Naples Federico II, Dept Clin & Mol Endocrinol & Oncol, Naples, Italy.
C3 Universita della Campania Vanvitelli; Universita della Campania
   Vanvitelli; University of Foggia; University of Naples Federico II
RP Pasquali, D (corresponding author), Univ Naples 2, Bldg 16,Via Pansini 5, I-80131 Naples, Italy.
EM daniela.pasquali@unina2.it
RI Gravina, Antonietta Gerarda/AAC-1528-2019; De Bellis,
   Andrea/P-9670-2015; Federico, Alessandro/AAB-3893-2019; Colao,
   Annamaria/A-7671-2011; Faggiano, Antongiulio/K-7771-2016
OI DE BELLIS, Annamaria/0000-0002-0611-4506; Federico,
   Alessandro/0000-0002-0885-0793; Gravina, Antonietta
   Gerarda/0000-0001-8049-0115; Pasquali, Daniela/0000-0002-5674-635X;
   ROMANO, Marco/0000-0002-3271-349X; Faggiano,
   Antongiulio/0000-0002-9324-3946
FU PRIN from MIUR (Ministero dell'Istruzione dell'Universita e della
   Ricerca), Italy [prot. 2008LFK7J5_002]
FX This work was supported by Grant: PRIN 2008 prot. 2008LFK7J5_002 to DP
   from MIUR (Ministero dell'Istruzione dell'Universita e della Ricerca),
   Italy.
CR Armitage P., STAT METHODS MED RES
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NR 20
TC 5
Z9 5
U1 0
U2 8
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1721-727X
EI 2058-7392
J9 EUR J INFLAMM
JI Eur. J. Inflamm.
PD SEP-DEC
PY 2013
VL 11
IS 3
BP 863
EP 870
DI 10.1177/1721727X1301100329
PG 8
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 287HS
UT WOS:000329533300029
DA 2025-06-01
ER

PT J
AU Mete, O
   Asa, SL
AF Mete, Ozgur
   Asa, Sylvia L.
TI Precursor lesions of endocrine system neoplasms
SO PATHOLOGY
LA English
DT Article
DE Adenoma-carcinoma sequence; adrenal medullary hyperplasia; C-cell
   hyperplasia; DIPNECH; endocrine cell hyperplasia; follicular epithelial
   dysplasia; microadenoma; multiple endocrine neoplasia; neuroendocrine
   tumour; pituitary adenoma; precursor lesions; tumourlets
ID NEUROENDOCRINE CELL HYPERPLASIA; ZOLLINGER-ELLISON-SYNDROME; LYMPH-NODE
   METASTASIS; PARATHYROID CARCINOMA; ADRENOCORTICAL TUMORS; GERMLINE
   MUTATION; THYROID-NODULES; PAPILLARY CARCINOMA; GASTRIC CARCINOIDS;
   MOLECULAR-GENETICS
AB The concept of precursor lesions of endocrine neoplasms is a new and interesting topic in endocrine pathology. A variety of clinicopathological conditions are associated with a sequence of cellular changes from hyperplasia to neoplasia; dysplasia is, in contrast, quite rare. The majority of precursor lesions is associated with familial genetic syndromes. These include C-cell hyperplasia in thyroid that is associated with familial medullary thyroid carcinoma, adrenal medullary hyperplasia as a precursor of phaeochromocytomas in MEN2 syndrome, rare pituitary adenohypophyseal cell hyperplasia in familial syndromes associated with pituitary adenomas, MEN1-related precursor gastric enterochromaffin-like cell (ECL) hyperplasia, and duodenal gastrin producing (G) and/or somatostatin producing (D) cell hyperplasia that give rise to type II gastric neuroendocrine tumours (NETs) and duodenal NETs, respectively, and MEN1- or VHL-related islet hyperplasia, islet dysplasia and ductulo-insular complexes that are associated with pancreatic NETs. Other hyperplasias are not thought to be associated with genetic predisposition. Some are attributed to inflammation; autoimmune chronic atrophic gastritis-related ECL hyperplasia can progress to type I gastric NETs, and EC (enterochromaffin) cell or L cell hyperplasia associated with inflammatory bowel diseases can progress to colorectal NETs. In the lung, diffuse idiopathic pulmonary neuroendocrine cell hyperplasia can give rise to peripherally-located low grade pulmonary NETs and tumourlets (neuroendocrine microtumours <5 mm). Rarely, secondary hyperplasias develop into autonomous neoplasms, as in tertiary hyperparathyroidism or pituitary thyrotroph adenomas in primary hypothyroidism. While some precursor lesions, such as thyroid C cell hyperplasia, represent frankly premalignant conditions, others may represent a sequence of proliferative changes from hyperplasia to benign neoplasia that may also progress to malignancy.
C1 [Mete, Ozgur; Asa, Sylvia L.] Univ Hlth Network, Dept Pathol, Toronto, ON M5G 2C4, Canada.
   [Mete, Ozgur; Asa, Sylvia L.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
C3 University of Toronto; University Health Network Toronto; University of
   Toronto
RP Mete, O (corresponding author), Univ Hlth Network, Dept Pathol, 200 Elizabeth St,11th Floor, Toronto, ON M5G 2C4, Canada.
EM ozgur.mete2@uhn.ca
RI ; Asa, Sylvia L./ACI-8408-2022
OI Mete, Ozgur/0000-0003-0469-2801; Asa, Sylvia L./0000-0001-8418-5054
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NR 129
TC 59
Z9 60
U1 0
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0031-3025
EI 1465-3931
J9 PATHOLOGY
JI Pathology
PD APR
PY 2013
VL 45
IS 3
BP 316
EP 330
DI 10.1097/PAT.0b013e32835f45c5
PG 15
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 107TT
UT WOS:000316244400011
PM 23478233
DA 2025-06-01
ER

PT J
AU Alakoski, A
   Salmi, TT
   Hervonen, K
   Kautiainen, H
   Salo, M
   Kaukinen, K
   Reunala, T
   Collin, P
AF Alakoski, Anna
   Salmi, Teea T.
   Hervonen, Kaisa
   Kautiainen, Hannu
   Salo, Maarit
   Kaukinen, Katri
   Reunala, Timo
   Collin, Pekka
TI Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study
SO CLINICAL & DEVELOPMENTAL IMMUNOLOGY
LA English
DT Article
ID HELICOBACTER-PYLORI INFECTION; GLUTEN-FREE DIET; ATROPHIC CORPUS
   GASTRITIS; CELIAC-DISEASE; ADULT-POPULATION; SKIN-LESIONS; FINLAND;
   TRANSGLUTAMINASE; AUTOANTIGEN; PREVALENCE
AB Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia. Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, and Helicobacter pylori. Duodenal biopsies were taken. Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp., P < 0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%, P = 0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P = 0.038) and H. pylori in 17 (18.3%) and 17 (9.3%) (P = 0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer. Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum. H. pylori will partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.
C1 [Salmi, Teea T.; Hervonen, Kaisa; Kaukinen, Katri; Reunala, Timo; Collin, Pekka] Univ Tampere, Sch Med, Tampere 33014, Finland.
   [Alakoski, Anna; Salmi, Teea T.; Hervonen, Kaisa; Reunala, Timo] Tampere Univ Hosp, Dept Dermatol, Tampere 33521, Finland.
   [Kautiainen, Hannu] Cent Finland Cent Hosp, Unit Family Practice, Kuopio 70211, Finland.
   [Kautiainen, Hannu] Kuopio Univ Hosp, Unit Primary Hlth Care, Kuopio 70211, Finland.
   [Salo, Maarit] Valkeakoski Reg Hosp, Dept Med, Valkeakoski 37600, Finland.
   [Kaukinen, Katri; Collin, Pekka] Tampere Univ Hosp, Dept Gastroenterol & Alimentary Tract Surg, Tampere 33521, Finland.
C3 Tampere University; Tampere University; Tampere University Hospital;
   Central Finland Central Hospital; Kuopio University Hospital; University
   of Eastern Finland; University of Eastern Finland Hospital; Tampere
   University; Tampere University Hospital
RP Collin, P (corresponding author), Univ Tampere, Sch Med, Tampere 33014, Finland.
EM pekka.collin@uta.fi
RI Salmi, Teea/HNQ-4705-2023
FU Tampere University Hospital [9L006, 9F063, 9M034, 9N062]
FX This study was financially supported by the Competitive Research Funding
   of the Tampere University Hospital (Grants 9L006, 9F063, 9M034, and
   9N062).
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NR 30
TC 14
Z9 14
U1 0
U2 2
PU HINDAWI PUBLISHING CORPORATION
PI NEW YORK
PA 410 PARK AVENUE, 15TH FLOOR, #287 PMB, NEW YORK, NY 10022 USA
SN 1740-2522
J9 CLIN DEV IMMUNOL
JI Clin. Dev. Immunol.
PY 2012
AR 640630
DI 10.1155/2012/640630
PG 5
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 938RF
UT WOS:000303749900001
OA Green Submitted, gold, Green Published
DA 2025-06-01
ER

PT J
AU Letko, E
   Gürcan, HM
   Papaliodis, GN
   Christen, W
   Foster, CS
   Ahmed, AR
AF Letko, E.
   Guercan, H. M.
   Papaliodis, G. N.
   Christen, W.
   Foster, C. S.
   Ahmed, A. R.
TI Relative risk for cancer in mucous membrane pemphigoid associated with
   antibodies to the β4 integrin subunit
SO CLINICAL AND EXPERIMENTAL DERMATOLOGY
LA English
DT Article
ID TERM-FOLLOW-UP; GASTRIC-CARCINOMA; INTRAVENOUS IMMUNOGLOBULIN;
   ANTIEPILIGRIN LAMININ-5; LUNG-CARCINOMA; EPILIGRIN; AUTOANTIBODIES;
   AUTOIMMUNE; INVASION; RECEPTOR
AB Background Mucous membrane pemphigoid (MMP) is a mucocutaneous vesiculobullous autoimmune disease characterized by autoantibodies to components of the basement membrane zone (BMZ). Recently, it has been reported that patients with MMP who have autoantibodies to laminin 5, known as anti-epiligrin cicatricial pemphigoid (AECP) have a high incidence of malignancy.
   Objective The purpose of this study was to determine the association between malignancy and MMP in patients with antibodies to beta 4 integrin.
   Methods The incidence of cancer was studied in 79 patients with MMP and/or ocular cicatricial pemphigoid (OCP) who had antibodies to human beta 4 integrin subunit. In each patient, the diagnosis was made by histology and confirmed by immunopathology of affected tissues. It was compared to the expected incidence, for age- and gender-matched individuals, in the National Cancer Institute's Surveillance, Epidemiology and End Results (NCISEER) database.
   Results Of 79 patients, 3 had cancer. The relative risk (RR) for cancer in patients with MMP and/or OCP, with autoantibodies to human beta 4 integrin subunit was 0.29 (95% CI 0.62-8.77). The expected number in the NCISEER database was 10.37. This difference was statistically significant (P < 0.01).
   Conclusions This incidence of cancer in MMP/OCP patients, with antibodies to human beta 4 integrin subunit is considerably lower than expected. Preliminary observations in this and other studies suggest that serological subsets of MMP, based on antigen reactivity, have a different clinical course, prognosis and associations with cancer.
C1 New England Baptist Hosp, Ctr Blistering Dis, Boston, MA 02120 USA.
   Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Immunol & Uveitis Serv, Boston, MA USA.
   Harvard Univ, Sch Med, Dept Ophthalmol, Boston, MA USA.
   Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
C3 New England Baptist Hospital; Harvard University; Harvard University
   Medical Affiliates; Massachusetts Eye & Ear Infirmary; Harvard Medical
   School; Harvard University; Harvard Medical School; Harvard University;
   Harvard University Medical Affiliates; Brigham & Women's Hospital
RP Gürcan, HM (corresponding author), New England Baptist Hosp, Ctr Blistering Dis, 70 Parker Hill Ave,Suite 208, Boston, MA 02120 USA.
EM arahmedmd@msn.com
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NR 25
TC 18
Z9 18
U1 0
U2 2
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0307-6938
EI 1365-2230
J9 CLIN EXP DERMATOL
JI Clin. Exp. Dermatol.
PD NOV
PY 2007
VL 32
IS 6
BP 637
EP 641
DI 10.1111/j.1365-2230.2007.02463.x
PG 5
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA 221UI
UT WOS:000250252400003
PM 17524068
DA 2025-06-01
ER

PT J
AU Miao, Q
   Zheng, ZQ
   Piao, MY
   Cao, HL
   Wang, BM
   Liu, WT
AF Miao, Qian
   Zheng, Zhongqing
   Piao, Meiyu
   Cao, Hailong
   Wang, Bangmao
   Liu, Wentian
TI Case report: Upper gastrointestinal bleeding associated with pancreatic
   segmental portal hypertension: six case reports and literature review
SO FRONTIERS IN MEDICINE
LA English
DT Article
DE pancreatic segmental portal hypertension; upper gastrointestinal
   bleeding; splenectomy; splenic artery embolization; case report
ID SPLENIC ARTERIAL EMBOLIZATION; GASTRIC VARICES; VEIN-THROMBOSIS;
   MANAGEMENT; INJECTION
AB Background Pancreatic segmental portal hypertension (PSPH) is a clinical syndrome in which splenic vein hypertension is caused by obstruction, stenosis, or thrombosis of the splenic veins in the primary pancreatic disease. Gastrointestinal hemorrhage caused by gastric varices (GVs) is one of the life-threatening complications in the patients with left portal hypertension. The aim was to report our experience and discuss the manifestations, management, and prognosis of PSPH with upper gastrointestinal bleeding (UGIB).Method We retrospectively analyzed six patients with PSPH and UGIB in our department. The clinical data were collected such as demographic information, medical history, and clinical presentation.Result The autoimmune pancreatitis, pancreatic tumor, pancreatic surgery, chronic pancreatitis and pancreatic pseudocyst were diagnosed in six patients, respectively. Five patients presented with hematemesis and/or melena on admission, and one patient presented with fatigue. All patients had isolated GVs. Follow-up patients were treated with portal vein stenting in one case, laparoscopic splenectomy in two cases, endoscopic gastric fundic vein embolization and injection of Cyanoacrylate Glue in one case, and improvement in conservative treatment in two cases. All patients were alive at the last follow-up.Conclusion PSPH should be seriously considered in patients with pancreatic disease with isolated GVs. It is particularly important to choose specific approaches for individual cases based on the primary disease, the severity of varicose veins and the general condition of the patients.
C1 [Miao, Qian; Zheng, Zhongqing; Piao, Meiyu; Cao, Hailong; Wang, Bangmao; Liu, Wentian] Tianjin Med Univ, Gen Hosp, Tianjin Inst Digest Dis,Dept Gastroenterol & Hepat, Tianjin Key Lab Digest Dis,Natl Key Clin Specialty, Tianjin, Peoples R China.
C3 Tianjin Medical University
RP Liu, WT (corresponding author), Tianjin Med Univ, Gen Hosp, Tianjin Inst Digest Dis,Dept Gastroenterol & Hepat, Tianjin Key Lab Digest Dis,Natl Key Clin Specialty, Tianjin, Peoples R China.
EM tliu01@tmu.edu.cn
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NR 38
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 2296-858X
J9 FRONT MED-LAUSANNE
JI Front. Med.
PD FEB 19
PY 2025
VL 12
AR 1522413
DI 10.3389/fmed.2025.1522413
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA Z1W6R
UT WOS:001436899500001
PM 40046926
OA gold
DA 2025-06-01
ER

PT J
AU Katsara, M
   Tselios, T
   Deraos, S
   Deraos, G
   Matsoukas, MT
   Lazoura, E
   Matsoukas, J
   Apostolopoulos, V
AF Katsara, Maria
   Tselios, Theodore
   Deraos, Spyros
   Deraos, George
   Matsoukas, Minos-Timotheos
   Lazoura, Eliada
   Matsoukas, John
   Apostolopoulos, Vasso
TI Round and round we go: Cyclic peptides in disease
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE cyclic peptides; myelin epitopes; angiotensin II; thrombin; gonadotropin
   releasing hormone
ID ALPHA-AMYLASE INHIBITOR; BASIC-PROTEIN EPITOPE;
   SER(42)-PHE-LEU-LEU-ARG(46) MOTIF SEQUENCE; EXPERIMENTAL ALLERGIC
   ENCEPHALOMYELITIS; RECEPTOR-DERIVED POLYPEPTIDES; FUNCTIONAL THROMBIN
   RECEPTOR; TERMINAL AROMATIC RESIDUE; CENTRAL-NERVOUS-SYSTEM; GASTRIC
   SMOOTH-MUSCLE; SYNOVIAL-FLUID CELLS
AB There is a need for novel drugs for the treatment of infectious diseases, autoimmunity and cancer. Cyclic peptides constitute a class of compounds that have made crucial contributions to the treatment of certain diseases. Penicillin, Vancomycin, Cyclosporin, the Echinocandins and Bleomycin are well-known cyclic peptides. Cyclic peptides, compared to linear peptides, have been considered to have greater potential as therapeutic agents due to their increased chemical and enzymatic stability, receptor selectively, and improved pharmacodynamic properties. They have been used as synthetic immunogens, transmembrane ion channels, antigens for Herpes Simplex Virus, potential immunotherapeutic vaccines for diabetes and Experimental Autoimmune Encephalomyelitis - an animal model of Multiple Sclerosis, as inhibitors against a-amylase and as protein stabilizers. Herein, we review important cyclic peptides as therapeutic agents in disease.
C1 Burnet Inst Austin, Immunol & Vaccine Lab, Heidelberg, Vic 3084, Australia.
   Univ Patras, Dept Chem, Sect Organ Chem Biochem & Nat Prod, GR-26500 Patras, Greece.
C3 Burnet Institute; University of Patras
RP Apostolopoulos, V (corresponding author), Burnet Inst Austin, Immunol & Vaccine Lab, Studley Rd, Heidelberg, Vic 3084, Australia.
EM vasso@burnet.edu.au
RI Apostolopoulos, Vasso/Q-4525-2019; Matsoukas, John/AAN-5039-2020;
   Deraos, George/AAN-1822-2020; Matsoukas, Minos-Timotheos/B-8746-2012
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NR 104
TC 136
Z9 143
U1 1
U2 63
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 0929-8673
EI 1875-533X
J9 CURR MED CHEM
JI Curr. Med. Chem.
PY 2006
VL 13
IS 19
BP 2221
EP 2232
DI 10.2174/092986706777935113
PG 12
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
   Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 066VN
UT WOS:000239258500001
PM 16918350
DA 2025-06-01
ER

PT J
AU Inagaki, H
AF Inagaki, Hiroshi
TI Mucosa-associated lymphoid tissue lymphoma: Molecular pathogenesis and
   clinicopathological significance
SO PATHOLOGY INTERNATIONAL
LA English
DT Review
DE API2-MALT1 fusion; autoimmune disease; chronic inflammation; cytogenetic
   alterations; Helicobacter pylori; lung; mucosa-associated lymphoid
   tissue (MALT) lymphoma; NF-kappa B; stomach; t(11 ; 18)(q21 ; q21)
ID B-CELL LYMPHOMA; HELICOBACTER-PYLORI ERADICATION; GASTRIC MALT LYMPHOMA;
   NF-KAPPA-B; SPLENIC MARGINAL ZONE; API2-MALT1 FUSION TRANSCRIPTS;
   NON-HODGKINS-LYMPHOMAS; IN-SITU HYBRIDIZATION; LOW-GRADE; CHROMOSOMAL
   TRANSLOCATION
AB Mucosa-associated lymphoid tissue (MALT) lymphoma is a low-grade tumor closely associated with chronic inflammation such as that of Helicobacter pylori gastritis, Sjogren's syndrome, and Hashimoto's thyroiditis. Tumor regression by H. pylori eradication alone is well known in gastric MALT lymphoma, but some tumors occur in the absence of pre-existing chronic inflammation. The understanding of MALT lymphoma biology has significantly improved, and recurrent cytogenetic alterations have been detected. These include the trisomies 3 and 18, and the translocations t(11;18)(q21;q21), t(1;14)(p22;q32), t(14;18)(q32;q21), and t(3;14)(p14.1;q32). At least some of these alterations result in the constitutive activation of the nuclear factor (NF)-kappa B pathway, and may exert anti-apoptotic action. Apoptosis inhibitor 2-MALT lymphoma-associated translocation 1 (API12-MALT1) fusion, resulting from t(11;18)(q21;q21), is specific to, and is the most common in, MALT lymphomas, and its clinicopathological significance has been studied extensively. The focus of the present review is on the recent progress made in elucidating MALT lymphomagenesis and its clinicopathological impact, especially in terms of the effect of API2-MALT1 fusion on this unique tumor.
C1 Nagoya City Univ, Grad Sch Med Sci, Dept Pathol, Mizuho Ku, Nagoya, Aichi 4678601, Japan.
C3 Nagoya City University
RP Inagaki, H (corresponding author), Nagoya City Univ, Grad Sch Med Sci, Dept Pathol, Mizuho Ku, 1 Kawasumi, Nagoya, Aichi 4678601, Japan.
EM hinagaki@med.nagoya-cu.ac.jp
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NR 131
TC 52
Z9 60
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1320-5463
EI 1440-1827
J9 PATHOL INT
JI Pathol. Int.
PD AUG
PY 2007
VL 57
IS 8
BP 474
EP 484
DI 10.1111/j.1440-1827.2007.02128.x
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 185IG
UT WOS:000247704000002
PM 17610471
DA 2025-06-01
ER

PT J
AU Shinohara, S
   Hanagiri, T
   So, T
   Yasuda, M
   Takenaka, M
   Nagata, Y
   Shimokawa, H
   Nakagawa, M
   Uramoto, H
   So, T
   Tanaka, F
AF Shinohara, Shinji
   Hanagiri, Takeshi
   So, Tetsuya
   Yasuda, Manabu
   Takenaka, Masaru
   Nagata, Yoshika
   Shimokawa, Hidehiko
   Nakagawa, Makoto
   Uramoto, Hidetaka
   So, Tomoko
   Tanaka, Fumihiro
TI Results of surgical resection for patients with thymoma according to
   World Health Organization histology and Masaoka staging
SO ASIAN JOURNAL OF SURGERY
LA English
DT Article
DE autoimmune disease; mediastinal tumor; prognosis; surgical resection;
   thymoma
ID MULTIDISCIPLINARY TREATMENT; POSTOPERATIVE RADIOTHERAPY; ADJUVANT
   RADIATION; MALIGNANT THYMOMA; II THYMOMA; CLASSIFICATION; THERAPY;
   DISEASE
AB Objectives: Thymomas are relatively rare tumors. In this study, we investigated the clinical features of patients who underwent surgical resection for thymoma.
   Patients and methods: This study clinicopathologically evaluated 54 consecutive patients who underwent a surgical resection of thymoma in our department between 1994 and 2006.
   Results: A complete resection was performed in 52 patients, while two patients underwent an incomplete resection due to pleural dissemination. Combined resection with adjacent organs was performed for the lung (n = 6), pericardium (n = 5), and large vessels (brachiocephalic vein in three, superior vena cava in two). The concomitant autoimmune diseases were observed in 20 patients (37%), and they included myasthenia gravis in 17 patients, macroglobulinemia in one, pemphigus vulgaris in one, and stiff person syndrome in one patient. The histologic types of the World Health Organization classification diagnosed as type A in four patients, type AB in 14, type B1 in eight, type B2 in 15, and type B3 in 11. There were 27, 17, eight, and two patients with Masaoka stages I, II, III, and IV, respectively. Four patients died, and the causes of death included recurrence of thymoma in two, gastric carcinoma in one, and respiratory failure due to myasthenia gravis in one patient. The overall survival rate at 10 years was 94.6% in patients with stages I and II disease and 77.1% in patients with stages III and IV disease.
   Conclusions: Long-term survival can be expected not only for patients at early stages, as well as for patients with stages III and IV disease if surgical resection is completed macroscopically. Copyright (c) 2012, Asian Surgical Association. Published by Elsevier Taiwan LLC. All rights reserved.
C1 [Hanagiri, Takeshi] Univ Occupat & Environm Hlth, Sch Med, Dept Surg 2, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan.
C3 University of Occupational & Environmental Health - Japan
RP Hanagiri, T (corresponding author), Univ Occupat & Environm Hlth, Sch Med, Dept Surg 2, Yahatanishi Ku, 1-1 Iseigaoka, Kitakyushu, Fukuoka 8078555, Japan.
EM hanagiri@med.uoeh-u.ac.jp
FU University of Occupational and Environmental Health (UOEH) Research
   Grant for the Promotion of Occupational Health; Grant-in-Aid for
   scientific research from the Ministry of Education, Culture, Sports,
   Science and Technology, Japan
FX This study was supported in part by a University of Occupational and
   Environmental Health (UOEH) Research Grant for the Promotion of
   Occupational Health and Grant-in-Aid for scientific research from the
   Ministry of Education, Culture, Sports, Science and Technology, Japan.
CR Chang JH, 2011, J THORAC ONCOL, V6, P1282, DOI 10.1097/JTO.0b013e31821f9662
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NR 25
TC 8
Z9 9
U1 0
U2 6
PU ELSEVIER SINGAPORE PTE LTD
PI SINGAPORE
PA 3 KILLINEY ROAD 08-01, WINSLAND HOUSE 1, SINGAPORE, 239519, SINGAPORE
SN 1015-9584
J9 ASIAN J SURG
JI Asian J. Surg.
PD OCT
PY 2012
VL 35
IS 4
BP 144
EP 148
DI 10.1016/j.asjsur.2012.08.005
PG 5
WC Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Surgery
GA 036EW
UT WOS:000311010200004
PM 23063086
DA 2025-06-01
ER

PT J
AU Yu, TF
   Wu, YX
   Liu, J
   Zhuang, YY
   Jin, XY
   Wang, LY
AF Yu, Tingfeng
   Wu, Yaxian
   Liu, Jia
   Zhuang, Yanyan
   Jin, Xiaoyan
   Wang, Lingyun
TI The risk of malignancy in patients with IgG4-related disease: a
   systematic review and meta-analysis
SO ARTHRITIS RESEARCH & THERAPY
LA English
DT Review
DE IgG4-RD; Malignancy; SIR; Meta-analysis
ID TYPE-1 AUTOIMMUNE PANCREATITIS; RETROSPECTIVE-ANALYSIS; CANCER;
   ASSOCIATION; DIAGNOSIS
AB Background The relationship between IgG4-related disease (IgG4-RD) and the risk of malignancy is still controversial. This article focused on assessing the risk of cancer in patients with IgG4-RD by meta-analysis. Methods We conducted a systematic review of the literature and meta-analysis characterizing the associated risk of overall malignancy and four site-specific malignancies (pancreas, lung, gastric and lymphoma) in patients with IgG4-RD. A search from 2003 to 2020 was performed using specified terms from PubMed, Embase, Web of Science and SinoMed. Random-effects model analysis was used to pool standardized incidence ratios (SIRs) and 95% confidence intervals (CIs). Subgroup and sensitivity analyses were conducted to clarify the heterogeneity of the included studies. Begg's funnel plot and Egger's linear regression test were used to evaluate the bias of the meta-analysis. A P value < 0.05 indicated the existence of publication bias. Results A total of 10 studies were included in the article. The overall SIR estimates suggested an increased risk of overall cancer in IgG4-RD patients (SIR 2.57 95% CI 1.72-3.84) compared with the general population. The specific SIRs for pancreas and lymphoma were higher than those of the general population in IgG4-RD patients (SIR 4.07 95% CI 1.04-15.92, SIR 69.17 95% CI 3.91-1223.04, respectively). No significant associations were revealed in respiratory and gastric cancer (SIR 2.14 95% CI 0.97-4.75, SIR 0.95 95% CI 0.24-3.95, respectively). Four studies were found to be the major sources of heterogeneity by sensitivity analysis. There was no evidence of publication bias via Egger's test. Conclusion Compared with the general population, patients with IgG4-RD appear to have a higher risk of overall cancer, especially pancreatic and lymphoma. The risk of lung and gastric cancer was not different between IgG4-RD patients and the general population.
C1 [Yu, Tingfeng; Wu, Yaxian; Liu, Jia; Zhuang, Yanyan; Wang, Lingyun] Sun Yat Sen Mem Hosp, Dept Gastroenterol, Guangzhou, Peoples R China.
   [Jin, Xiaoyan] Sun Yat Sen Mem Hosp, Dept Gen Practice, Guangzhou, Peoples R China.
C3 Sun Yat Sen University; Sun Yat Sen University
RP Wang, LY (corresponding author), Sun Yat Sen Mem Hosp, Dept Gastroenterol, Guangzhou, Peoples R China.; Jin, XY (corresponding author), Sun Yat Sen Mem Hosp, Dept Gen Practice, Guangzhou, Peoples R China.
EM jinxy@mail.sysu.edu.cn; wanglyun@mail.sysu.edu.cn
RI Jin, Xiaoyan/LCD-9031-2024
FU Medical Research Foundation of Guangdong Province [C2018059]; Guangzhou
   Science and Technology Project [201704020121]
FX This work was supported by the Medical Research Foundation of Guangdong
   Province (Grant numbers: C2018059) and the Guangzhou Science and
   Technology Project (Grants 201704020121). The funding organization was
   not involved in the design of the study or collection, analysis and
   interpretation of data or in writing the manuscript.
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NR 48
TC 52
Z9 52
U1 0
U2 11
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1478-6354
EI 1478-6362
J9 ARTHRITIS RES THER
JI Arthritis Res. Ther.
PD JAN 5
PY 2022
VL 24
IS 1
AR 14
DI 10.1186/s13075-021-02652-2
PG 9
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA YC0MS
UT WOS:000739395000001
PM 34986892
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Takuse, Y
   Watanabe, M
   Inoue, N
   Ozaki, R
   Ohtsu, H
   Saeki, M
   Katsumata, Y
   Hidaka, Y
   Iwatani, Y
AF Takuse, Yukina
   Watanabe, Mikio
   Inoue, Naoya
   Ozaki, Ritsuko
   Ohtsu, Hiroshi
   Saeki, Minori
   Katsumata, Yuka
   Hidaka, Yoh
   Iwatani, Yoshinori
TI Association of IL-10-Regulating MicroRNAs in Peripheral Blood
   Mononuclear Cells with the Pathogenesis of Autoimmune Thyroid Disease
SO IMMUNOLOGICAL INVESTIGATIONS
LA English
DT Article
DE Graves' disease; Hashimoto's; disease; IL-10; miRNA; polymorphism
ID CIRCULATING MICRORNA; GASTRIC-CANCER; GRAVES-DISEASE; EXPRESSION;
   INTERLEUKIN-10; POLYMORPHISMS; DIFFERENTIATION; SUSCEPTIBILITY;
   BIOGENESIS; PROPORTION
AB Interleukin (IL)-10 is known to suppress inflammation in autoimmune diseases. IL-10 can be regulated by miRNAs. To elucidate the involvement of miRNAs that regulate IL-10 expression with the pathogenesis of autoimmune thyroid disease (AITD), we examined the expression levels of hsa-miR-27a-3p, hsa-miR-98-5p, hsa-miR-106a-5p, and hsamiR- 223-3p in peripheral blood mononuclear cells (PBMCs) from 43 patients with Graves' disease (GD), 38 patients with Hashimoto's disease (HD), and 21 healthy volunteers. We evaluated the association between the expression levels of four miRNAs and intracellular expression of IL-10 in PBMCs from 11 healthy volunteers. We also genotyped MIR27A rs895819 G/A and MIR106A rs3747440 C/G polymorphisms, which may be related to the expression of these miRNAs in 141 patients with GD, 178 patients with HD, and 84 healthy volunteers. The expression level of hsa-miR-106a-5p was significantly higher in patients with intractable GD than in those with GD in remission (p = 0.0113). The expression level of hsa-miR-223-3p was significantly lower in GD than in HD and lower in patients with intractable GD than in healthy volunteers (p = 0.0094, 0.0340). We found a negative correlation between the expression levels of hsa-miR-98-5p and the proportions of IL-10(+) cells in stimulated PBMCs from healthy volunteers (p = 0.0092). The G allele of the MIR27A polymorphism was significantly more frequent in patients with mild HD than in healthy volunteers (p = 0.0432). In conclusion, the expression levels of hsa-miR106a- 5p and hsa-miR-223-3p were associated with the pathogenesis of AITDs. hsa-miR-98-5p may negatively regulate the expression of IL-10. The functional polymorphism of MIR27A was associated with HD severity.
C1 [Takuse, Yukina; Watanabe, Mikio; Inoue, Naoya; Ozaki, Ritsuko; Ohtsu, Hiroshi; Saeki, Minori; Katsumata, Yuka; Iwatani, Yoshinori] Osaka Univ, Grad Sch Med, Dept Biomed Informat, Div Hlth Sci, Yamadaoka 1-7, Suita, Osaka 5650871, Japan.
   [Inoue, Naoya; Hidaka, Yoh] Osaka Univ Hosp, Lab Clin Invest, Suita, Osaka, Japan.
C3 The University of Osaka; The University of Osaka
RP Iwatani, Y (corresponding author), Osaka Univ, Grad Sch Med, Dept Biomed Informat, Div Hlth Sci, Yamadaoka 1-7, Suita, Osaka 5650871, Japan.
EM iwatani@sahs.med.osaka-u.ac.jp; iwatani@sahs.med.osaka-u.ac.jp
RI WATANABE, Mikio/AFK-8755-2022
FU Japan Society for the Promotion of Science (JSPS) KAKENHI [JP26293128];
   Grants-in-Aid for Scientific Research [17H04111] Funding Source: KAKEN
FX This work was supported by Japan Society for the Promotion of Science
   (JSPS) KAKENHI (grant number: JP26293128).
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NR 38
TC 19
Z9 22
U1 0
U2 5
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0882-0139
EI 1532-4311
J9 IMMUNOL INVEST
JI Immunol. Invest.
PY 2017
VL 46
IS 6
BP 590
EP 602
DI 10.1080/08820139.2017.1322975
PG 13
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FC0RM
UT WOS:000406546400006
PM 28742402
DA 2025-06-01
ER

PT J
AU Müller, A
   Oertli, M
   Arnold, IC
AF Mueller, Anne
   Oertli, Mathias
   Arnold, Isabelle C.
TI H. pylori exploits and manipulates innate and adaptive
   immune cell signaling pathways to establish persistent infection
SO CELL COMMUNICATION AND SIGNALING
LA English
DT Review
DE immune evasion; innate immune signaling; immunomodulation; persistent
   infection
ID REGULATORY T-CELLS; HELICOBACTER-PYLORI; VACUOLATING TOXIN;
   EPITHELIAL-CELLS; BACTERIAL PEPTIDOGLYCAN; ANTIBODIES IMPAIR; NOD1;
   ACTIVATION; RESPONSES; ASTHMA
AB Persistent infection with the gastric bacterial pathogen Helicobacter pylori causes gastritis and predisposes carriers to a high gastric cancer risk, but has also been linked to protection from allergic, chronic inflammatory and autoimmune diseases. In the course of tens of thousands of years of co-existence with its human host, H. pylori has evolved elaborate adaptations that allow it to persist in the hostile environment of the stomach in the face of a vigorous innate and adaptive immune response. For this review, we have identified several key immune cell types and signaling pathways that appear to be preferentially targeted by the bacteria to establish and maintain persistent infection. We explore the mechanisms that allow the bacteria to avoid detection by innate immune cells via their pattern recognition receptors, to escape T-cell mediated adaptive immunity, and to reprogram the immune system towards tolerance rather than immunity. The implications of the immunomodulatory properties of the bacteria for the prevention of allergic and auto-immune diseases in chronically infected individuals are also discussed.
C1 [Mueller, Anne; Oertli, Mathias; Arnold, Isabelle C.] Univ Zurich, Inst Mol Canc Res, Zurich, Switzerland.
   [Arnold, Isabelle C.] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
C3 University of Zurich; University of Oxford
RP Müller, A (corresponding author), Univ Zurich, Inst Mol Canc Res, Zurich, Switzerland.
EM mueller@imcr.uzh.ch
RI Arnold, Isabelle/JMB-4984-2023
OI Arnold, Isabelle C./0000-0001-8679-9666; Muller,
   Anne/0000-0002-1368-8276
FU University of Zurich; Swiss National Science Foundation; Swiss and
   Zurich Cantonal Cancer Leagues
FX Work in the laboratory of A.M. is supported by the University of Zurich
   Research Priority Program in Systems Biology, the Swiss National Science
   Foundation and the Swiss and Zurich Cantonal Cancer Leagues.
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NR 56
TC 66
Z9 72
U1 0
U2 16
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1478-811X
J9 CELL COMMUN SIGNAL
JI Cell Commun. Signal.
PD NOV 1
PY 2011
VL 9
AR 25
DI 10.1186/1478-811X-9-25
PG 9
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 846OI
UT WOS:000296912700001
PM 22044597
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Alfurjani, BH
   Sabi, SH
   Almaaytah, AM
   Masadeh, MM
   Abualhaijaa, AK
AF Alfurjani, Batool H.
   Sabi, Salsabeel H.
   Almaaytah, Ammar M.
   Masadeh, Majd M.
   Abualhaijaa, Ahmad K.
TI Helicobacter pylori and the immune system: Genetics,
   epigenetics and treatment aspects
SO PHARMACIA
LA English
DT Review
DE anti-Helicobacter therapy; epigenetics; genetics; Helicobacter pylori;
   immune system
ID ABERRANT DNA METHYLATION; SUCCESSFUL ERADICATION; ANTIBIOTIC-RESISTANCE;
   EVASION STRATEGIES; VIRULENCE FACTORS; TRIPLE THERAPY; FIELD DEFECT;
   PEPTIC-ULCER; FOLLOW-UP; REINFECTION
AB Helicobacter pylori infects more than 50% of the human population worldwide. Persistence and colonization of this bacterium in the host result in genetic and epigenetic alteration and intra-complicated reactions that enhance innate and adaptive immune responses, which lead to the development of several gastrointestinal illnesses and increase the risk for gastric cancer progression. Even the World Health Organization (WHO) classified a bacterium in the first group of carcinogens; also, it has been associated with multiple extra gastric implications such as autoimmune disease and cardiovascular disease, thereby being considered a highly infectious pathogen and a critical health problem globally. Detection of the infection facilitates prognosis for suitable treatment that enhances eradication of this bacterium to prevent further implication. The aim of this review is to convey several aspects related to the Helicobacter pylori infection, to understand and clarify the epigenetic changes, host immune response, and the pathogenicity of multiple virulence factors involved in the infection, as well as diagnostic options, the fundamental strategy of treatment and the rate of reinfection among variable individuals.
C1 [Alfurjani, Batool H.] Jordan Univ Sci & Technol, Fac Appl Med Sci, Dept Med Lab Sci, Irbid, Jordan.
   [Sabi, Salsabeel H.] Hashemite Univ, Fac Sci, Basic Sci Dept, Zarqa, Jordan.
   [Almaaytah, Ammar M.; Abualhaijaa, Ahmad K.] Jordan Univ Sci & Technol, Fac Pharm, Dept Pharmaceut Technol, Irbid, Jordan.
   [Masadeh, Majd M.] Univ Sains Malaysia, Fac Pharmaceut Sci, Dept Clin Pharm, Sains, Malaysia.
C3 Jordan University of Science & Technology; Hashemite University; Jordan
   University of Science & Technology; Universiti Sains Malaysia
RP Sabi, SH (corresponding author), Hashemite Univ, Fac Sci, Basic Sci Dept, Zarqa, Jordan.
EM salsabeel@hu.edu.jo
RI Almaaytah, Ammar/AAD-3195-2019
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NR 120
TC 0
Z9 0
U1 0
U2 0
PU PENSOFT PUBLISHERS
PI SOFIA
PA 12 PROF GEORGI ZLATARSKI ST, SOFIA, 1700, BULGARIA
SN 0428-0296
EI 2603-557X
J9 PHARMACIA
JI Pharmacia
PD MAR 25
PY 2025
VL 72
AR e144177
DI 10.3897/pharmacia.72.e144177
PG 15
WC Pharmacology & Pharmacy
WE Emerging Sources Citation Index (ESCI)
SC Pharmacology & Pharmacy
GA 1TF7T
UT WOS:001473101000001
OA gold
DA 2025-06-01
ER

PT J
AU Gregorio, GV
   Jones, H
   Choudhuri, K
   Vegnente, A
   Bortolotti, F
   MieliVergani, G
   Vergani, D
AF Gregorio, GV
   Jones, H
   Choudhuri, K
   Vegnente, A
   Bortolotti, F
   MieliVergani, G
   Vergani, D
TI Autoantibody prevalence in chronic hepatitis B virus infection: Effect
   of interferon alfa
SO HEPATOLOGY
LA English
DT Article
ID ALPHA-INTERFERON; AUTOIMMUNE-DISEASE; THERAPY; INDUCTION; CANCER; DNA
AB The most effective treatment of chronic hepatitis B virus (HBV) infection is interferon alfa (IFN-alpha), a potentially severe side effect of which is the induction of autoimmunity, To assess whether IFN-alpha causes clinical or seroloscal autoimmune manifestations, we studied 61 children randomized to receive 5 MU/m(2) of IFN-alpha three times per week for 12 weeks, with or without steroid priming or no treatment, Autoantibodies to antinuclei (ANA), smooth muscle (SMA), gastric parietal cell (GPC), liver kidney microsomal type 1, mitochondrial, Liver cytosolic antigen, thyroid microsomal, and thyroid globulin were detected by standard techniques. Over a median of 4 years (range, 1-5 years) from randomization, no clinical signs of autoimmunity were observed, Autoantibody positivity for nuclei, smooth muscle, and/or gastric parietal cells was observed on at least one occasion in 42 of 61 children (89%), with no overall difference in the prevalence between patients treated with interferon alone (19 of 24 [79%]), steroids plus interferon (13 of 20 [65%]), or untreated controls (10 of 17 [59%]). There was also no difference in the autoantibody prevalence before, during, and at follow-up after cessation of treatment in both interferon-treated and interferon-untreated patients, Autoantibodies are common in chronic HBV infection, and their prevalence is uninfluenced by IFN-alpha.
C1 UNIV LONDON KINGS COLL,SCH MED & DENT,DEPT IMMUNOL,LONDON SE5 9PJ,ENGLAND.
   UNIV LONDON KINGS COLL,SCH MED & DENT,DEPT CHILD HLTH,LONDON SE5 9PJ,ENGLAND.
   UNIV NAPLES FEDERICO II,DEPT PAEDIAT,NAPLES,ITALY.
   UNIV PADUA,IST MED CLIN,I-35100 PADUA,ITALY.
C3 University of London; King's College London; University of London;
   King's College London; University of Naples Federico II; University of
   Padua
RI Vergani, Diego/H-7610-2019; Mieli-Vergani, Giorgina/G-5616-2011
OI Choudhuri, Kaushik/0000-0002-3911-027X
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NR 18
TC 51
Z9 53
U1 0
U2 2
PU W B SAUNDERS CO
PI PHILADELPHIA
PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA
   19106-3399
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD SEP
PY 1996
VL 24
IS 3
BP 520
EP 523
DI 10.1053/jhep.1996.v24.pm0008781317
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA VF567
UT WOS:A1996VF56700009
PM 8781317
OA Bronze
DA 2025-06-01
ER

PT J
AU Mostafa, NR
   Ali, AAM
   Alkaphoury, MG
   Marzo, RR
AF Mostafa, Neveen Rashad
   Ali, Abeer A. M.
   Alkaphoury, Mona Gamalludin
   Marzo, Roy Rillera
TI Helicobacter Pylori infection and non-alcoholic fatty liver disease. Is
   there a relationship?
SO HEALTHCARE IN LOW-RESOURCE SETTINGS
LA English
DT Article
DE Helicobacter Pylori; lipid; non-alcoholic fatty liver
ID CARDIOVASCULAR-DISEASE; NAFLD; PATHOGENESIS; PROGRESSION; PREVALENCE;
   FIBROSIS
AB The most prevalent infection that causes chronic gastritis, gas-tric ulcers, and gastric cancer is Helicobacter pylori infection. Recent research has implicated H. pylori in the pathogenesis of non-gastrointestinal diseases such as cardiovascular, autoimmune, and metabolic disorders. In addition, since H. pylori is believed to be implicated in insulin resistance, numerous studies have been conducted to determine the relationship between H. pylori infec-tion and nonalcoholic fatty liver diseases (NAFLD), but the results have been contested. The purpose of this study is to determine the relationship between H. Pylori infection and nonalcoholic fatty liver diseases. One hundred patients were examined via urea breath test for the presence of H. pylori infection and vibration-controlled transient elastography for the diagnosis of non-alcoholic fatty liver disease. After adjusting for other variables, age, body mass index (BMI), and H. pylori infection were associated with elastography 248dB/m. Infection with H. pylori contributes to the development of NAFLD, and its eradication may influence prognosis.
C1 [Mostafa, Neveen Rashad] Alexandria Univ, Med Res Inst, Dept Expt & Clin Internal Med, Alexandria, Egypt.
   [Ali, Abeer A. M.] Alexandria Univ, Med Res Inst, Dept Chem Pathol, Alexandria, Egypt.
   [Alkaphoury, Mona Gamalludin] Ain Shams Univ, Dept Diagnost Radiol, Cairo, Egypt.
   [Marzo, Roy Rillera] Management & Sci Univ, Int Med Sch, Dept Community Med, Shah Alam, Malaysia.
   [Marzo, Roy Rillera] Monash Univ Malaysia, Jeffrey Cheah Sch Med & Hlth Sci, Global Publ Hlth, Kuala Lumpur, Malaysia.
C3 Egyptian Knowledge Bank (EKB); Alexandria University; Egyptian Knowledge
   Bank (EKB); Alexandria University; Egyptian Knowledge Bank (EKB); Ain
   Shams University; Management Science University; Monash University;
   Monash University Malaysia
RP Mostafa, NR (corresponding author), Alexandria Univ, Med Res Inst, Dept Expt & Clin Internal Med, Alexandria, Egypt.
EM doctor.aj.2000@gmail.com
RI MARZO, ROY/ABA-4304-2020
OI MARZO, ROY/0000-0001-9414-4010
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NR 34
TC 1
Z9 1
U1 4
U2 9
PU PAGEPRESS PUBL
PI PAVIA
PA MEDITGROUP, VIA G BELLI, 4, PAVIA, 27100, ITALY
EI 2281-7824
J9 HEALTHC LOW-RESOUR S
JI Healthc. Low-resource Settings
PY 2023
VL 11
SU 2
AR 11379
DI 10.4081/hls.2023.11379
PG 6
WC Health Care Sciences & Services
WE Emerging Sources Citation Index (ESCI)
SC Health Care Sciences & Services
GA K7GT0
UT WOS:001018093900001
OA gold
DA 2025-06-01
ER

PT J
AU Fan, JH
   Lv, ZL
   Yang, GH
   Liao, TT
   Xu, JJ
   Wu, F
   Huang, Q
   Guo, MF
   Hu, GR
   Zhou, M
   Duan, LM
   Liu, SQ
   Jin, Y
AF Fan, Jinshuo
   Lv, Zhilei
   Yang, Guanghai
   Liao, Ting Ting
   Xu, Juanjuan
   Wu, Feng
   Huang, Qi
   Guo, Mengfei
   Hu, Guorong
   Zhou, Mei
   Duan, Limin
   Liu, Shuqing
   Jin, Yang
TI Retinoic Acid Receptor-Related Orphan Receptors: Critical Roles in
   Tumorigenesis
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE retinoic acid receptor-related orphan receptors; ROR alpha; ROR beta;
   ROR gamma; cancer
ID ROR-GAMMA EXPRESSION; NUCLEAR RECEPTOR; TH17 CELLS; VITAMIN-D; T-CELLS;
   CIRCADIAN TRANSCRIPTION; MELANOMA PROGRESSION; COLORECTAL-CANCER;
   PERIPHERAL-BLOOD; GENE-EXPRESSION
AB Retinoic acid receptor-related orphan receptors (RORs) include ROR alpha (NR1F1), ROR beta (NR1F2), and ROR gamma (NR1F3). These receptors are reported to activate transcription through ligand-dependent interactions with co-regulators and are involved in the development of secondary lymphoid tissues, autoimmune diseases, inflammatory diseases, the circadian rhythm, and metabolism homeostasis. Researches on RORs contributing to cancer-related processes have been growing, and they provide evidence that RORs are likely to be considered as potential therapeutic targets in many cancers. ROR alpha has been identified as a potential therapeutic target for breast cancer and has been investigated in melanoma, colorectal colon cancer, and gastric cancer. ROR beta is mainly expressed in the central nervous system, but it has also been studied in pharyngeal cancer, uterine leiomyosarcoma, and colorectal cancer, in addition to neuroblastoma, and recent studies suggest that ROR gamma is involved in various cancers, including lymphoma, melanoma, and lung cancer. Some studies found ROR gamma to be upregulated in cancer tissues compared with normal tissues, while others indicated the opposite results. With respect to the mechanisms of RORs in cancer, previous studies on the regulatory mechanisms of RORs in cancer were mostly focused on immune cells and cytokines, but lately there have been investigations concentrating on RORs themselves. Thus, this review summarizes reports on the regulation of RORs in cancer and highlights potential therapeutic targets in cancer.
C1 [Fan, Jinshuo; Lv, Zhilei; Liao, Ting Ting; Xu, Juanjuan; Wu, Feng; Huang, Qi; Guo, Mengfei; Hu, Guorong; Zhou, Mei; Duan, Limin; Liu, Shuqing; Jin, Yang] Huazhong Univ Sci & Technol, Dept Resp & Crit Care Med, Tongji Med Coll, Key Lab Resp Dis,Minist Hlth,Union Hosp, Wuhan, Hubei, Peoples R China.
   [Yang, Guanghai] Huazhong Univ Sci & Technol, Union Hosp, Dept Thorac Surg, Tongji Med Coll, Wuhan, Hubei, Peoples R China.
C3 Huazhong University of Science & Technology; Huazhong University of
   Science & Technology
RP Jin, Y (corresponding author), Huazhong Univ Sci & Technol, Dept Resp & Crit Care Med, Tongji Med Coll, Key Lab Resp Dis,Minist Hlth,Union Hosp, Wuhan, Hubei, Peoples R China.
EM whuhjy@126.com
RI Guo, Mengfei/IWM-4794-2023; Hu, Guorong/AAI-9354-2020; Jin,
   Yang/AAX-2586-2021; Huang, Qi/JLK-9804-2023
OI zhou, mei/0000-0002-8510-5287
FU National Natural Science Foundation of China [81572942, 81770096]; Hubei
   province technical innovation special major project [2017ACA094];
   Natural Science Foundation of Hubei Province [2014CFA057]; Health and
   Planning Commission Fund of Hubei Province [WJ2017M098]; Science and
   Technology Support Program of Hubei Province [YSF2015001294]; Wuhan
   Planning Project of Science and Technology [2014060101010036]; Special
   Fund for Industrial Transformation and Upgrading; Independent Innovation
   Research Fund for Huazhong University of Science and Technology
   [017KFYXJJ253]; Scientific Training Program for Young Talents from Union
   Hospital of Tongji Medical College, Huazhong University of Science and
   Technology; National major new drug discovery technology major special
   projects [2018ZX09301001001]
FX This paper was supported by the National Natural Science Foundation of
   China (no. 81572942, no. 81770096), Hubei province technical innovation
   special major project (2017ACA094), the Natural Science Foundation of
   Hubei Province (no. 2014CFA057), the Health and Planning Commission Fund
   of Hubei Province (WJ2017M098), the Science and Technology Support
   Program of Hubei Province (YSF2015001294), the Wuhan Planning Project of
   Science and Technology (no. 2014060101010036), the Special Fund for
   Industrial Transformation and Upgrading, the Independent Innovation
   Research Fund for Huazhong University of Science and Technology (no.
   017KFYXJJ253), the Scientific Training Program for Young Talents from
   Union Hospital of Tongji Medical College, Huazhong University of Science
   and Technology (to JF), and the National major new drug discovery
   technology major special projects (2018ZX09301001001).
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NR 80
TC 45
Z9 56
U1 1
U2 21
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD MAY 31
PY 2018
VL 9
AR 1187
DI 10.3389/fimmu.2018.01187
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA GH6TD
UT WOS:000433576100001
PM 29904382
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Loosen, SH
   Mertens, A
   Klein, I
   Leyh, C
   Krieg, S
   Kandler, J
   Luedde, T
   Roderburg, C
   Kostev, K
AF Loosen, Sven Heiko
   Mertens, Alexander
   Klein, Isabel
   Leyh, Catherine
   Krieg, Sarah
   Kandler, Jennis
   Luedde, Tom
   Roderburg, Christoph
   Kostev, Karel
TI Association between Helicobacter pylori and its eradication and
   the development of cancer
SO BMJ OPEN GASTROENTEROLOGY
LA English
DT Article
DE HELICOBACTER PYLORI; CANCER; HELICOBACTER PYLORI - TREATMENT; CANCER
   PREVENTION; CANCER EPIDEMIOLOGY
ID INFECTION; METAANALYSIS; CAGA; PREVALENCE; DISEASE; RISK
AB Background: Helicobacter pylori (H. pylori) is a gram-negative gastrointestinal pathogen that colonises the human stomach and is considered a major risk factor for gastric cancer and mucosa-associated lymphoid tissue lymphoma. Furthermore, H. pylori is a potential trigger of a wide spectrum of extragastric cancer entities, extraintestinal chronic inflammatory processes and autoimmune diseases. In the present study, we evaluated the association between H. pylori infection and its eradication with the development of subsequent gastrointestinal and non-gastrointestinal cancer. Methods: We identified 25 317 individuals with and 25 317 matched individuals without a diagnosis of H. pylori from the Disease Analyzer database (IQVIA). A subsequent cancer diagnosis was analysed using Kaplan-Meier and conditional Cox-regression analysis as a function of H. pylori and its eradication. Results: After 10 years of follow-up, 12.8% of the H. pylori cohort and 11.8% of the non-H. pylori cohort were diagnosed with cancer (p=0.002). Results were confirmed in regression analysis (HR: 1.11; 95% CI 1.04 to 1.18). Moreover, a non-eradicated H. pylori status (HR: 1.18; 95% CI 1.07 to 1.30) but not an eradicated H. pylori status (HR: 1.06; 95% CI 0.97 to 1.15) was associated with a subsequent diagnosis of cancer. In subgroup analyses, H. pylori eradication was negatively associated with bronchus and lung cancer (HR: 0.60; 95% CI 0.44 to 0.83). Conclusion: Our data from a large outpatient cohort in Germany reveal a distinct association between H. pylori infection and the subsequent development of cancer. These data might help to identify patients at risk and support eradication strategies in the future.
C1 [Loosen, Sven Heiko; Mertens, Alexander; Leyh, Catherine; Krieg, Sarah; Kandler, Jennis; Luedde, Tom; Roderburg, Christoph] Univ Hosp Dusseldorf, Dept Gastroenterol Hepatol & Infect Dis, Dusseldorf, Germany.
   [Klein, Isabel; Kostev, Karel] IQVIA Germany, Frankfurt, Hessen, Germany.
C3 Heinrich Heine University Dusseldorf; Heinrich Heine University
   Dusseldorf Hospital
RP Mertens, A (corresponding author), Univ Hosp Dusseldorf, Dept Gastroenterol Hepatol & Infect Dis, Dusseldorf, Germany.
EM sven.loosen@med.uni-duesseldorf.de;
   alexander.mertens@med.uni-duesseldorf.de; Isabel.Klein@iqvia.com;
   catherine.leyh@med.uni-duesseldorf.de;
   sarah.krieg@med.uni-duesseldorf.de;
   jennis.kandler@med.uni-duesseldorf.de;
   tom.luedde@med.uni-duesseldorf.de;
   christoph.roderburg@med.uni-duesseldorf.de; Karel.Kostev@iqvia.com
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   Tom/AAE-9135-2022
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NR 40
TC 4
Z9 4
U1 0
U2 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 2054-4774
J9 BMJ OPEN GASTROENTER
JI BMJ Open Gastroenterol.
PD AUG 23
PY 2024
VL 11
IS 1
AR e001377
DI 10.1136/bmjgast-2024-001377
PG 7
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA F9N4N
UT WOS:001312998900001
PM 39181567
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Rubio, CA
AF Rubio, Carlos A.
TI An Easy Method to Highlight Chief Cells in Gastric Biopsies
SO IN VIVO
LA English
DT Article
DE Toluidine blue; gastric biopsies; inflammation
ID HELICOBACTER-PYLORI; PARIETAL-CELLS; METAPLASIA; MUCOSA; CANCER
AB Background: Hematoxylin and eosin (H&E) is not an optimal stain to discriminate chief cells from parietal cells in gastric biopsies Materials and Methods: Fifteen sets of biopsies from the gastric corpus were consecutively stained with H&E and toluidine blue stains; chief cells stained deep blue with toluidine blue, thus contrasting with lightly-stained parietal cells. In well-oriented sections, the continuity of the chief cell zone was studied at x4 magnification and its thickness in one field at x10 magnification. Results: Toluidine blue stained fundic sections that exhibited normal mucosa or chronic gastritis without glandular atrophy displayed a distinct deep-blue chief cell zone, intercalated between the lightly-stained parietal cells on top and the muscularis mucosae underneath (Group A). In chronic gastritis with focal glandular atrophy or focal intestinal metaplasia, at least one focally fragmented toluidine blue chief cell zone was seen (Group B). In one case with severe autoimmune gastritis and in a case with extensive intestinal metaplasia, an absence of toluidine blue chief cells zone was recorded in the entire section (Group C). Conclusion: This quick and easy staining method made it possible to group sections from the gastric corpus into those with a continuous chief cell zone, with fragmented or with an absent chief cell zone, modalities that seem to correlate with different stages of fundic mucosal inflammation. These preliminary results should be validated in a larger cohort of gastric biopsies from patients with various diseases affecting the corpus mucosa.
C1 [Rubio, Carlos A.] Karolinska Inst, Dept Pathol, Gastrointestinal & Liver Pathol Res Lab, S-17176 Stockholm, Sweden.
   [Rubio, Carlos A.] Univ Hosp, S-17176 Stockholm, Sweden.
C3 Karolinska Institutet
RP Rubio, CA (corresponding author), Karolinska Inst, Dept Pathol, Gastrointestinal & Liver Pathol Res Lab, S-17176 Stockholm, Sweden.
EM Carlos.Rubio@ki.se
RI Rubio-Navarro, Carlos-Enrique/A-4166-2009
OI RUBIO CHACON, CARLOS/0000-0001-5106-2912
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NR 23
TC 2
Z9 2
U1 0
U2 0
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD JAN-FEB
PY 2011
VL 25
IS 1
BP 137
EP 140
PG 4
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA 720RC
UT WOS:000287296800020
PM 21282747
DA 2025-06-01
ER

PT J
AU Marglous, S
   Brown, CE
   Padler-Karavani, V
   Cummings, RD
   Gildersleeve, JC
AF Marglous, Samantha
   Brown, Claire E.
   Padler-Karavani, Vered
   Cummings, Richard D.
   Gildersleeve, Jeffrey C.
TI Serum antibody screening using glycan arrays
SO CHEMICAL SOCIETY REVIEWS
LA English
DT Review
ID POLYSACCHARIDE MICROARRAY TECHNOLOGY; CANCER-ASSOCIATED AUTOANTIBODIES;
   CONJUGATE VACCINE CANDIDATE; KEYHOLE LIMPET HEMOCYANIN; HUMORAL
   IMMUNE-RESPONSE; INFLUENZAE TYPE-B; GASTRIC-CANCER; CAPSULAR
   POLYSACCHARIDE; CLOSTRIDIUM-DIFFICILE; SCHISTOSOMA-MANSONI
AB Humans and other animals produce a diverse collection of antibodies, many of which bind to carbohydrate chains, referred to as glycans. These anti-glycan antibodies are a critical part of our immune systems' defenses. Whether induced by vaccination or natural exposure to a pathogen, anti-glycan antibodies can provide protection against infections and cancers. Alternatively, when an immune response goes awry, antibodies that recognize self-glycans can mediate autoimmune diseases. In any case, serum anti-glycan antibodies provide a rich source of information about a patient's overall health, vaccination history, and disease status. Glycan microarrays provide a high-throughput platform to rapidly interrogate serum anti-glycan antibodies and identify new biomarkers for a variety of conditions. In addition, glycan microarrays enable detailed analysis of the immune system's response to vaccines and other treatments. Herein we review applications of glycan microarray technology for serum anti-glycan antibody profiling.
   Glycan microarrays provide a high-throughput platform to rapidly interrogate serum anti-glycan antibodies, identify new biomarkers for a variety of conditions, and analyze the immune system's response to vaccines and other treatments.
C1 [Marglous, Samantha; Brown, Claire E.; Gildersleeve, Jeffrey C.] NCI, Chem Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA.
   [Padler-Karavani, Vered] Tel Aviv Univ, George S Wise Fac Life Sci, Shmunis Sch Biomed & Canc Res, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel.
   [Cummings, Richard D.] Beth Israel Deaconess Med Ctr, Harvard Med Sch, Dept Surg, Boston, MA 02115 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); Tel Aviv University; Harvard University; Harvard University
   Medical Affiliates; Beth Israel Deaconess Medical Center; Harvard
   Medical School
RP Gildersleeve, JC (corresponding author), NCI, Chem Biol Lab, Ctr Canc Res, Frederick, MD 21702 USA.; Padler-Karavani, V (corresponding author), Tel Aviv Univ, George S Wise Fac Life Sci, Shmunis Sch Biomed & Canc Res, Dept Cell Res & Immunol, IL-69978 Tel Aviv, Israel.; Cummings, RD (corresponding author), Beth Israel Deaconess Med Ctr, Harvard Med Sch, Dept Surg, Boston, MA 02115 USA.
EM vkaravani@tauex.tau.ac.il; rcummin1@bidmc.harvard.edu;
   gildersj@mail.nih.gov
RI PADLER-KARAVANI, VERED/AAC-6055-2022; Gildersleeve, Jeffrey/N-3392-2014
OI PADLER-KARAVANI, VERED/0000-0002-4761-3571; Gildersleeve,
   Jeffrey/0000-0002-3744-6423; Brown, Claire/0000-0002-1840-7840;
   Marglous, Samantha/0000-0002-2892-6150
FU NCI; NIH; NIH [R24GM137763]; European Research Council Consolidator
   Grant [ERC-2020-COG-101003021]
FX This work was supported in part by the intramural research program of
   the NCI, NIH, by NIH grant R24GM137763 to RDC, and by European Research
   Council Consolidator Grant ERC-2020-COG-101003021 to VPK
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NR 330
TC 8
Z9 8
U1 6
U2 32
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
   ENGLAND
SN 0306-0012
EI 1460-4744
J9 CHEM SOC REV
JI Chem. Soc. Rev.
PD MAR 4
PY 2024
VL 53
IS 5
BP 2603
EP 2642
DI 10.1039/d3cs00693j
EA FEB 2024
PG 40
WC Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Chemistry
GA JM7G5
UT WOS:001155375600001
PM 38305761
DA 2025-06-01
ER

PT J
AU Tzellos, TG
   Tahmatzidis, DK
   Lallas, A
   Apostolidou, K
   Goulis, DG
AF Tzellos, Thrasivoulos G.
   Tahmatzidis, Dimitrios K.
   Lallas, Aimilios
   Apostolidou, Kiriaki
   Goulis, Dimitrios G.
TI Pernicious anemia in a patient with Type 1 diabetes mellitus and
   alopecia areata universalis
SO JOURNAL OF DIABETES AND ITS COMPLICATIONS
LA English
DT Article
DE Alopecia areata universalis; Pernicious anemia; Diabetes mellitus Type 1
ID PARIETAL-CELL ANTIBODY; AUTOIMMUNE GASTRITIS; PREVALENCE; DISEASE; RISK
AB A 27-year-old male, who had developed diabetes mellitus type 1 (DMT1) since the age of eighteen and alopecia. areata universalis nine months later, attended the outpatient clinics complaining of general fatigue and shortness of breath. A Schilling test was indicative of pernicious anemia. Antigastric parietal cell (AGPA) and anti-intrinsic factor antibodies were positive, confirming diagnosis of pernicious anemia. Thyroid and Addison's disease were excluded. Gastroscopy revealed atrophic gastritis without any evidence of carcinoid tumors. The aim of this case, which, to our knowledge, is the first one to describe a correlation between diabetes mellitus Type 1 (DMT1), pernicious anaemia, and alopecia areata universalis, is to remind the clinician of the increased risk of pernicious anaemia and gastric carcinoids in DMT1 patients. Screening for AGPA followed by serum gastrin and vitamin B-12 levels constitute the most evidence-based diagnostic approach. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Tzellos, Thrasivoulos G.; Tahmatzidis, Dimitrios K.; Lallas, Aimilios; Apostolidou, Kiriaki] Mamatseio Gen Hosp, Dept Internal Med, Kozani, Greece.
   [Goulis, Dimitrios G.] Aristotle Univ Thessaloniki, Unit Reprod Endocrinol, Dept Obstet & Gynecol 1, Thessaloniki 56403, Greece.
C3 Aristotle University of Thessaloniki
RP Goulis, DG (corresponding author), Aristotle Univ Thessaloniki, Unit Reprod Endocrinol, Dept Obstet & Gynecol 1, Papageorgiou Gen Hosp Nea Efkarpia, Thessaloniki 56403, Greece.
EM dimitrios.goulis@otenet.gr
RI Tachmatzidis, Dimitrios/IVV-3451-2023; Lallas, Aimilios/O-4986-2019;
   Goulis, Dimitrios/AAG-4589-2020
OI Lallas, Aimilios/0000-0002-7193-0964; Goulis,
   Dimitrios/0000-0002-5005-1995; Tzellos, Thrasivoulos/0000-0003-2356-0847
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NR 25
TC 12
Z9 14
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1056-8727
EI 1873-460X
J9 J DIABETES COMPLICAT
JI J. Diabetes Complications
PD NOV-DEC
PY 2009
VL 23
IS 6
BP 434
EP 437
DI 10.1016/j.jdiacomp.2008.05.003
PG 4
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 519TM
UT WOS:000271791300009
PM 18614380
DA 2025-06-01
ER

PT J
AU Borghese, F
   Clanchy, FIL
AF Borghese, Federica
   Clanchy, Felix I. L.
TI CD74: an emerging opportunity as a therapeutic target in cancer and
   autoimmune disease
SO EXPERT OPINION ON THERAPEUTIC TARGETS
LA English
DT Review
DE antigen presentation; cancer; cathepsin; CD44; CD74; inflammatory
   disease; invariant chain; MIF
ID MHC CLASS-II; MIGRATION-INHIBITORY FACTOR; REGULATED INTRAMEMBRANE
   PROTEOLYSIS; INVARIANT CHAIN DEGRADATION; COLLAGEN-INDUCED ARTHRITIS;
   CHONDROITIN SULFATE FORM; GASTRIC EPITHELIAL-CELLS; HELICOBACTER-PYLORI;
   CATHEPSIN-S; ANTIGEN PRESENTATION
AB Introduction: CD74, also known as the invariant chain, participates in several key processes of the immune system, including antigen presentation, B-cell differentiation and inflammatory signaling. Despite being described more than 3 decades ago, new functions and novel interactions for this evolutionarily conserved molecule are still being unraveled. As a participant in several immunological processes and an indicator of disease in some conditions, it has potential as a therapeutic target.
   Areas covered: The relationship between the structure of CD74 variants and their physiological functions is detailed in this review. The function of CD74 in several cell lineages is examined with a focus on the interactions with cathepsins and, in an inflammatory milieu, the pro-inflammatory cytokine macrophage migratory inhibitory factor. The role of CD74 signaling in inflammatory and carcinogenic processes is outlined as is the use of CD74 as a therapeutic target (in cancer) and tool (as a vaccine).
   Expert opinion: CD74 has several roles within the cell and throughout the immune system. Most prominent amongst these are the complex relationships with MIF and cathepsins. Modulation of CD74 function shows promise for the effective amelioration of disease.
C1 [Clanchy, Felix I. L.] Univ London Imperial Coll Sci Technol & Med, Fac Med, Div Rheumatol, Kennedy Inst, London W6 8LH, England.
   [Borghese, Federica] Univ Roma La Sapienza, Dept Clin Med, Clin Immunol Unit, Umberto Policlin Roma 1, IT-00161 Rome, Italy.
C3 University of Oxford; Kennedy Institute for Rheumatology; Imperial
   College London; Sapienza University Rome; University Hospital Sapienza
   Rome
RP Clanchy, FIL (corresponding author), Univ London Imperial Coll Sci Technol & Med, Fac Med, Div Rheumatol, Kennedy Inst, 65 Aspenlea Rd, London W6 8LH, England.
EM f.clanchy@imperial.ac.uk
FU Sapienza University of Rome; European Commission
FX F Borghese is supported by Sapienza University of Rome. F Clanchy is
   supported by the European Commission FP7 Masterswitch (mechanisms to
   attack steering effectors of rheumatoid syndromes with innovative
   therapy choices) project. The authors have no conflicts of interests.
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NR 154
TC 126
Z9 144
U1 0
U2 29
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 2-4 PARK SQUARE, MILTON PARK, ABINGDON OR14 4RN, OXON, ENGLAND
SN 1472-8222
EI 1744-7631
J9 EXPERT OPIN THER TAR
JI Expert Opin. Ther. Targets
PD MAR
PY 2011
VL 15
IS 3
BP 237
EP 251
DI 10.1517/14728222.2011.550879
PG 15
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 719KL
UT WOS:000287203500002
PM 21208136
DA 2025-06-01
ER

PT J
AU Takeuchi, C
   Sato, J
   Yamamichi, N
   Kageyama-Yahara, N
   Sasaki, A
   Akahane, T
   Aoki, R
   Nakajima, S
   Ito, M
   Yamamichi, M
   Liu, YY
   Sakuma, N
   Takahashi, Y
   Sakaguchi, Y
   Tsuji, Y
   Sakurai, K
   Tomida, S
   Niimi, K
   Ushijima, T
   Fujishiro, M
AF Takeuchi, Chihiro
   Sato, Junichi
   Yamamichi, Nobutake
   Kageyama-Yahara, Natsuko
   Sasaki, Akiko
   Akahane, Takemi
   Aoki, Rika
   Nakajima, Shigemi
   Ito, Masayoshi
   Yamamichi, Mitsue
   Liu, Yu-Yu
   Sakuma, Nobuyuki
   Takahashi, Yu
   Sakaguchi, Yoshiki
   Tsuji, Yosuke
   Sakurai, Kouhei
   Tomida, Shuta
   Niimi, Keiko
   Ushijima, Toshikazu
   Fujishiro, Mitsuhiro
TI Marked intestinal trans-differentiation by autoimmune gastritis along
   with ectopic pancreatic and pulmonary trans-differentiation
SO JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
DE Autoimmune gastritis; Diverse trans-differentiation; Intestinal
   differentiation; Increased pH; Molecular epidemiology
ID HELICOBACTER-PYLORI INFECTION; ABERRANT DNA METHYLATION; ATROPHIC
   GASTRITIS; CPG ISLANDS; STEM-CELLS; EXPRESSION; METAPLASIA; GENE;
   IDENTIFICATION; PATHOLOGY
AB BackgroundAutoimmune gastritis (AIG) is a prevalent chronic inflammatory disease with oncogenic potential that causes destruction of parietal cells and severe mucosal atrophy. We aimed to explore the distinctive gene expression profiles, activated signaling pathways, and their underlying mechanisms.MethodsA comprehensive gene expression analysis was conducted using biopsy specimens from AIG, Helicobacter pylori-associated gastritis (HPG), and non-inflammatory normal stomachs. Gastric cancer cell lines were cultured under acidic (pH 6.5) conditions to evaluate changes in gene expression.ResultsGastric mucosa with AIG had a unique gene expression profile compared with that with HPG and normal mucosa, such as extensively low expression of ATP4A and high expression of GAST and PAPPA2, which are involved in neuroendocrine tumorigenesis. Additionally, the mucosa with AIG and HPG showed the downregulation of stomach-specific genes and upregulation of small intestine-specific genes; however, intestinal trans-differentiation was much more prominent in AIG samples, likely in a CDX-dependent manner. Furthermore, AIG induced ectopic expression of pancreatic digestion-related genes, PNLIP, CEL, CTRB1, and CTRC; and a master regulator gene of the lung, NKX2-1/TTF1 with alveolar fluid secretion-related genes, SFTPB and SFTPC. Mechanistically, acidic conditions led to the downregulation of master regulator and stemness control genes of small intestine, suggesting that increased environmental pH may cause abnormal intestinal differentiation in the stomach.ConclusionsAIG induces diverse trans-differentiation in the gastric mucosa, characterized by the transactivation of genes specific to the small intestine, pancreas, and lung. Increased environmental pH owing to AIG may cause abnormal differentiation of the gastric mucosa.
C1 [Takeuchi, Chihiro; Sato, Junichi; Yamamichi, Nobutake; Kageyama-Yahara, Natsuko; Yamamichi, Mitsue; Sakuma, Nobuyuki; Takahashi, Yu; Sakaguchi, Yoshiki; Tsuji, Yosuke; Niimi, Keiko; Fujishiro, Mitsuhiro] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138655, Japan.
   [Takeuchi, Chihiro; Liu, Yu-Yu; Ushijima, Toshikazu] Natl Canc Ctr, Res Inst, Div Epigen, Tokyo, Japan.
   [Takeuchi, Chihiro; Liu, Yu-Yu; Ushijima, Toshikazu] Hoshi Univ, Inst Adv Life Sci, Dept Epigen, Tokyo, Japan.
   [Yamamichi, Nobutake; Sakuma, Nobuyuki; Niimi, Keiko] Univ Tokyo Hosp, Ctr Epidemiol & Prevent Med, Tokyo, Japan.
   [Sasaki, Akiko] Shonan Kamakura Gen Hosp, Dept Gastroenterol, Med Ctr, Kamakura, Kanagawa, Japan.
   [Akahane, Takemi] Nara Med Univ, Dept Gastroenterol, Nara, Japan.
   [Aoki, Rika] Tokushima Hlth Screening Ctr, Tokushima, Japan.
   [Nakajima, Shigemi] Shiga Univ Med Sci, Japan Community Healthcare Org, Dept Gen Med, Consortium Community Med,Shiga Hosp, Otsu, Shiga, Japan.
   [Ito, Masayoshi] Yotsuya Med Cube, Dept Gastroenterol, Tokyo, Japan.
   [Sakurai, Kouhei] Fujita Hlth Univ, Sch Med, Dept Pathol, Aichi, Japan.
   [Tomida, Shuta] Okayama Univ Hosp, Ctr Comprehens Genom Med, Okayama, Japan.
C3 University of Tokyo; National Cancer Center - Japan; Hoshi University;
   University of Tokyo; Nara Medical University; Shiga University of
   Medical Science; Fujita Health University; Okayama University
RP Yamamichi, N (corresponding author), Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Tokyo 1138655, Japan.; Yamamichi, N (corresponding author), Univ Tokyo Hosp, Ctr Epidemiol & Prevent Med, Tokyo, Japan.
EM nobutakeyamamichi@gmail.com
RI Tsuji, Yosuke/IYS-9042-2023; Takeuchi, Chihiro/LXA-1618-2024; Liu,
   Yu-Yu/MTB-5851-2025; Akahane, Takemi/O-4509-2018; Takahashi,
   Yu/I-4665-2015; Ushijima, Toshikazu/AAP-5742-2021; 坂口, 賀基/IUN-9262-2023
OI Ushijima, Toshikazu/0000-0003-3405-7817; Sakurai,
   Kouhei/0000-0003-2428-0310; Takeuchi, Chihiro/0000-0002-2746-9189
FU This research was supported by JSPS KAKENHI [Grant Number: 21H03178] for
   NY and the Research Grant of the Princess Takamatsu Cancer Research Fund
   [Grant Number: 19-25138] for NY. [21H03178]; JSPS KAKENHI [19-25138];
   Princess Takamatsu Cancer Research Fund; Grants-in-Aid for Scientific
   Research [23K07425, 21H03178, 21K09862, 22K08073, 23K27688] Funding
   Source: KAKEN
FX This research was supported by JSPS KAKENHI [Grant Number: 21H03178] for
   NY and the Research Grant of the Princess Takamatsu Cancer Research Fund
   [Grant Number: 19-25138] for NY.
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NR 51
TC 5
Z9 5
U1 0
U2 2
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 0944-1174
EI 1435-5922
J9 J GASTROENTEROL
JI J. Gastroenterol.
PD FEB
PY 2024
VL 59
IS 2
BP 95
EP 108
DI 10.1007/s00535-023-02055-x
EA NOV 2023
PG 14
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA FT3F0
UT WOS:001101625600001
PM 37962678
OA Green Published, hybrid
DA 2025-06-01
ER

PT J
AU Sirajudeen, S
   Shah, I
   Al Menhali, A
AF Sirajudeen, Shaima
   Shah, Iltaf
   Al Menhali, Asma
TI A Narrative Role of Vitamin D and Its Receptor: With Current Evidence on
   the Gastric Tissues
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE 1 alpha,25(OH)(2)D; vitamin D deficiency; vitamin D epimers; cytochrome
   P450; 1,25-MARRS; stomach
ID RESPONSE STEROID-BINDING; 1,25D(3)-MEMBRANE-ASSOCIATED RAPID RESPONSE;
   SERUM 25-HYDROXYVITAMIN D; CALCIUM-SENSING RECEPTOR; BONE-MINERAL
   DENSITY; 1,25-DIHYDROXYVITAMIN D-3; PARATHYROID-HORMONE;
   NUCLEAR-RECEPTOR; GENE-EXPRESSION; CANCER CELLS
AB Vitamin D is a major steroid hormone that is gaining attention as a therapeutic molecule. Due to the general awareness of its importance for the overall well-being, vitamin D deficiency (VDD) is now recognized as a major health issue. The main reason for VDD is minimal exposure to sunlight. The vitamin D receptor (VDR) is a member of the steroid hormone receptors that induces a cascade of cell signaling to maintain healthy Ca2+ levels that serve to regulate several biological functions. However, the roles of vitamin D and its metabolism in maintaining gastric homeostasis have not yet been completely elucidated. Currently, there is a need to increase the vitamin D status in individuals worldwide as it has been shown to improve musculoskeletal health and reduce the risk of chronic illnesses, including some cancers, autoimmune and infectious diseases, type 2 diabetes mellitus, neurocognitive disorders, and general mortality. The role of vitamin D in gastric homeostasis is crucial and unexplored. This review attempts to elucidate the central role of vitamin D in preserving and maintaining the overall health and homeostasis of the stomach tissue.
C1 [Sirajudeen, Shaima; Al Menhali, Asma] UAEU, Dept Biol, Coll Sci, POB 15551, Al Ain, U Arab Emirates.
   [Shah, Iltaf] UAEU, Dept Chem, Coll Sci, POB 15551, Al Ain, U Arab Emirates.
C3 United Arab Emirates University; United Arab Emirates University
RP Al Menhali, A (corresponding author), UAEU, Dept Biol, Coll Sci, POB 15551, Al Ain, U Arab Emirates.
EM asmaa@uaeu.ac.ae
OI SHAH, ILTAF/0000-0002-3739-6083; Al Menhali, Asma/0000-0001-5081-561X;
   Sirajudeen, Shaima/0000-0002-6357-4787
FU Zayed bin Sultan Center for Health Sciences, UAE University [31R138]
FX This research was funded by Zayed bin Sultan Center for Health Sciences,
   UAE University, grant number 31R138.
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NR 180
TC 77
Z9 87
U1 0
U2 9
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD AUG
PY 2019
VL 20
IS 15
AR 3832
DI 10.3390/ijms20153832
PG 29
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA IS8ET
UT WOS:000482383000225
PM 31387330
OA Green Submitted, gold, Green Published
DA 2025-06-01
ER

PT J
AU Bocian, KM
   Jagusztyn-Krynicka, EK
AF Bocian, Katarzyna M.
   Jagusztyn-Krynicka, Elzbieta K.
TI The Controversy over Anti-Helicobacter pylori Therapy
SO POLISH JOURNAL OF MICROBIOLOGY
LA English
DT Review
DE Helicobacter pylori; allergy; GERD; NAP protein; obesity; therapy
ID NEUTROPHIL-ACTIVATING PROTEIN; BODY-MASS INDEX; PLASMA GHRELIN;
   CIRCULATING GHRELIN; LEPTIN CONCENTRATIONS; GASTRIC LEPTIN; INFECTION;
   ERADICATION; MICROBIOTA; POPULATION
AB Helicobacter pylori is a Gram-negative spiral-shaped bacterium, member of epsilon-Proteobacteria specifically colonizing the gastric epithelium of humans. It causes one of the most common infections worldwide, affecting about half of the world's population. However, it should be noted that the prevalence of H. pylori, particularly in the Western world, has significantly decreased coinciding with an increase of some autoimmune and allergic diseases, such as asthma. Various epidemiological studies have also documented a negative association between H. pylori colonization and the presence of GERD (gastroesophageal reflux disease) and risk of esophageal cancer. Additionally, an upward trend of obesity recently observed in inhabitants of developed countries raised a question about the relationship between H. pylori infection and the human body mass index. The first part of this review describes common, recommended anti-H. pylon treatments. The second part, presents the results of recent experiments aimed at evaluating the association between H. pylon infections and gastro-esophageal diseases, the level of stomach hormones, the human body mass index and allergic diseases. Although some studies suggest an inverse association of H. pylori infection with some health problems of the modern world such as asthma, obesity or GERD, H. pylori should be considered as a harmful human pathogen responsible for serious and sometimes lethal diseases. Thus, many scientists advocate the eradication of H. pylori.
C1 [Bocian, Katarzyna M.; Jagusztyn-Krynicka, Elzbieta K.] Univ Warsaw, Fac Biol, Inst Microbiol, Dept Bacterial Genet, PL-02096 Warsaw, Poland.
C3 University of Warsaw
RP Jagusztyn-Krynicka, EK (corresponding author), Univ Warsaw, Fac Biol, Inst Microbiol, Dept Bacterial Genet, Miecznikowa 1, PL-02096 Warsaw, Poland.
EM kjkryn@biol.uw.edu.pl
OI Jagusztyn-Krynicka, Elzbieta/0000-0003-0484-9290; Bocian-Ostrzycka,
   Katarzyna Marta/0000-0003-3271-0325
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NR 85
TC 5
Z9 6
U1 0
U2 8
PU POLSKIE TOWARZYSTWO MIKROBIOLOGOW-POLISH SOCIETY OF MICROBIOLOGISTS
PI WARSAW
PA CHELMSKA STR 30-34, WARSAW, 00-725, POLAND
SN 1733-1331
J9 POL J MICROBIOL
JI Pol. J. Microbiol.
PY 2012
VL 61
IS 4
BP 239
EP 246
DI 10.33073/pjm-2012-033
PG 8
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA 119HL
UT WOS:000317088300001
PM 23484406
OA gold
DA 2025-06-01
ER

PT J
AU Jenkins, BJ
AF Jenkins, Brendan John
TI Transcriptional Regulation of Pattern Recognition Receptors by JAK/STAT
   Signaling, and the Implications for Disease Pathogenesis
SO JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
LA English
DT Review
ID TOLL-LIKE RECEPTOR-2; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; GASTRIC
   TUMORIGENESIS; NLRP3 INFLAMMASOME; INTESTINAL INFLAMMATION; SERINE
   PHOSPHORYLATION; RHEUMATOID-ARTHRITIS; SUSCEPTIBILITY LOCI;
   INSULIN-RESISTANCE; STAT1 ACTIVATION
AB Cytokines are well known for their pleiotropism, affecting a large number of cellular responses, including proliferation, survival, functional maturation, and immunomodulation. It is, therefore, not surprising that both the deregulated expression of cytokines and the subsequent activation of their downstream signaling pathways is a common feature of many cancers, as well as chronic inflammatory, autoimmune, metabolic, and cardiovascular diseases. In this regard, activation of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway is the predominant intracellular signaling event triggered by cytokines, with STAT1 and STAT3 having the greatest diversity of biological functions among the 7 known members of the STAT family of latent transcription factors. Notably, over recent years, it has emerged that STAT1 and STAT3 are employed by various cytokines to manipulate the signal output of heterologous receptors of the innate immune system, namely pattern recognition receptors (PRRs), with both immune and nonimmune (eg, oncogenic, metabolic) cellular processes being affected. This review highlights these pivotal advancements in our understanding of how a cross talk between cytokine and PRR signaling networks can impact on a variety of cellular responses during disease pathogenesis, and the potential therapeutic implications of targeting these networks.
C1 MIMR PHI Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic 3168, Australia.
C3 Prince Henry's Institute of Medical Research
RP Jenkins, BJ (corresponding author), MIMR PHI Inst Med Res, Ctr Innate Immun & Infect Dis, 27-31 Wright St, Clayton, Vic 3168, Australia.
EM brendan.jenkins@monash.edu
RI jenkins, brendan/J-7854-2012
OI Jenkins, Brendan/0000-0002-7552-4656
FU Association for International Cancer Research; Cancer Council of
   Victoria; Sylvia and Charles Viertel Charitable Foundation; Operational
   Infrastructure Support Program by Victorian Government of Australia
FX Dr. R. Smith (MIMR-PHI) is thanked for reviewing this article. This
   study was supported by grants from the Association for International
   Cancer Research, the Cancer Council of Victoria, and the Sylvia and
   Charles Viertel Charitable Foundation, as well as the Operational
   Infrastructure Support Program by the Victorian Government of Australia.
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NR 102
TC 16
Z9 21
U1 2
U2 25
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1079-9907
EI 1557-7465
J9 J INTERF CYTOK RES
JI J. Interferon Cytokine Res.
PD OCT 1
PY 2014
VL 34
IS 10
BP 750
EP 758
DI 10.1089/jir.2014.0081
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA AQ1SR
UT WOS:000342561800002
PM 25051239
DA 2025-06-01
ER

PT J
AU Jafarzadeh, A
   Larussa, T
   Nemati, M
   Jalapour, S
AF Jafarzadeh, Abdollah
   Larussa, Tiziana
   Nemati, Maryam
   Jalapour, Shila
TI T cell subsets play an important role in the determination of the
   clinical outcome of Helicobacter pylori infection
SO MICROBIAL PATHOGENESIS
LA English
DT Review
DE Helicobacter pylori; Th1 cells; Th2 cells; Th17 cells; Treg cells
ID VIRULENCE FACTOR CAGA; HUMAN GASTRIC-MUCOSA; PEPTIC-ULCER DISEASE;
   ROR-GAMMA-T; DENDRITIC CELLS; IMMUNE-RESPONSES; TH17 RESPONSES; IN-VIVO;
   TRANSCRIPTION FACTOR; AUTOIMMUNE-DISEASES
AB Helicobacter pylori (H. pylori) is one of the most prevalent human pathogen and a persistent infection with this bacterium causes common pathologies, such as gastritis or peptic ulcers, and also less common but more serious pathologies, such as gastric cancer or gastric mucosa-associated lymphoid tissue (MALT) lymphoma. The clinical outcome of gastrointestinal infection sustained by H. pylori is determined by the reciprocal interactions between virulence factors of the bacterium and host factors, including immune response genes. Although H. pylori induces a strong immune response, the bacterium is not eliminated. The eradication failure could be attributed to the bacterial capability to regulate helper T (Th) cell-related responses. H. pylori specific CD4(+) T cells play a fundamental role in regulating host immunity and immunopathologic events. It has been documented that Th1, Th2, Th9, Th17, Th22 and T regulatory (Treg) cells, separately or in coordination with each other, can affect the outcome of the infection sustained by of H. pylori. Some studies indicated that both Th1 and Th17 cells may be protective or pathogenic, whereas Treg and Th2 cells perform anti-inflammatory impacts during H. pylori infection. This review gathers recent information regarding the association of the CD4(+) T cells-mediated immunological responses and the clinical consequence of H. pylori infection.
C1 [Jafarzadeh, Abdollah] Rafsanjan Univ Med Sci, Immunol Infect Dis Res Ctr, Rafsanjan, Iran.
   [Jafarzadeh, Abdollah] Rafsanjan Univ Med Sci, Sch Med, Dept Immunol, Rafsanjan, Iran.
   [Jafarzadeh, Abdollah] Kerman Univ Med Sci, Sch Med, Dept Immunol, Kerman, Iran.
   [Larussa, Tiziana] Univ Catanzaro Magna Graecia, Dept Hlth Sci, I-88100 Catanzaro, Italy.
   [Nemati, Maryam] Kerman Univ Med Sci, Sch Para Med, Dept Lab Sci, Kerman, Iran.
   [Jalapour, Shila] Rafsanjan Univ Med Sci, Mol Med Res Ctr, Rafsanjan, Iran.
C3 Kerman University of Medical Sciences; Magna Graecia University of
   Catanzaro; Kerman University of Medical Sciences
RP Jalapour, S (corresponding author), Rafsanjan Univ Med Sci, Mol Med Res Ctr, Rafsanjan, Iran.
EM Jafarzadeh14@rums.ac.ir; shilla.jalalpoor@yahoo.com
RI Jafarzadeh, Abdollah/AAX-2558-2020; Larussa, Tiziana/K-9991-2016
OI Nemati, Maryam/0000-0001-5861-1224; Larussa,
   Tiziana/0000-0001-6998-8502; Jafarzadeh, Abdollah/0000-0002-8180-0602
FU Rafsanjan University of Medical Sciences, Rafsanjan, Iran
FX This work was supported by Rafsanjan University of Medical Sciences,
   Rafsanjan, Iran.
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PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0882-4010
J9 MICROB PATHOGENESIS
JI Microb. Pathog.
PD MAR
PY 2018
VL 116
BP 227
EP 236
DI 10.1016/j.micpath.2018.01.040
PG 10
WC Immunology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Microbiology
GA GB5EF
UT WOS:000429085200037
PM 29407232
DA 2025-06-01
ER

PT J
AU Butnaru, D
   Shoenfeld, Y
AF Butnaru, Dana
   Shoenfeld, Yehuda
TI Adjuvants and lymphoma risk as part of the ASIA spectrum
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Adjuvant; Autoimmunity; Vaccines; Autoimmune syndromes induced by
   adjuvants (ASIA); Lymphoma
ID B-CELL LYMPHOMA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; PRIMARY
   SJOGRENS-SYNDROME; GASTRIC MALT LYMPHOMA; TERM-FOLLOW-UP;
   RHEUMATOID-ARTHRITIS; CHRONIC INFLAMMATION; ALUMINUM-HYDROXIDE;
   MALIGNANT-LYMPHOMA; CANCER-RISK
AB The emerging epidemic of Hodgkin and non-Hodgkin lymphomas worldwide continues to defy our understanding and forces the search for the causative factors. Adjuvants are known to act as triggers of immune and inflammatory responses. Animal experiments have demonstrated that long-term inflammation is related to aggravation of the immune network resulting in cellular and humoral responses leading to autoimmunity and lymphoma development. Chronic stimulation of the immune system is thought to be the key mechanism through which infectious diseases as well as autoimmune diseases can lead to lymphomagenesis. Many adjuvants can act similarly perturbing immune system's function, inducing a state of prolonged immune activation related to chronic lymphatic drainage. Several mechanisms were proposed by which adjuvants induce inflammation, and they are discussed herein. Some of them are triggering inflammasome; others bind DNA, lipid moieties in cells, induce uric acid production or act as lipophilic and/or hydrophobic substances. The sustained inflammation increases the risk of genetic aberrations, where the initial polyclonal activation ends in monoclonality. The latter is the hallmark of malignant lymphoma. Thus, chronic adjuvant stimulation may lead to lymphoma.
C1 [Butnaru, Dana; Shoenfeld, Yehuda] Chaim Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-52621 Tel Hashomer, Israel.
   [Butnaru, Dana] Hosp Gen Univ Gregorio Maranon, Div Clin Immunol, Madrid, Spain.
   [Shoenfeld, Yehuda] Tel Aviv Univ, Sackler Fac Med, Incumbent Laura Schwarz Kipp Chair Res Autoimmune, IL-69978 Tel Aviv, Israel.
C3 Chaim Sheba Medical Center; Tel Aviv University; Sackler Faculty of
   Medicine
RP Butnaru, D (corresponding author), Chaim Sheba Med Ctr, Zabludowicz Ctr Autoimmune Dis, IL-52621 Tel Hashomer, Israel.
EM dana_medis@iberserv.es
RI Schoenfeld, Yehuda/I-1525-2016
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NR 103
TC 14
Z9 15
U1 0
U2 4
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD FEB
PY 2015
VL 61
IS 1-2
SI SI
BP 79
EP 89
DI 10.1007/s12026-014-8622-0
PG 11
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CA6FK
UT WOS:000349004900012
PM 25582758
DA 2025-06-01
ER

PT J
AU Bonamichi-Santos, R
   Castells, M
AF Bonamichi-Santos, Rafael
   Castells, Mariana
TI Diagnoses and Management of Drug Hypersensitivity and Anaphylaxis in
   Cancer and Chronic Inflammatory Diseases: Reactions to Taxanes and
   Monoclonal Antibodies
SO CLINICAL REVIEWS IN ALLERGY & IMMUNOLOGY
LA English
DT Review
DE Taxanes; Monoclonal antibodies; Rapid drug desensitization;
   Drughypersensitivity reaction; Adverse drug reaction
ID CETUXIMAB PLUS IRINOTECAN; METASTATIC COLORECTAL-CANCER;
   WORLD-ALLERGY-ORGANIZATION; INFUSION-RELATED REACTIONS; RAPID
   DESENSITIZATION; GENERAL-CONSIDERATIONS; BRENTUXIMAB VEDOTIN;
   NORTH-CAROLINA; PHASE-III; SKIN-TEST
AB Due to the increase in utilization of chemotherapies and antibodies, drug hypersensitivity reactions have increased dramatically worldwide, preventing the use of first-line therapies and impacting patients' survival and quality of life. Some of the more frequently used medications in cancer include taxanes for ovarian, lung, breast, and prostate cancers. Monoclonal antibodies are used in the treatment of neoplastic, autoimmune, and inflammatory diseases, and their clinical applications are becoming broader. Monoclonal antibody targets include CD20, HER-2, EGFR, IL-6 receptor, TNF-alpha, CD30, VEGF-A, IgE, and more, and examples of immune-mediated and inflammatory diseases that respond to monoclonal antibodies include rheumatoid arthritis, Crohn's disease, ulcerative colitis, juvenile idiopathic arthritis, psoriasis and psoriatic arthritis, Wegener's granulomatosis, microscopic polyangiitis, ankylosing spondylitis, plaque psoriasis, and asthma. Neoplastic diseases include non-Hodgkin's lymphoma, chronic lymphocytic leukemia, and colorectal, breast, gastric, and lung cancer. The clinical presentation of drug hypersensitivity reactions ranges from mild cutaneous reactions to life-threatening symptoms including anaphylaxis. Rapid drug desensitization (RDD) has become a groundbreaking approach to the management of immediate drug hypersensitivity reactions IgE and non-IgE mediated. It is the only effective procedure that enables sensitized patients to receive the full treatment dose safely, thus representing an important advance in the patients' treatment and prognosis. The aim of this review is to provide an update on hypersensitivity reactions to commonly used monoclonal and taxanes, their clinical presentations, diagnosis, and the use of RDD for their management.
C1 [Bonamichi-Santos, Rafael; Castells, Mariana] Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA.
   [Bonamichi-Santos, Rafael] Univ Sao Paulo, Div Clin Immunol, Sao Paulo, SP, Brazil.
   [Bonamichi-Santos, Rafael] Univ Sao Paulo, Div Allergy, Sao Paulo, SP, Brazil.
C3 Harvard University; Harvard Medical School; Harvard University Medical
   Affiliates; Brigham & Women's Hospital; Universidade de Sao Paulo;
   Universidade de Sao Paulo
RP Bonamichi-Santos, R (corresponding author), Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Rheumatol Immunol & Allergy, Boston, MA 02115 USA.; Bonamichi-Santos, R (corresponding author), Univ Sao Paulo, Div Clin Immunol, Sao Paulo, SP, Brazil.; Bonamichi-Santos, R (corresponding author), Univ Sao Paulo, Div Allergy, Sao Paulo, SP, Brazil.
EM rafaelbonamichi@hotmail.com
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NR 77
TC 44
Z9 48
U1 0
U2 21
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1080-0549
EI 1559-0267
J9 CLIN REV ALLERG IMMU
JI Clin. Rev. Allergy Immunol.
PD JUN
PY 2018
VL 54
IS 3
BP 375
EP 385
DI 10.1007/s12016-016-8556-5
PG 11
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA GJ5LF
UT WOS:000435421900003
PM 27277133
DA 2025-06-01
ER

PT J
AU Zhang, QY
   Yan, WZ
   Li, H
   Peng, HL
AF Zhang, Qingyang
   Yan, Wenzhe
   Li, Heng
   Peng, Hongling
TI Advances in the Pathogenesis, Diagnosis, Treatment, and Prognosis of
   Marginal Zone Lymphoma
SO CURRENT TREATMENT OPTIONS IN ONCOLOGY
LA English
DT Review
DE Marginal zone lymphoma; Pathogenesis; Diagnosis; Treatment; Prognosis
ID B-CELL LYMPHOMA; NON-HODGKIN-LYMPHOMA; NF-KAPPA-B; GASTRIC MALT
   LYMPHOMA; PHASE-II TRIAL; HELICOBACTER-PYLORI; COMBINATION CHEMOTHERAPY;
   RITUXIMAB MONOTHERAPY; CLINICAL PRESENTATION; IMPROVING SURVIVAL
AB The management of marginal zone lymphoma (MZL), an indolent B-cell non-Hodgkin lymphoma, requires a personalized and adaptive approach due to its clinical and prognostic heterogeneity. We believe treatment should emphasize a balanced strategy considering the subtype, disease burden, symptoms, and actionable genetic or environmental factors, such as infections or autoimmune diseases. For asymptomatic patients with low tumor burden or disseminated disease, a watch-and-wait approach remains appropriate, given MZL's indolent nature and the risks of overtreatment. Conversely, for symptomatic or high-burden cases, early intervention with chemoimmunotherapy is recommended for effective disease control. Surgery remains essential for both diagnosis and the treatment of localized disease. Incorporating molecular profiling and prognostic models, such as MZL-IPI and POD24, is crucial for decision-making and risk stratification. Testing for infectious agents like Helicobacter pylori or Hepatitis C virus should be standard practice, as eradication therapy offers a targeted, less toxic, and effective option in select patients. With ongoing advancements in understanding dysregulated signaling pathways and the tumor microenvironment, we anticipate novel targeted therapies and combination regimens will further improve outcomes. We advocate for molecular testing at diagnosis to identify actionable biomarkers, particularly for patients with refractory or relapsed disease. Finally, MZL management requires vigilant follow-up with adjustments based on evolving disease features. Treatment decisions should integrate patient preferences, clinical context, and the latest evidence to maximize survival while preserving quality of life.
C1 [Zhang, Qingyang; Yan, Wenzhe; Li, Heng; Peng, Hongling] Cent South Univ, Xiangya Hosp 2, Dept Hematol, 139th Renmin Middle Rd, Changsha 410011, Hunan, Peoples R China.
   [Peng, Hongling] Hunan Engn Res Ctr Cell Immunotherapy Hematopoiet, Changsha 410011, Hunan, Peoples R China.
C3 Central South University
RP Peng, HL (corresponding author), Cent South Univ, Xiangya Hosp 2, Dept Hematol, 139th Renmin Middle Rd, Changsha 410011, Hunan, Peoples R China.; Peng, HL (corresponding author), Hunan Engn Res Ctr Cell Immunotherapy Hematopoiet, Changsha 410011, Hunan, Peoples R China.
EM zhangqingyang1107@163.com; penghongling@csu.edu.cn
OI Peng, Hongling/0000-0003-2770-5150
FU National Natural Science Foundation of China [82070175]
FX This work was generously supported by the National Natural Science
   Foundation of China (82070175).
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NR 134
TC 0
Z9 0
U1 2
U2 2
PU SPRINGER
PI NEW YORK
PA ONE NEW YORK PLAZA, SUITE 4600, NEW YORK, NY, UNITED STATES
SN 1527-2729
EI 1534-6277
J9 CURR TREAT OPTION ON
JI Curr. Treat. Options Oncol.
PD FEB
PY 2025
VL 26
IS 2
BP 142
EP 155
DI 10.1007/s11864-025-01293-w
EA FEB 2025
PG 14
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA X3O6F
UT WOS:001410561700001
PM 39891871
DA 2025-06-01
ER

PT J
AU Kaltsas, G
   Grozinsky-Glasberg, S
   Alexandraki, KI
   Thomas, D
   Tsolakis, AV
   Gross, D
   Grossman, AB
AF Kaltsas, Gregory
   Grozinsky-Glasberg, Simona
   Alexandraki, Krystallenia I.
   Thomas, Dimitrios
   Tsolakis, Apostolos V.
   Gross, David
   Grossman, Ashley B.
TI Current concepts in the diagnosis and management of type 1 gastric
   neuroendocrine neoplasms
SO CLINICAL ENDOCRINOLOGY
LA English
DT Review
ID HELICOBACTER-PYLORI INFECTION; OCTREOTIDE SUPPRESSION TEST;
   ENTEROCHROMAFFIN-LIKE CELLS; CHRONIC ATROPHIC GASTRITIS; TERM-FOLLOW-UP;
   PERNICIOUS-ANEMIA; CARCINOID-TUMORS; LONG-TERM; RISK; ANTRECTOMY
AB The vast majority of gastrin-related gastrointestinal neuroendocrine neoplasms (GI-NENs) develop in the context of chronic atrophic gastritis (type 1), a condition closely related to autoimmune thyroid diseases. These neoplasms are defined as gastric NENs type 1 (GNEN1) and have recently been shown to constitute the commonest GI-NENs in a prospective study. GNEN1s are usually multiple and follow a relative indolent course, raising questions regarding the extent that such patients should be investigated and the appropriate therapeutic interventions needed. Recently, a number of consensus statements and guidelines have been published from various societies dealing with the diagnosis and management of GI-NENs. Endocrinologists are among the many different medical specialties involved in GNEN1s diagnosis and management. However, despite recent advances, few randomized trials are available, and thus existing evidence remains relatively weak compared to other malignancies. The purpose of this review is to provide recent evidence along with currently employed modalities addressing the diagnosis, management, long-term follow-up and potential comorbidities of GNEN1s.
C1 [Kaltsas, Gregory; Alexandraki, Krystallenia I.; Thomas, Dimitrios] Natl Univ Athens, Dept Pathophysiol, Athens, Greece.
   [Grozinsky-Glasberg, Simona] Hadassah Hebrew Univ Hosp, Neuroendocrine Tumor Unit, Endocrinol & Metab Serv, Dept Med, Jerusalem, Israel.
   [Tsolakis, Apostolos V.] Dept Med Sci, Sect Endocrine Oncol, Uppsala, Sweden.
   [Grossman, Ashley B.] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford, England.
C3 National & Kapodistrian University of Athens; Hebrew University of
   Jerusalem; Hadassah University Medical Center; Hadassah University
   Hospital; University of Oxford
RP Kaltsas, G (corresponding author), Med Sch Athens, Dept Pathophysiol, Mikras Asias 75, Athens 11527, Greece.
EM gkaltsas@endo.gr
RI Tsolakis, Apostolos/AAK-3974-2020; Kaltsas, Gregory/AAD-7193-2019;
   Alexandraki, Krystallenia/S-4058-2019
OI Alexandraki, Krystallenia/0000-0003-2398-6768; Kaltsas,
   Gregory/0000-0002-5876-7883
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NR 70
TC 19
Z9 24
U1 0
U2 7
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0300-0664
EI 1365-2265
J9 CLIN ENDOCRINOL
JI Clin. Endocrinol.
PD AUG
PY 2014
VL 81
IS 2
BP 157
EP 168
DI 10.1111/cen.12476
PG 12
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA AM2HF
UT WOS:000339670500001
PM 24750249
OA Bronze
DA 2025-06-01
ER

PT J
AU Sabzali, S
   Pazhouhnia, S
   Shahzamani, K
   Sedeh, PA
AF Sabzali, Somaieh
   Pazhouhnia, Setareh
   Shahzamani, Kiana
   Sedeh, Peyman Adibi
TI Role of phage therapy in acute gastroenteritis
SO JOURNAL OF RESEARCH IN MEDICAL SCIENCES
LA English
DT Review
DE Bacteria; bacteriophage; gastroenteritis; gastrointestinal diseases
ID BACTERIOPHAGE THERAPY; ESCHERICHIA-COLI; ANTIMICROBIAL SUSCEPTIBILITY;
   TOXIN PRODUCTION; RESISTANCE; CAMPYLOBACTER; SALMONELLA; PREVALENCE;
   MECHANISMS; MICROBES
AB The gut ecosystem, comprising the gut microbiota and its interactions, plays a crucial role in human health and disease. This complex ecosystem involves a diverse array of microorganisms such as viruses, fungi, and bacteria, collectively known as the gut microbiota. These microorganisms contribute to various functions, including nutrient metabolism and immune modulation, thereby impacting human health. Dysbiosis, or an imbalance in the gut microbiota, has been associated with the pathogenesis of several diseases, ranging from intestinal disorders such as inflammatory bowel disease to extra-intestinal conditions such as metabolic and neurological disorders. The implications of dysbiosis in the gut ecosystem are far-reaching, affecting not only gastrointestinal health but also contributing to the development and progression of conditions such as autoimmune gastritis and gastric cancer. Furthermore, the burden of antimicrobial use and subsequent side effects, including antibiotic resistance, poses additional challenges in managing gastrointestinal diseases. In light of these complexities, investigating the role of bacteriophages as regulators of the gut ecosystem and their potential clinical applications presents a promising opportunity to tackle antibiotic resistance and fight infectious diseases.
C1 [Sabzali, Somaieh] Lorestan Univ, Fac Basic Sci, Dept Biol, Khorramabad, Iran.
   [Pazhouhnia, Setareh] Univ Isfahan, Fac Biol Sci & Technol, Dept Cell & Mol Biol & Microbiol, Esfahan, Iran.
   [Shahzamani, Kiana] Lorestan Univ Med Sci, Fac Med, Hepatitis Res Ctr, Khorramabad, Iran.
   [Sedeh, Peyman Adibi] Isfahan Univ Med Sci, Fac Med, Gastroenterol & Hepatol Res Ctr, Esfahan, Iran.
C3 Lorestan University; University of Isfahan; Lorestan University of
   Medical Sciences; Isfahan University of Medical Sciences
RP Shahzamani, K (corresponding author), Lorestan Univ Med Sci, Fac Med, Hepatitis Res Ctr, Khorramabad, Iran.
EM shahzamani.k@lums.ac.ir
RI Sabzali, Somaieh/JGD-2374-2023; Shahzamani, Kiana/R-9794-2017
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NR 74
TC 0
Z9 0
U1 1
U2 1
PU WOLTERS KLUWER MEDKNOW PUBLICATIONS
PI MUMBAI
PA WOLTERS KLUWER INDIA PVT LTD , A-202, 2ND FLR, QUBE, C T S  NO 1498A-2
   VILLAGE MAROL, ANDHERI EAST, MUMBAI, Maharashtra, INDIA
SN 1735-1995
EI 1735-7136
J9 J RES MED SCI
JI J. Res. Med. Sci.
PD JAN
PY 2025
VL 30
IS 1
AR 2
DI 10.4103/jrms.jrms_464_24
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA U0X0X
UT WOS:001409116600001
PM 40200968
OA gold
DA 2025-06-01
ER

PT J
AU Tandon, R
   Srivastava, N
AF Tandon, Reetika
   Srivastava, Nidhi
TI Unravelling exosome paradigm: Therapeutic, diagnostic and theranostics
   application and regulatory consideration
SO LIFE SCIENCES
LA English
DT Article
DE Extracellular vesicles; Exosomes; Classification; Therapeutics;
   Challenges; Diagnostics
ID INFLAMMATORY-BOWEL-DISEASE; HUMAN URINARY EXOSOMES; CELL-DERIVED
   EXOSOMES; EXTRACELLULAR VESICLES; STEM-CELLS; IN-VITRO;
   TOXOPLASMA-GONDII; MEMBRANE-VESICLES; ANALYSIS REVEALS; T-CELLS
AB In the recent decade, extracellular vesicles (EVs) have been released from nearly all the kingdoms, modulating intercellular communication and maintaining the human body's homeostasis by regulating different cellular processes. Among EVs, exosomes are the emerging field in biopharmaceuticals. They have lipid bilayer ranging from 30 to 150 nm in size and encompass DNA, RNA, protein lipids, etc. Their sources are widespread, easy to acquire, and cost-effective in manufacturing. This review focuses on the detailed classification of exosomes existing in nature, knowledge and application of omics, therapeutic, diagnostic and theranostic application of exosomes. It covers diseases such as cancer, infectious diseases (viral, bacterial, fungal infections), neurodegenerative diseases, metabolic diseases, lifestyle diseases (diabetes, cardiovascular, gastric disorder (IBD)), autoimmune disorders and their biodistribution. This article unfolds the recent progress in the exosomes arena and covers all the regulatory considerations (FDA, EMA, and other nations) involved with it. Moreover, a detailed discussion about clinical trials and its manifestation with exosomes and challenges associated with their isolation procedures, reproducibility, and safety concerns.
C1 [Tandon, Reetika; Srivastava, Nidhi] Natl Inst Pharmaceut Educ & Res Raebareli, Dept Biotechnol, Lucknow 226002, India.
RP Srivastava, N (corresponding author), Natl Inst Pharmaceut Educ & Res Raebareli, Dept Biotechnol, Lucknow 226002, India.
EM nidhi1.srivastava@niperraebareli.edu.in
RI S, N/KCL-3312-2024
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NR 279
TC 1
Z9 1
U1 3
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0024-3205
EI 1879-0631
J9 LIFE SCI
JI Life Sci.
PD APR 1
PY 2025
VL 366
AR 123472
DI 10.1016/j.lfs.2025.123472
EA FEB 2025
PG 31
WC Medicine, Research & Experimental; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pharmacology & Pharmacy
GA Y1D7C
UT WOS:001429625800001
PM 39956185
DA 2025-06-01
ER

PT J
AU Kapadia, CR
AF Kapadia, Cyrus R.
TI Gastric Atrophy, Metaplasia, and Dysplasia A Clinical Perspective
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Chronic atrophic gastritis; Intestinal metaplasia; Helicobacter pylori;
   Cobalamin deficiency
ID HELICOBACTER-PYLORI INFECTION; LASER-INDUCED FLUORESCENCE; HIGH-GRADE
   DYSPLASIA; INTESTINAL METAPLASIA; FOLLOW-UP; COBALAMIN DEFICIENCY;
   NATURAL-HISTORY; ACID-SECRETION; CANCER; ULCER
AB Gastric carcinoma of the intestinal type originates in dysplastic epithelium, which in turn develops in the milieu of atrophic gastritis and intestinal metaplasia. Cancers also may develop less often from gastric adenomatous polyps, which represent dysplastic epithelium arising in a raised lesion. The main causes of chronic atrophic gastritis and gastric atrophy are autoimmune due to pernicious anemia or chronic Helicobacter pylori infection. In the former condition, there is severe atrophy of the corpus (oxyntic mucosa), with the antrum being speared. In contrast, chronic atrophic gastritis consequent to H. pylori infection is a multifocal pangastritis, involving independent foci in the corpus and antrum of the stomach. For the most part, these clinical conditions are silent; the only manifestation of both these forms of chronic atrophic gastritis is cobalamin (vitamin B 12) deficiency. In the case of the autoimmune gastritis of pernicious anemia, cobalamin deficiency results form the absence of intrinsic factor. When cobalamin deficiency occurs in patients with H. pylori-related gastritis, for the most part, it is because these patients have hypochlorhydria and are therefore unable to release cobalamin from its bound form in food. Patients may have advanced neuropsychiatric manifestations of cobalamin deficiency and yet not be anemic, have a normal blood smear, and even have serum cobalamin levels in the normal range. The condition may be identified by demonstrating elevated levels of homocysteine and methylmalonic acid. Intestinal metaplasia may be of the enteric (grade I), enterocolic (grade II), or colonic (grade III) type. Grade III intestinal metaplasia has traditionally been thought of as the most sinister variety, although the extent of atrophy and metaplasia may be a better marker for premalignancy than the mere identification of small areas of grade III intestinal metaplasia. Over the years, there has been much disagreement and a high degree of interrater variability, especially between Western and Japanese pathologists, as to the different grades of dysplasia and early gastric cancer. Recent consensus conferences at Vienna and Padova have resulted in better understanding of what constitutes these lesions, and it is hoped that in the near future agreement between pathologists will improve as a consequence. For the present, it is imperative that clinicians obtain second opinions from two or more expert pathologists on biopsy specimens before arriving at a diagnosis of either low-or highgrade dysplasia. The former histologic diagnosis is tantamount to subjecting the patient to endoscopic surveillance and the latter is tantamount to a decision regarding the resection of the lesion, both decisions being psychologically disturbing for patients. At this time, population screening for H. pylori is not recommended in Western countries, but most experts would agree that H. pylori should be eradicated if detected as part of the appropriate investigation of a clinical disorder such as dyspepsia. Certain other specific conditions may also be considered to be precancerous, such as the gastric remnant after a partial gastrectomy and the gastric mucosa in familial adenomatous polyposis syndrome and in familial Peutz-Jeghers syndrome and perhaps Menetrier disease.
C1 Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA.
C3 Yale University
RP Kapadia, CR (corresponding author), Yale Univ, Sch Med, Dept Internal Med, LMP 1074,POB 208030, New Haven, CT 06520 USA.
EM cyrus.kapadia@yale.edu
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NR 44
TC 81
Z9 100
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAY
PY 2003
VL 36
BP S29
EP S36
DI 10.1097/00004836-200305001-00006
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA V16QJ
UT WOS:000207883800006
PM 12702963
DA 2025-06-01
ER

PT J
AU Soluri, MF
   Puccio, S
   Caredda, G
   Edomi, P
   D'Elios, MM
   Cianchi, F
   Troilo, A
   Santoro, C
   Sblattero, D
   Peano, C
AF Soluri, Maria Felicia
   Puccio, Simone
   Caredda, Giada
   Edomi, Paolo
   D'Elios, Mario Milco
   Cianchi, Fabio
   Troilo, Arianna
   Santoro, Claudio
   Sblattero, Daniele
   Peano, Clelia
TI Defining theHelicobacter pyloriDisease-Specific Antigenic
   Repertoire
SO FRONTIERS IN MICROBIOLOGY
LA English
DT Article
DE H; pyloriinfection; interactome; gastric cancer; MALT lymphoma;
   autoimmune gastritis; phage display; next generation sequencing
ID HELICOBACTER-PYLORI INFECTION; IMMUNE-RESPONSE; GENOME SEQUENCE;
   INCREASED RISK; PROTEIN; MUCOSA; CAGA; IMMUNOPROTEOMICS; POLYMORPHISMS;
   PATHOGENESIS
AB The analysis of the interaction betweenHelicobacter pylori(HP) and the hostin vivois an extremely informative way to enlighten the molecular mechanisms behind the persistency/latency of the bacterium as well as in the progression of the infection. An important source of information is represented by circulating antibodies targeting the bacteria that define a specific "disease signature" with prospective diagnostic implications. The diagnosis of some of the HP induced diseases such as gastric cancer (GC), MALT lymphoma (MALT), and autoimmune gastritis (AIG) is not easy because patients do not show symptoms of illness in early-onset stages, at the same time they progress rapidly. The possibility of identifying markers able to provide an early diagnosis would be extremely beneficial since a late diagnosis results in a delay in undergoing active therapy and reduces the survival rate of patients. With the aim to identify the HP antigens recognized during the host immune-response to the infection and possibly disease progression, we applied a discovery-driven approach, that combines "phage display" and deep sequencing. The procedure is based on the selection of ORF phage libraries, specifically generated from the pathogen's genome, with sera antibodies from patients with different HP-related diseases. To this end two phage display libraries have been constructed starting from genomic DNA from the reference HP 26695 and the pathogenic HP B128 strains; libraries were filtered for ORFs by using an ORF selection vector developed by our group (Di Niro et al., 2005;Soluri et al., 2018), selected with antibodies from patients affected by GC, MALT, and AIG and putative HP antigens/epitopes were identified after Sequencing and ranking. The results show that individual selection significantly reduced the library diversity and comparison of individual ranks for each condition allowed us to highlight a pattern of putative antigens specific for the different pathological outcomes or common for all of them. Within the putative antigens enriched after selection, we have validated protein CagY/Cag7 by ELISA assay as a marker of HP infection and progression. Overall, we have defined HP antigenic repertoire and identified a panel of putative specific antigens/epitopes for three different HP infection pathological outcomes that could be validated in the next future.
C1 [Soluri, Maria Felicia; Santoro, Claudio] Univ Piemonte Orientale, Dept Hlth Sci, Novara, Italy.
   [Soluri, Maria Felicia; Santoro, Claudio] Univ Piemonte Orientale, IRCAD, Novara, Italy.
   [Soluri, Maria Felicia; Santoro, Claudio] Univ Piemonte Orientale, Ctr Translat Res Autoimmune & Allerg Dis, Novara, Italy.
   [Puccio, Simone] IRCCS, Humanitas Clin & Res Ctr, Lab Translat Immunol, Rozzano, Italy.
   [Caredda, Giada] Univ Milan, Dept Excellence Pharmacol & Bimol Sci, Milan, Italy.
   [Edomi, Paolo; Sblattero, Daniele] Univ Trieste, Dept Life Sci, Trieste, Italy.
   [D'Elios, Mario Milco; Cianchi, Fabio; Troilo, Arianna] Univ Florence, Sch Human Hlth Sci, Dept Expt & Clin Med, Florence, Italy.
   [Peano, Clelia] CNR, Inst Genet & Biomed Res, UoS Milan, Milan, Italy.
   [Peano, Clelia] IRCCS, Humanitas Clin & Res Ctr, Genom Unit, Milan, Italy.
C3 University of Eastern Piedmont Amedeo Avogadro; University of Eastern
   Piedmont Amedeo Avogadro; University of Eastern Piedmont Amedeo
   Avogadro; IRCCS Humanitas Research Hospital; University of Milan;
   University of Trieste; University of Florence; Consiglio Nazionale delle
   Ricerche (CNR); Istituto di Ricerca Genetica e Biomedica (IRGB-CNR)
RP Sblattero, D (corresponding author), Univ Trieste, Dept Life Sci, Trieste, Italy.; Peano, C (corresponding author), CNR, Inst Genet & Biomed Res, UoS Milan, Milan, Italy.; Peano, C (corresponding author), IRCCS, Humanitas Clin & Res Ctr, Genom Unit, Milan, Italy.
EM dsblattero@units.it; clelia.peano@humanitasresearch.it
RI Peano, Clelia/C-4015-2018; Edomi, Paolo/AAL-7596-2021; D'Elios, Mario
   Milco/Y-9573-2019; Puccio, Simone/P-9571-2018
OI CIANCHI, FABIO/0000-0002-6936-8693; PEANO, CLELIA/0000-0001-7055-3629;
   D'Elios, Mario Milco/0000-0001-9160-0930; Puccio,
   Simone/0000-0003-4007-4365
FU Italian Ministry of University and Research [2010P3S8BR_002]
FX This work was supported by Grants from the Italian Ministry of
   University and Research (2010P3S8BR_002 to CP).
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NR 77
TC 8
Z9 8
U1 0
U2 3
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
EI 1664-302X
J9 FRONT MICROBIOL
JI Front. Microbiol.
PD JUL 9
PY 2020
VL 11
AR 1551
DI 10.3389/fmicb.2020.01551
PG 14
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA MU3FT
UT WOS:000555559000001
PM 32849324
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Davidson, WF
   Giese, T
   Fredrickson, TN
AF Davidson, WF
   Giese, T
   Fredrickson, TN
TI Spontaneous development of plasmacytoid tumors in mice with defective
   Fas-Fas ligand interactions
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
DE lpr; gld; Fas; Fas ligand; lymphoma
ID MATURE T-CELLS; NECROSIS-FACTOR-ALPHA; LPR MICE; B-CELLS;
   LYMPHOPROLIFERATIVE SYNDROME; MONOCLONAL-ANTIBODY; AUTOIMMUNE SYNDROME;
   GASTRIC LYMPHOMA; GENE-MUTATIONS; DEFICIENT MICE
AB B cell malignancies arise with increased frequency in aging individuals and in patients with genetic or acquired immunodeficiency (e.g., AIDS) or autoimmune diseases. The mechanisms of lymphomagenesis in these individuals are poorly understood. In this report we investigated the possibility that mutations at the Fas (lpr) and Fasl (gld) loci, which prevent Fas-mediated apoptosis and cause an early onset benign lymphoid hyperplasia and autoimmunity, also predispose mice to malignant lymphomas later in life. Up to 6 mo of age, hyperplasia in lpr and gld mice results from the predominant accumulation of polyclonal T cell subsets and smaller numbers of polyclonal B cells and plasma cells. Here, we examined C3H-lpr, C3H-gld, and BALB-gld mice 6-15 mo of age for the emergence of clonal T and B cell populations and found that a significant proportion of aging mice exclusively developed B cell malignancies with many of the hallmarks of immunodeficiency-associated B lymphomas. By 1 yr of age,similar to 60% of BALB-gld and 30% of C3H-gld mice had monoclonal B cell populations that grew and metastasized in scid recipients but in most cases were rejected by immunocompetent mice. The tumors developed in a milieu greatly enriched for plasma cells, CD23(-) B cells and immunodeficient memory T cells and variably depleted of B220(+) DN T cells. Growth factor-independent cell lines were established from five of the tumors. The majority of the tumors were CD23(-) and IgH isotype switched and a high proportion was CD5(+) and dull Mac-1(+). Considering their Ig secretion and morphology in vivo, most tumors were classified as malignant plasmacytoid lymphomas. The delayed development of the gld tumors indicated that genetic defects in addition to the Fas/Fasl mutations were necessary for malignant transformation. Interestingly, none of the tumors showed changes in the genomic organization of c-Myc but many had one of more somatically-acquired MuLV proviral integrations that were transmitted in scid passages and cell lines. Therefore, insertional mutagenesis may be a mechanism for transformation in gld B cells. Our panel of in vivo passaged and in vitro adapted gld lymphomas will be a valuable tool for the future identification of genetic abnormalities associated with B cell transformation in aging and autoimmune mice.
C1 NCI, Genet Lab, NIH, Bethesda, MD 20892 USA.
   NCI, Registry Expt Canc, NIH, Bethesda, MD 20892 USA.
C3 National Institutes of Health (NIH) - USA; NIH National Cancer Institute
   (NCI); National Institutes of Health (NIH) - USA; NIH National Cancer
   Institute (NCI)
RP Amer Red Cross, Holland Lab, Dept Immunol, 15601 Crabbs Branch Way, Rockville, MD 20855 USA.
EM davidson@hlsun.redcross.org
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NR 67
TC 141
Z9 156
U1 0
U2 2
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA
SN 0022-1007
EI 1540-9538
J9 J EXP MED
JI J. Exp. Med.
PD JUN 1
PY 1998
VL 187
IS 11
BP 1825
EP 1838
DI 10.1084/jem.187.11.1825
PG 14
WC Immunology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Research & Experimental Medicine
GA ZT738
UT WOS:000074120200010
PM 9607923
OA Green Published, Bronze
DA 2025-06-01
ER

PT J
AU Shartouni, R
   Shartouni, R
   Mahmoodi, M
   Nikas, IP
AF Shartouni, Ranim
   Shartouni, Roy
   Mahmoodi, Maryam
   Nikas, Ilias P.
TI The Value of Cytology in the Evaluation of Malignant Pericardial
   Effusions: A Systematic Review
SO DIAGNOSTICS
LA English
DT Article
DE pericardial fluid; sensitivity and specificity; diagnosis; prognosis;
   survival analysis; metastasis; pathology; cytopathology; lung neoplasms;
   cancer
ID PROGNOSTIC-FACTORS; CARDIAC-TAMPONADE; PLEURAL EFFUSION;
   CANCER-PATIENTS; POOR-PROGNOSIS; FLUID CYTOLOGY; MANAGEMENT; DIAGNOSIS;
   DRAINAGE; CYTOPATHOLOGY
AB Pericardial effusions can be caused by diverse etiologies, including heart-related conditions, kidney failure, trauma, infections, autoimmune diseases, and cancer. This systematic review aimed to assess the role of cytology in identifying the most prevalent cancers related to malignant pericardial effusions (MPEs), the ability of cytology, compared to histology, to detect cancer while evaluating pericardial effusions, and the prognostic impact of MPEs. Four electronic databases were investigated using a predefined algorithm, and specific inclusion and exclusion criteria. We found that the most prevalent primaries associated with MPEs were lung (especially NSCLCs), breast, hematolymphoid, and gastrointestinal cancers. MPEs tended to be hemorrhagic rather than serous or serosanguinous and to occupy larger volumes compared to non-neoplastic effusions. In addition, cytology was shown to exhibit an enhanced ability to detect cancer compared to biopsy in most of the included studies. Lastly, the presence of an MPE was associated with poor prognosis, while survival depended on the specific cancer type detected. Particularly, prognosis was found to be worse when MPEs were caused by lung or gastric cancer, rather than breast or hematolymphoid malignancies. In conclusion, evidence suggests that cytologic evaluation has a significant diagnostic and prognostic impact in patients with MPEs.
C1 [Shartouni, Ranim; Shartouni, Roy; Mahmoodi, Maryam; Nikas, Ilias P.] European Univ Cyprus, Sch Med, CY-2404 Nicosia, Cyprus.
C3 European University Cyprus
RP Nikas, IP (corresponding author), European Univ Cyprus, Sch Med, CY-2404 Nicosia, Cyprus.
EM ranimshartounimd@gmail.com; roy.shartouni7@gmail.com;
   mariya.mahmoodi@gmail.com; i.nikas@euc.ac.cy
RI mahmoodi, maryam/S-2424-2017
OI Nikas, Ilias/0000-0001-8625-2556
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NR 58
TC 11
Z9 11
U1 0
U2 6
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2075-4418
J9 DIAGNOSTICS
JI Diagnostics
PD FEB
PY 2022
VL 12
IS 2
AR 367
DI 10.3390/diagnostics12020367
PG 14
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA ZL8JN
UT WOS:000763917700001
PM 35204458
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bai, Y
   Pan, YD
   Liu, X
AF Bai, Yang
   Pan, Youdong
   Liu, Xing
TI Mechanistic insights into gasdermin-mediated pyroptosis
SO NATURE REVIEWS MOLECULAR CELL BIOLOGY
LA English
DT Review; Early Access
ID NONSYNDROMIC HEARING IMPAIRMENT; SINGLE NUCLEOTIDE POLYMORPHISM; DFNA5
   GENE; INFLAMMASOME ACTIVATION; GASTRIC-CANCER; HAIR FOLLICLE;
   GASTROINTESTINAL-TRACT; MACROPHAGE APOPTOSIS; NLRP3 INFLAMMASOME; INDUCE
   PYROPTOSIS
AB Pyroptosis, a novel mode of inflammatory cell death, is executed by membrane pore-forming gasdermin (GSDM) family members in response to extracellular or intracellular injury cues and is characterized by a ballooning cell morphology, plasma membrane rupture and the release of inflammatory mediators such as interleukin-1 beta (IL-1 beta), IL-18 and high mobility group protein B1 (HMGB1). It is a key effector mechanism for host immune defence and surveillance against invading pathogens and aberrant cancerous cells, and contributes to the onset and pathogenesis of inflammatory and autoimmune diseases. Manipulating the pore-forming activity of GSDMs and pyroptosis could lead to novel therapeutic strategies. In this Review, we discuss the current knowledge regarding how GSDM-mediated pyroptosis is initiated, executed and regulated, its roles in physiological and pathological processes, and the crosstalk between different modes of programmed cell death. We also highlight the development of drugs that target pyroptotic pathways for disease treatment.
C1 [Bai, Yang; Liu, Xing] Chinese Acad Sci, Shanghai Inst Immun & Infect, Shanghai, Peoples R China.
   [Pan, Youdong] Harvard Med Sch, Brigham & Womens Hosp, Dept Dermatol, Boston, MA USA.
   [Liu, Xing] Shanghai Acad Nat Sci SANS, Shanghai, Peoples R China.
C3 Chinese Academy of Sciences; Shanghai Institute of Immunity and
   Infection, CAS; Harvard University; Harvard Medical School; Harvard
   University Medical Affiliates; Brigham & Women's Hospital
RP Liu, X (corresponding author), Chinese Acad Sci, Shanghai Inst Immun & Infect, Shanghai, Peoples R China.; Liu, X (corresponding author), Shanghai Acad Nat Sci SANS, Shanghai, Peoples R China.
EM xingliu@ips.ac.cn
OI Liu, Xing/0000-0002-6277-3856
FU National Natural Science Foundation of China [32425023, 32400723,
   32122034]; National Key R&D Program of China [2020YFA0509600]; Shanghai
   Pilot Program for Basic Research-Chinese Academy of Sciences
   [JCYJ-SHFY-2021-009]; Strategic Priority Research Program of Chinese
   Academy of Sciences [XDB0570000]; Innovative Research Team of High-Level
   Local Universities in Shanghai [SHSMU-ZDCX20211002]; National
   Postdoctoral Program for Innovative Talents [BX20240395]; Chinese
   Postdoctoral Science Foundation [2024M753367]; Shanghai Sailing Program
   [24YF2754200]
FX This work was partly supported by the National Natural Science
   Foundation of China (32425023, 32400723, 32122034), the National Key R&D
   Program of China (2020YFA0509600), the Shanghai Pilot Program for Basic
   Research-Chinese Academy of Sciences, Shanghai Branch
   (JCYJ-SHFY-2021-009), the Strategic Priority Research Program of Chinese
   Academy of Sciences (XDB0570000), the Innovative Research Team of
   High-Level Local Universities in Shanghai (SHSMU-ZDCX20211002), the
   National Postdoctoral Program for Innovative Talents (BX20240395), the
   Chinese Postdoctoral Science Foundation (2024M753367) and the Shanghai
   Sailing Program (24YF2754200). X.L. is a SANS Exploration Scholar. The
   authors apologize to colleagues whose work could not be cited owing to
   space limitations.
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NR 245
TC 0
Z9 0
U1 12
U2 12
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1471-0072
EI 1471-0080
J9 NAT REV MOL CELL BIO
JI Nat. Rev. Mol. Cell Biol.
PD 2025 MAR 24
PY 2025
DI 10.1038/s41580-025-00837-0
EA MAR 2025
PG 21
WC Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology
GA 0MG0P
UT WOS:001450718800001
PM 40128620
DA 2025-06-01
ER

PT J
AU Fukiishi, Y
   Fukuhara, H
   Kurano, Y
   Shugimoto, H
   Yamashita, E
   Karasima, T
   Inoue, K
AF Fukiishi, Yousuke
   Fukuhara, Hideo
   Kurano, Yoshitaka
   Shugimoto, Hiroki
   Yamashita, Erika
   Karasima, Takashi
   Inoue, Keiji
TI A case of acute lymphocytic gastritis related to treatment with
   pembrolizumab for metastatic urothelial carcinoma
SO IJU CASE REPORTS
LA English
DT Article
DE acute lymphocytic gastritis; metastatic urothelial carcinoma;
   pembrolizumab
ID CASE SERIES
AB IntroductionImmune checkpoint inhibitors such as programmed cell death/-ligand 1 inhibitor and cytotoxic T-lymphocyte-associated antigen-4 inhibitors have been widely used for various advanced malignancies. The mechanism of action for these inhibitors is the improvement of antitumor immunity via T-cell modulation. On the contrary, immune-related adverse events such as autoimmune colitis might arise in association with T-cell activation. Upper gastrointestinal adverse events related to pembrolizumab have rarely been reported.Case presentationA 72-year-old man underwent laparoscopic radical cystectomy for muscle-invasive bladder cancer (pT2N0M0). Multiple lymph node metastases appeared in the paraaortic region. First-line chemotherapy comprising gemcitabine and carboplatin failed to stop disease progression. After the administration of pembrolizumab as second-line treatment, the patient showed symptomatic gastroesophageal reflux disease. Esophagogastroduodenoscopic biopsy of the gastric body showed severe lymphoplasmacytic and neutrophilic infiltration.ConclusionWe present acute gastritis related to pembrolizumab. Early eradication therapy may be able to control immune checkpoint inhibitor-related gastritis.
C1 [Fukiishi, Yousuke] Natl Hosp Org Kochi Natl Hosp, Dept Urol, Kochi, Japan.
   [Fukuhara, Hideo; Kurano, Yoshitaka; Shugimoto, Hiroki; Yamashita, Erika; Karasima, Takashi; Inoue, Keiji] Kochi Med Sch, Dept Urol, Kohasu,Oko, Kochi 7838505, Japan.
C3 Kochi University
RP Fukuhara, H (corresponding author), Kochi Med Sch, Dept Urol, Kohasu,Oko, Kochi 7838505, Japan.
EM jm-fukuhara@kochi-u.ac.jp
OI Karashima, Takashi/0000-0001-7338-8059
FX We thank Hung Wei Lai for English language editing from the center for
   photodynamic medicine, Kochi Medical School.
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NR 9
TC 1
Z9 1
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
EI 2577-171X
J9 IJU CASE REP
JI IJU Case Rep.
PD MAR
PY 2023
VL 6
IS 2
BP 128
EP 132
DI 10.1002/iju5.12568
PG 5
WC Urology & Nephrology
WE Emerging Sources Citation Index (ESCI)
SC Urology & Nephrology
GA A6X0B
UT WOS:001283935100009
PM 36874988
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Amato, G
   Vita, F
   Quattrocchi, P
   Minciullo, PL
   Pioggia, G
   Gangemi, S
AF Amato, Giuliana
   Vita, Federica
   Quattrocchi, Paolina
   Minciullo, Paola Lucia
   Pioggia, Giovanni
   Gangemi, Sebastiano
TI Involvement of miR-142 and miR-155 in Non-Infectious Complications of
   CVID
SO MOLECULES
LA English
DT Review
DE common variable immunodeficiency; microRNAs; miR-142; miR-155;
   autoimmunity; cancer
ID GASTRIC-CANCER; CELL LYMPHOMA; EXPRESSION; IMMUNODEFICIENCY
AB Background and objectives: Common variable immunodeficiency (CVID) is the most prevalent antibody impairment. It is characterized by failure in immunoglobulin and protective antibody generation and defined by an increased tendency toward bacterial infections, autoimmunity, and malignancy. Most CVID diagnoses do not follow a classical Mendelian pattern of inheritance. In recent years, CVID has been considered an epigenetic phenomenon in the majority of cases, overtaking previous monogenetic and/or polygenetic theories. The aim of this study was to review the role of microRNAs (miRNAs) in CVID, focusing on the involvement of the same miRNAs in various non-infectious clinical complications of CVID, mainly autoimmunity and/or cancer. Materials and Methods: A bibliographic search of the scientific literature was carried out independently by two researchers in scientific databases and search engines. The MeSH terms "microRNAs" and "common variable immunodeficiency" were used. All research articles from inception to May 2020 were considered. Results: The literature data showed the involvement of two miRNAs in primary immunodeficiency: miR-142 and miR-155. Both of these miRNAs have been investigated through mice models, in which miR-142 and miR-155 were deleted. These knock-out (KO) mice models showed phenotypic analogies to CVID patients with hypogammaglobulinemia, adaptive immunodeficiency, polyclonal proliferation, lung disease, and enteric inflammation. miR-142 and miR-155 have been found to be involved in the following autoimmune and neoplastic clinical complications of CVID: Gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, natural killer/Tcell lymphoma (NKTCL), and immune thrombocytopenia. Conclusions: miR-142 and miR-155 deregulation leads to similar CVID phenotypesin KO mice models. Although no data are available on the involvement of these miRNAs in human CVID, their dysregulation has been detected in human CVID comorbidities. The literature data show that miRNA sequences in murine models are comparable to those in humans; therefore, miR-142 and miR-155 involvement in human CVID could be hypothesized.
C1 [Amato, Giuliana; Vita, Federica; Quattrocchi, Paolina; Minciullo, Paola Lucia; Gangemi, Sebastiano] Univ Messina, Dept Clin & Expt Med, Operat Unit, I-98125 Messina, Italy.
   [Amato, Giuliana; Vita, Federica; Quattrocchi, Paolina; Minciullo, Paola Lucia; Gangemi, Sebastiano] Univ Messina, Dept Clin & Expt Med, Sch Allergy & Clin Immunol, I-98125 Messina, Italy.
   [Pioggia, Giovanni] Natl Res Council Italy CNR, Inst Biomed Res & Innovat IRIB, I-98164 Messina, Italy.
C3 University of Messina; University of Messina; Consiglio Nazionale delle
   Ricerche (CNR); Istituto Ricerca l'Innovazione Biomedica (IRIB-CNR)
RP Pioggia, G (corresponding author), Natl Res Council Italy CNR, Inst Biomed Res & Innovat IRIB, I-98164 Messina, Italy.
EM giulianaamato89@hotmail.it; federica.vita75@gmail.com;
   pquattrocchi@unime.it; pminciullo@unime.it; giovanni.pioggia@cnr.it;
   gangemis@unime.it
RI vita, Federica/HQF-9850-2023; gangemi, sebastiano/GLR-3109-2022;
   Pioggia, Giovanni/C-8119-2016
OI Pioggia, Giovanni/0000-0002-8089-7449; gangemi,
   sebastiano/0000-0001-7001-6532
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NR 38
TC 9
Z9 9
U1 0
U2 5
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1420-3049
J9 MOLECULES
JI Molecules
PD OCT
PY 2020
VL 25
IS 20
AR 4760
DI 10.3390/molecules25204760
PG 10
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA OL7MJ
UT WOS:000585518800001
PM 33081305
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Irshaid, L
   Robert, ME
   Zhang, XC
AF Irshaid, Lina
   Robert, Marie E.
   Zhang, Xuchen
TI Immune Checkpoint Inhibitor Induced Upper Gastrointestinal Tract
   Inflammation Shows Morphologic Similarities to, but Is Immunologically
   Distinct From, Helicobacter pylori Gastritis and Celiac Disease
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID ADVERSE EVENTS; COLITIS; BLOCKADE; CANCER
AB Context.-Immune checkpoint inhibitor (CPI) therapies are associated with multi-organ immune-related adverse events. Although colonic mucosal changes have been described, inflammatory changes incited by CPIs in the upper gastrointestinal tract have not been well characterized.
   Objective.-To investigate morphologic and immunologic changes incited by CPI therapy in the upper gastrointestinal tract.
   Design.-We compared the morphology and immune cell phenotype of gastric and duodenal biopsies from patients treated with anti-cytotoxic T-lymphocyte associated protein 4 (CTLA-4) or anti-programmed death receptor-1/programmed death ligand-1 (PD-1/PD-L1) antibodies with biopsies from patients with Helicobacter pylori gastritis, patients with celiac disease, and normal controls.
   Results.-Gastric biopsies from patients on CPIs showed chronic gastritis mimicking H pylori gastritis. However, CPI gastritis demonstrated greater numbers of CD8(+) intraepithelial lymphocytes, less lamina propria inflamma- tion, fewer plasma cells and CD20(+) 8 cells, fewer lymphoid aggregates, and reduced CD4:CD8 ratio in both the lamina propria and the epithelial layer. There were no differences between anti-CTLA-4 and anti-PD-1/PD-L1 gastritis, except for more lymphoid aggregates in anti-PD-1/PD-L1 gastritis. Duodenal biopsies from patients on CPIs revealed chronic duodenitis with villous blunting, mimicking celiac disease. Compared with celiac disease, CPI duodenitis demonstrated higher prevalence of neutrophilic infiltrates and erosions, increased lamina propria CD3 and CD8 T cells, and reduced CD4:CD8 ratio. Upper gastrointestinal biopsies were more inflamed than concomitant colonic biopsies in the majority of patients.
   Conclusions.-The morphologic and immunophenotypic distinctions between CPI-associated upper gastrointestinal injuries and common infectious and autoimmune diseases may provide useful discriminators when clinicians are confronted with gastric and duodenal inflammatory changes in patients receiving CPI therapy.
C1 [Irshaid, Lina; Robert, Marie E.; Zhang, Xuchen] Yale Univ, Dept Pathol, Sch Med, 310 Cedar St,POB 208023, New Haven, CT 06520 USA.
C3 Yale University
RP Zhang, XC (corresponding author), Yale Univ, Dept Pathol, Sch Med, 310 Cedar St,POB 208023, New Haven, CT 06520 USA.
EM Xuchen.zhang@yale.edu
CR Aslanian H, 2012, DIGEST DIS SCI, V57, P720, DOI 10.1007/s10620-011-1938-x
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NR 26
TC 29
Z9 30
U1 0
U2 1
PU COLL AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
EI 1543-2165
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD FEB
PY 2021
VL 145
IS 2
BP 191
EP 200
DI 10.5858/arpa.2019-0700-OA
PG 10
WC Medical Laboratory Technology; Medicine, Research & Experimental;
   Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology; Research & Experimental Medicine;
   Pathology
GA QA2NA
UT WOS:000613283900010
PM 33501492
OA gold
DA 2025-06-01
ER

PT J
AU Shu, X
   Ji, J
   Li, X
   Sundquist, J
   Sundquist, K
   Hemminki, K
AF Shu, X.
   Ji, J.
   Li, X.
   Sundquist, J.
   Sundquist, K.
   Hemminki, K.
TI Cancer risk among patients hospitalized for Type 1 diabetes mellitus: a
   population-based cohort study in Sweden
SO DIABETIC MEDICINE
LA English
DT Article
DE age at first hospitalization; cancer risk; national registry; Type 1
   diabetes mellitus
ID VIRAL-INFECTIONS; CELIAC-DISEASE; MANIFESTATIONS; ENDOMETRIAL; CHILDREN;
   INSULIN
AB P>Aims
   Type 1 diabetes mellitus (T1DM) is an autoimmune disease with potential mechanistic links to immune-related cancers. We aimed at examining the overall and specific cancer risks among hospitalized T1DM patients from the national registers in Sweden.
   Methods
   A T1DM research cohort was created by identifying T1DM patients from the Hospital Discharge Register and linking them with the Cancer Registry. Standardized incidence ratios (SIRs) for subsequent cancers were calculated among patients with T1DM compared with those without T1DM.
   Results
   Two hundred and fifty-eight cases were ascertained with subsequent cancers during the follow-up duration from 1964 to 2006, with an increased overall SIR of 1.17 (95% CI 1.04-1.33) among 24 052 T1DM patients identified at baseline. Significant excess was noted for gastric and skin (squamous cell carcinoma) cancers and for leukaemia. Increased risk of acute lymphatic leukaemia accounted for most of the variation of leukaemia risk (SIR = 5.31, 95% CI 3.32-8.05). Cancer risk varied with sex, age at first hospitalization and numbers of hospitalizations. The risk was higher in women compared with men and in those hospitalized for T1DM at age over 10 years compared with the younger patients. Higher risks were also found among those with more hospital visits.
   Conclusion
   By quantifying the variations of overall and site-specific cancer risks after T1DM, the current study provides novel associations between T1DM and subsequent cancers, the mechanisms of which remain to be established.
C1 [Shu, X.; Sundquist, K.; Hemminki, K.] Karolinska Inst, Ctr Family & Community Med, SE-14183 Huddinge, Sweden.
   [Shu, X.; Ji, J.; Li, X.; Sundquist, J.; Sundquist, K.; Hemminki, K.] Lund Univ, Ctr Primary Hlth Care Res, Malmo, Sweden.
   [Sundquist, J.] Stanford Univ, Sch Med, Stanford Prevent Res Ctr, Stanford, CA 94305 USA.
   [Hemminki, K.] German Canc Res Ctr, Div Mol Genet Epidemiol, Heidelberg, Germany.
C3 Karolinska Institutet; Lund University; Stanford University; Helmholtz
   Association; German Cancer Research Center (DKFZ)
RP Shu, X (corresponding author), Karolinska Inst, Ctr Family & Community Med, Alfred Nobels Alle 12, SE-14183 Huddinge, Sweden.
EM xiaochen.shu@ki.se
RI Ji, Jianguang/E-9579-2011
OI Ji, Jianguang/0000-0003-0324-9496; Li, Xinjun/0000-0002-5559-4657
FU Swedish Cancer Society; Swedish Council for Working Life and Social
   Research; Deutsche Krebshilfe
FX Source of funding: this research was supported by the Swedish Cancer
   Society, the Swedish Council for Working Life and Social Research and
   the Deutsche Krebshilfe. The registers used in the current study are
   maintained by the National Board of Health and Welfare and Statistics
   Sweden.
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NR 31
TC 91
Z9 94
U1 0
U2 9
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0742-3071
EI 1464-5491
J9 DIABETIC MED
JI Diabetic Med.
PD JUL
PY 2010
VL 27
IS 7
BP 791
EP 797
DI 10.1111/j.1464-5491.2010.03011.x
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 619OX
UT WOS:000279440600011
PM 20636960
DA 2025-06-01
ER

PT J
AU Escalante, GM
   Mutsvunguma, LZ
   Muniraju, M
   Rodriguez, E
   Ogembo, JG
AF Escalante, Gabriela M.
   Mutsvunguma, Lorraine Z.
   Muniraju, Murali
   Rodriguez, Esther
   Ogembo, Javier Gordon
TI Four Decades of Prophylactic EBV Vaccine Research: A Systematic Review
   and Historical Perspective
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Review
DE Epstein-Barr virus; infectious mononucleosis; cancer; prophylactic
   vaccine; glycoprotein; neutralizing antibody; herpesvirus; pre-clinical
ID EPSTEIN-BARR-VIRUS; ENVELOPE GLYCOPROTEIN GP340; PHASE-I TRIAL; MEMBRANE
   ANTIGEN GP340; NEUTRALIZING ANTIBODIES; COTTONTOP TAMARINS; COMMON
   MARMOSETS; INFECTIOUS-MONONUCLEOSIS; RHESUS LYMPHOCRYPTOVIRUS; GASTRIC
   ADENOCARCINOMA
AB Background: Epstein-Barr virus (EBV) is the causal agent of infectious mononucleosis and has been associated with various cancers and autoimmune diseases. Despite decades of research efforts to combat this major global health burden, there is no approved prophylactic vaccine against EBV. To facilitate the rational design and assessment of an effective vaccine, we systematically reviewed pre-clinical and clinical prophylactic EBV vaccine studies to determine the antigens, delivery platforms, and animal models used in these studies. Methods: We searched Cochrane Library, ClinicalTrials.gov, Embase, PubMed, Scopus, Web of Science, WHO's Global Index Medicus, and Google Scholar from inception to June 20, 2020, for EBV prophylactic vaccine studies focused on humoral immunity. Results: The search yielded 5,614 unique studies. 36 pre-clinical and 4 clinical studies were included in the analysis after screening against the exclusion criteria. In pre-clinical studies, gp350 was the most commonly used immunogen (33 studies), vaccines were most commonly delivered as monomeric proteins (12 studies), and mice were the most used animal model to test immunogenicity (15 studies). According to an adaptation of the CAMARADES checklist, 4 pre-clinical studies were rated as very high, 5 as high, 13 as moderate quality, 11 as poor, and 3 as very poor. In clinical studies, gp350 was the sole vaccine antigen, delivered in a vaccinia platform (1 study) or as a monomeric protein (3 studies). The present study was registered in PROSPERO (CRD42020198440). Conclusions: Four major obstacles have prevented the development of an effective prophylactic EBV vaccine: undefined correlates of immune protection, lack of knowledge regarding the ideal EBV antigen(s) for vaccination, lack of an appropriate animal model to test vaccine efficacy, and lack of knowledge regarding the ideal vaccine delivery platform. Our analysis supports a multivalent antigenic approach including two or more of the five main glycoproteins involved in viral entry (gp350, gB, gH/gL, gp42) and a multimeric approach to present these antigens. We anticipate that the application of two underused challenge models, rhesus macaques susceptible to rhesus lymphocryptovirus (an EBV homolog) and common marmosets, will permit the establishment of in vivo correlates of immune protection and attainment of more generalizable data.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?RecordID=198440, identifier PROSPERO I.D. CRD4202019844.
C1 [Escalante, Gabriela M.; Rodriguez, Esther] City Hope Natl Med Ctr, Irell & Manella Grad Sch Biol Sci, Duarte, CA USA.
   [Escalante, Gabriela M.; Mutsvunguma, Lorraine Z.; Muniraju, Murali; Ogembo, Javier Gordon] City Hope Natl Med Ctr, Dept Immuno Oncol, Beckman Res Inst, Duarte, CA 91010 USA.
C3 City of Hope; City of Hope; Beckman Research Institute of City of Hope
RP Ogembo, JG (corresponding author), City Hope Natl Med Ctr, Dept Immuno Oncol, Beckman Res Inst, Duarte, CA 91010 USA.
EM jogembo@coh.org
OI Escalante, Gabriela/0000-0003-3182-1947
FU National Institute for Allergy and Infectious Diseases [R56AI148295];
   Department of Defense [W81XWH-20-1-0401]
FX This study was funded by the National Institute for Allergy and
   Infectious Diseases R56AI148295 grant to JO, and Department of Defense
   W81XWH-20-1-0401 Horizon Award to GE. The funding agencies were not
   involved in the design of the study, data analysis or interpretation,
   nor manuscript preparation or study publication.
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NR 156
TC 19
Z9 22
U1 4
U2 16
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD APR 14
PY 2022
VL 13
AR 867918
DI 10.3389/fimmu.2022.867918
PG 44
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 1H1IP
UT WOS:000796300500001
PM 35493498
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Sun, T
   Zhou, YF
   Yang, M
   Hu, ZB
   Tan, W
   Han, XH
   Shi, YK
   Yao, JR
   Guo, YL
   Yu, DK
   Tian, T
   Zhou, XY
   Shen, HB
   Lin, DX
AF Sun, Tong
   Zhou, Yifeng
   Yang, Ming
   Hu, Zhibin
   Tan, Wen
   Han, Xiaohong
   Shi, Yuankai
   Yao, Jiarui
   Guo, Yongli
   Yu, Dianke
   Tian, Tian
   Zhou, Xiaoyi
   Shen, Hongbing
   Lin, Dongxin
TI Functional genetic variations in cytotoxic T-lymphocyte antigen 4
   and susceptibility to multiple types of cancer
SO CANCER RESEARCH
LA English
DT Article
ID T-LYMPHOCYTE ANTIGEN-4; SYSTEMIC-LUPUS-ERYTHEMATOSUS; AUTOIMMUNE
   THYROID-DISEASE; SQUAMOUS-CELL CARCINOMA; CTLA-4 GENE; METASTATIC
   MELANOMA; BREAST-CANCER; PROSTATE-CANCER; GRAVES-DISEASE; POLYMORPHISM
AB Antitumor T lymphocytes play a pivotal role in immunosurveillance of malignancy. The CTL antigen 4 (CTLA-4) is a vital negative regulator of T-cell activation and proliferation. This study examined whether genetic polymorphisms in CTLA-4 are associated with cancer susceptibility. A two-stage investigation using haplotype-tagging single nucleotide polymorphism approach and multiple independent case-control analyses was performed to assess the association between CTLA-4 genotypes and cancer risk. Functional relevance of the polymorphisms was examined by biochemical assays. We found that the 49G>A polymorphism in the CTLA-4 leading sequence causing (17)Ala to (17)Thr amino acid substitution is associated with increased susceptibility to multiple cancers, including lung, breast, esophagus, and gastric cardia cancers. Genotyping in 5,832 individuals with cancer and 5,831 control subjects in northern and southern Chinese populations showed that the CTLA-4 49AA genotype had an odds ratio of 1.72 (95% confidence interval, 1.50-2.10; P = 3.4 x 10(-7)) for developing cancer compared with the 49GG genotype. Biochemical analyses showed that CTLA-4-(17)Thr had higher capability to bind B7.1 and stronger inhibitory effect on T-cell activation compared with CTLA-4-(17)Ala. T cells carrying the 49AA genotype had significantly lower activation and proliferation rates compared with T cells carrying the 49GG genotype upon stimulation. These results are consistent with our hypothesis and indicate that genetic polymorphisms influencing T-cell activation modify cancer susceptibility.
C1 [Sun, Tong; Zhou, Yifeng; Yang, Ming; Tan, Wen; Guo, Yongli; Yu, Dianke; Lin, Dongxin] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Etiol & Carcinogenesis, Beijing 100021, Peoples R China.
   [Han, Xiaohong; Shi, Yuankai; Yao, Jiarui] Chinese Acad Med Sci, Canc Inst & Hosp, Dept Med Oncol, Beijing 100021, Peoples R China.
   [Han, Xiaohong; Shi, Yuankai; Yao, Jiarui] Peking Union Med Coll, Beijing 100021, Peoples R China.
   [Hu, Zhibin; Tian, Tian; Zhou, Xiaoyi; Shen, Hongbing] Nanjing Med Univ, Ctr Canc, Dept Epidemiol & Biostat, Nanjing, Peoples R China.
C3 Chinese Academy of Medical Sciences - Peking Union Medical College;
   Cancer Institute & Hospital - CAMS; Chinese Academy of Medical Sciences
   - Peking Union Medical College; Cancer Institute & Hospital - CAMS;
   Chinese Academy of Medical Sciences - Peking Union Medical College;
   Peking Union Medical College; Nanjing Medical University
RP Lin, DX (corresponding author), Chinese Acad Med Sci, Inst Canc, Dept Etiol & Carcinogenesis, Beijing 100021, Peoples R China.
EM dlin@public.bta.net.cn
RI Tian, Tongguan/MVX-5598-2025; Yang, Ming/G-4705-2012; Li,
   Xingchuan/JFB-4764-2023; shen, hong/HTQ-6147-2023; Sun,
   Tong/LZI-7687-2025; xi, li/JZC-6279-2024; Yu, Dianke/LDE-9085-2024
OI Lin, Dongxin/0000-0002-8723-8868; Shen, Hongbing/0000-0002-2581-5906
FU National Natural Science Foundation [30530710, 30425001, 30730080];
   State Key Basic Research Program [2004CB518701, 2002CB512902]
FX National Natural Science Foundation (grant 30530710 for 1). Lin: grant
   30425001 and 30730080 for H. Shen) and State Key Basic Research Program
   (grant 2004CB518701 for D. Lin. and grant 2002CB512902 for H. Shen).
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NR 46
TC 145
Z9 156
U1 0
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD SEP 1
PY 2008
VL 68
IS 17
BP 7025
EP 7034
DI 10.1158/0008-5472.CAN-08-0806
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 346PF
UT WOS:000259080300022
PM 18757416
OA Green Submitted
DA 2025-06-01
ER

PT J
AU Buzás, GM
AF Buzas, Gyorgy M.
TI Benign and malignant gastroduodenal diseases associated with
   Helicobacter pylori: a narrative review and personal remarks in
   2018
SO MINERVA GASTROENTEROLOGICA E DIETOLOGICA
LA English
DT Review
DE Dyspepsia; Stomach neoplasms; Polyps; Gastritis; Helicobacter pylori,
   Lymphoma
ID FUNDIC GLAND POLYPS; GLOBAL CONSENSUS REPORT; GASTRIN-RECEPTOR
   ANTAGONIST; FUNCTIONAL DYSPEPSIA; CARBONIC-ANHYDRASE; TRIPLE THERAPY;
   DOUBLE-BLIND; ATROPHIC GASTRITIS; CANCER STATISTICS; N-ACETYLCYSTEINE
AB The subject of Helicobacter pylori continues to elicit worldwide interest in many research fields. Epidemiological data suggest that the prevalence of the infection is decreasing in Western/developed countries and even in some developing regions, but this is masked by the high prevalence in the most populous regions. Chronic gastritis, caused invariably by the bacterium, was again classified in Kyoto and Helicobacter pylori-associated gastritis was included as a distinct entity. The prevalence of peptic ulcers is decreasing, but bleeding ulcers are a challenging problem, with stable mortality levels even in the endoscopic era. With the extended use of endoscopy, gastric polyps (GP) have become more prevalent: some are associated with the infection, some are not. Autoimmune and Helicobacter-induced gastritis can share common pathogenetic mechanisms. Gastric cancer (GC) is ranked highly on mortality lists worldwide. Its surgical treatment has registered some progress though. Little, if any improvement has been achieved in the medical treatment of advanced GC. With proper organization, GC seems a preventable disease. In spite of many guidelines, the Pan-European registry of Helicobacter pylori management shows that eradication rates obtained in many places are suboptimal. A new therapeutic regimen was compiled with promising pilot results. The results obtained with vonaprazan are limited to Asia. New avenues of both antibiotic and non-antibiotic treatments are expected to accelerate the eradication of this ulcerogenic and carcinogenic bacterium.
C1 [Buzas, Gyorgy M.] Ferencvaros Hlth Ctr, Dept Gastroenterol, Mester Utca 45, H-1095 Budapest, Hungary.
RP Buzás, GM (corresponding author), Ferencvaros Hlth Ctr, Dept Gastroenterol, Mester Utca 45, H-1095 Budapest, Hungary.
EM drbgym@gmail.com
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NR 100
TC 26
Z9 26
U1 0
U2 11
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 0026-4776
EI 1827-1642
J9 MINERVA GASTROENT D
JI Minerva Gastroenterol. Dietol.
PD SEP
PY 2018
VL 64
IS 3
BP 280
EP 296
DI 10.23736/S1121-421X.18.02481-9
PG 17
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA GU5AX
UT WOS:000445298000012
PM 29458240
DA 2025-06-01
ER

PT J
AU Chao, C
   Page, JH
   Yang, SJ
   Rodriguez, R
   Huynh, J
   Chia, VM
AF Chao, C.
   Page, J. H.
   Yang, S. -J.
   Rodriguez, R.
   Huynh, J.
   Chia, V. M.
TI History of chronic comorbidity and risk of chemotherapy-induced febrile
   neutropenia in cancer patients not receiving G-CSF prophylaxis
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE febrile neutropenia; neutropenia; chemotherapy; toxicity; comorbidities;
   cancer
ID TREATMENT-RELATED TOXICITY; BODY-MASS INDEX; INFECTION; OUTCOMES;
   FAILURE; DISEASE; COPD
AB Background: Chemotherapy-induced febrile neutropenia (FN) is a clinically important complication that affects patient outcome by delaying chemotherapy doses or reducing dose intensity. Risk of FN depends on chemotherapy-and patient-level factors. We sought to determine the effects of chronic comorbidities on risk of FN.
   Design: We conducted a cohort study to examine the association between a variety of chronic comorbidities and risk of FN in patients diagnosed with six types of cancer (non-Hodgkin lymphoma and breast, colorectal, lung, ovary, and gastric cancer) from 2000 to 2009 who were treated with chemotherapy at Kaiser Permanente Southern California, a large managed care organization. We excluded those patients who received primary prophylactic granulocyte colony-stimulating factor. History of comorbidities and FN events were identified using electronic medical records. Cox models adjusting for propensity score, stratified by cancer type, were used to determine the association between comorbid conditions and FN. Models that additionally adjusted for cancer stage, baseline neutrophil count, chemotherapy regimen, and dose reduction were also evaluated.
   Results: A total of 19 160 patients with mean age of 60 years were included; 963 (5.0%) developed FN in the first chemotherapy cycle. Chronic obstructive pulmonary disease [hazard ratio (HR) = 1.30 (1.07-1.57)], congestive heart failure [HR = 1.43 (1.00-1.98)], HIV infection [HR = 3.40 (1.90-5.63)], autoimmune disease [HR = 2.01 (1.10-3.33)], peptic ulcer disease [HR = 1.57 (1.05-2.26)], renal disease [HR = 1.60 (1.21-2.09)], and thyroid disorder [HR = 1.32 (1.06-1.64)] were all associated with a significantly increased FN risk.
   Conclusions: These results provide evidence that history of several chronic comorbidities increases risk of FN, which should be considered when managing patients during chemotherapy.
C1 [Chao, C.; Yang, S. -J.] Kaiser Permanente So Calif, Dept Res & Evaluat, Pasadena, CA 91101 USA.
   [Page, J. H.; Chia, V. M.] Amgen Inc, Ctr Observat Res, Thousand Oaks, CA 91320 USA.
   [Rodriguez, R.] Kaiser Permanente So Calif, Los Angeles Med Ctr, Dept Hematol Oncol, Los Angeles, CA USA.
   [Huynh, J.] Harbor UCLA Med Ctr, Dept Hematol & Oncol, Los Angeles, CA USA.
C3 Kaiser Permanente; Amgen; Kaiser Permanente; University of California
   System; University of California Los Angeles; University of California
   Los Angeles Medical Center; University of California System; University
   of California Los Angeles; University of California Los Angeles Medical
   Center
RP Chao, C (corresponding author), Kaiser Permanente So Calif, Dept Res & Evaluat, 100 S Los Robles Ave,2nd Floor, Pasadena, CA 91101 USA.
EM chun.r.chao@kp.org
FU Amgen, Inc. [51812]
FX This work was supported by Amgen, Inc. (Grant number 51812).
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NR 23
TC 50
Z9 51
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
EI 1569-8041
J9 ANN ONCOL
JI Ann. Oncol.
PD SEP
PY 2014
VL 25
IS 9
BP 1821
EP 1829
DI 10.1093/annonc/mdu203
PG 9
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AP8UB
UT WOS:000342353600022
OA Bronze
DA 2025-06-01
ER

PT J
AU Repetto, O
   Zanussi, S
   Casarotto, M
   Canzonieri, V
   De Paoli, P
   Cannizzaro, R
   De Re, V
AF Repetto, Ombretta
   Zanussi, Stefania
   Casarotto, Mariateresa
   Canzonieri, Vincenzo
   De Paoli, Paolo
   Cannizzaro, Renato
   De Re, Valli
TI Differential Proteomics of Helicobacter pylori Associated with
   Autoimmune Atrophic Gastritis
SO MOLECULAR MEDICINE
LA English
DT Article
ID 2-DIMENSIONAL GEL-ELECTROPHORESIS; CLINICAL STRAINS; VACCINE CANDIDATES;
   MASS-SPECTROMETRY; CELLULAR-PROTEINS; SEQUENCE-ANALYSIS;
   ESCHERICHIA-COLI; OXIDATIVE STRESS; EPITHELIAL-CELLS; GENOME SEQUENCE
AB Atrophic autoimmune gastritis (AAG) is a condition of chronic inflammation and atrophy of stomach mucosa, for which development can be partially triggered by the bacterial pathogen Helicobacter pylori (HP). HP can cause a variety of gastric diseases, such as duodenal ulcer (DU) or gastric cancer (GC). In this study, a comparative proteomic approach was used by two-dimensional fluorescence difference gel electrophoresis (DIGE) to identify differentially expressed proteins of HP strains isolated from patients with AAG, to identify markers of HP strain associated with AAG. Proteome profiles of HP isolated from GC or DU were used as a reference to compare proteomic levels. Proteomics analyses revealed 27 differentially expressed spots in AAG-associated HP in comparison with GC, whereas only 9 differential spots were found in AAG-associated HP profiles compared with DU. Proteins were identified after matrix- assisted laser desorption ionization (MALDI)-TOF and peptide mass fingerprinting. Some AAG-HP differential proteins were common between DU-and GC-HP (peroxiredoxin, heat shock protein 70 [HSP70], adenosine 5'- triphosphate [ATP] synthase subunit a, flagellin A). Our results presented here may suggest that comparative proteomes of HP isolated from AAG and DU share more common protein expression than GC and provide subsets of putative AAG-specific upregulated or downregulated proteins that could be proposed as putative markers of AAG-associated HP. Other comparative studies by two-dimensional maps integrated with functional genomics of candidate proteins will undoubtedly contribute to better decipher the biology of AAG-associated HP strains.
C1 [Repetto, Ombretta; De Paoli, Paolo; De Re, Valli] CRO, Facil Bioprote, Aviano Natl Canc Inst, I-33081 Aviano, PN, Italy.
   [Zanussi, Stefania; Casarotto, Mariateresa] CRO, Aviano Natl Canc Inst, I-33081 Aviano, PN, Italy.
   [Canzonieri, Vincenzo] CRO, Pathol Unit, Aviano Natl Canc Inst, I-33081 Aviano, PN, Italy.
   [Cannizzaro, Renato] CRO, Gastroenterol Unit, Aviano Natl Canc Inst, I-33081 Aviano, PN, Italy.
C3 IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano
   (CRO)
RP De Re, V (corresponding author), CRO, Facil Bioprote, Aviano Natl Canc Inst, Via F Gallini 2, I-33081 Aviano, PN, Italy.
EM vdere@cro.it
RI De Re, Valli/K-4121-2016; De Paoli, Paolo/AAG-2586-2021; Canzonieri,
   Vincenzo/AAA-7951-2019; Repetto, Ombretta/V-6342-2019; CASAROTTO,
   MARIATERESA/D-3947-2019; Canzonieri, Vincenzo/K-3141-2018; DE RE,
   VALLI/AAA-1374-2019; ZANUSSI, STEFANIA/I-2558-2018; Cannizzaro,
   Renato/V-3804-2018
OI Repetto, Ombretta/0000-0002-0785-5066; De Paoli,
   Paolo/0000-0002-9502-1781; CASAROTTO, MARIATERESA/0000-0001-5832-2895;
   Canzonieri, Vincenzo/0000-0001-6010-0976; DE RE,
   VALLI/0000-0001-6100-9373; ZANUSSI, STEFANIA/0000-0003-0608-9766;
   Cannizzaro, Renato/0000-0002-2020-222X
FU Associazione Italiana per la Ricerca sul Cancro (AIRC) [10266, 12214];
   Bio-Proteomics Core Facility, CRO Scientific Direction
FX This work was supported by Associazione Italiana per la Ricerca sul
   Cancro (AIRC) grant #10266 (to V De Re); AIRC grant #12214 (to R
   Cannizzaro); and the Bio-Proteomics Core Facility, CRO Scientific
   Direction. We thank Bruno Bacher for the use of DeCyder.
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NR 87
TC 19
Z9 20
U1 0
U2 27
PU FEINSTEIN INST MED RES
PI MANHASSET
PA 350 COMMUNITY DR, MANHASSET, NY 11030 USA
SN 1076-1551
EI 1528-3658
J9 MOL MED
JI Mol. Med.
PD JAN-JUN
PY 2014
VL 20
BP 57
EP 71
DI 10.2119/molmed.2013.00076
PG 15
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
   Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
   Medicine
GA AD3VF
UT WOS:000333173600008
PM 24395566
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bica, T
   Castelló, R
   Toussaint, LL
   Montesó-Curto, P
AF Bica, Teodora
   Castello, Ruth
   Toussaint, Loren L.
   Monteso-Curto, Pilar
TI Depression as a Risk Factor of Organic Diseases: An International
   Integrative Review
SO JOURNAL OF NURSING SCHOLARSHIP
LA English
DT Review
DE Depression; disease risk factor; modifiable factors; physical illnesses;
   triggers
ID COGNITIVE IMPAIRMENT; COMORBIDITIES; DISORDERS; SYMPTOMS; DEMENTIA
AB Purpose and Design: This integrative review offers a systematic synthesis of the international literature regarding the role of depression as a risk factor in physical illnesses and the mechanisms of this connection. Special attention is paid to those modifiable factors.
   Findings: Published studies of depression and physical illness and disease (N = 24) from five countries that were indexed in PubMed, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), APA PsycNET, Scopus, Dialnet, and CUIDEN were examined. Results suggest that depression is a significant risk factor for the development of physical illnesses and diseases. More commonly studied were the connections between depression and cardiovascular disease, metabolic syndrome, biochemical alterations, diabetes, dementia, cognitive impairment, Alzheimer's disease, somatization and chronic pain, asthma, arthritis, and hyperlipidemia. Less frequently studied conditions connected to depression were cancer, infections, allergies, autoimmune disease, gastric ulcer, rhinitis, thyroiditis, bronchitis, migraines, fractures, and osteoporosis.
   Conclusions: Mechanisms connecting depression to physical illness appear to involve alterations in the hypothalamic-pituitary axis, unhealthy lifestyle, chronic or acute stressors including posttraumatic stress, an increase in C-reactive protein (CRP) in men, taking antidepressant medication, and social and emotional loneliness.
C1 [Bica, Teodora] Comarcal Mora dEbre Hosp, Mora Debre, Spain.
   [Castello, Ruth] Brighton & Sussex Univ Hosp NHS Trust, Emergency Dept, Brighton, E Sussex, England.
   [Toussaint, Loren L.] Luther Coll, Dept Psychol, Decorah, IA USA.
   [Monteso-Curto, Pilar] Rovira & Virgili Univ, Dept Nursing, Avda Remolins 13-15,Campus Terres de lEbre, Tortosa 43500, Spain.
C3 Brighton and Sussex University Hospitals NHS Trust; University of
   Brighton; Universitat Rovira i Virgili
RP Montesó-Curto, P (corresponding author), Rovira & Virgili Univ, Dept Nursing, Avda Remolins 13-15,Campus Terres de lEbre, Tortosa 43500, Spain.
EM mariapilar.monteso@urv.cat
RI Montesó-Curto, Pilar/I-5875-2019; Monteso-Curto, Pilar/A-6749-2018
OI Monteso-Curto, Pilar/0000-0002-0833-2152
CR Aguilar-Navarro S, 2007, GAC MED MEX, V143, P141
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NR 29
TC 54
Z9 60
U1 2
U2 23
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1527-6546
EI 1547-5069
J9 J NURS SCHOLARSHIP
JI J. Nurs. Scholarsh.
PD JUL
PY 2017
VL 49
IS 4
BP 389
EP 399
DI 10.1111/jnu.12303
PG 11
WC Nursing
WE Science Citation Index Expanded (SCI-EXPANDED); Social Science Citation Index (SSCI)
SC Nursing
GA FC8SI
UT WOS:000407110900005
PM 28692781
OA Bronze
DA 2025-06-01
ER

PT J
AU De Re, V
   Orzes, E
   Canzonieri, V
   Maiero, S
   Fornasarig, M
   Alessandrini, L
   Cervo, S
   Steffan, A
   Zanette, G
   Mazzon, C
   De Paoli, P
   Cannizzaro, R
AF De Re, Valli
   Orzes, Enrico
   Canzonieri, Vincenzo
   Maiero, Stefania
   Fornasarig, Mara
   Alessandrini, Lara
   Cervo, Silvia
   Steffan, Agostino
   Zanette, Giorgio
   Mazzon, Cinzia
   De Paoli, Paolo
   Cannizzaro, Renato
TI Pepsinogens to Distinguish Patients With Gastric Intestinal Metaplasia
   and Helicobacter pylori Infection Among Populations at Risk for
   Gastric Cancer
SO CLINICAL AND TRANSLATIONAL GASTROENTEROLOGY
LA English
DT Article
ID FAMILY-HISTORY; FOLLOW-UP; AUTOIMMUNE GASTRITIS; ATROPHIC GASTRITIS;
   SERUM PEPSINOGENS; ASSOCIATION; MANAGEMENT; PATHOLOGY; RELATIVES;
   LESIONS
AB OBJECTIVES: The objectives of this study were to investigate the serum pepsinogen test for the prediction of OLGIM (Operative Link on Gastric Intestinal Metaplasia Assessment) stages in first-degree relatives (FDR-GC) of patients with gastric cancer (GC) and autoimmune chronic atrophic gastritis (ACAG).
   METHODS: In 67 consecutive patients with ACAG, 82 FDR-GC, and 53 controls (CTRL) without gastric disease (confirmed by biopsy), serum levels of pepsinogen 1 (PG1), pepsinogen 2 (PG2), G17, and the PG1/2 ratio were assessed by enzyme-linked immunosorbent assay kit. All ACAG patients had positive antiparietal cell antibody levels, estimated by indirect immunofluorescence. Biopsies taken in duplicate from the antrum, corpus, and fundus were stained with Giemsa for Helicobacter pylori detection. Endoscopic detection of metaplasia was confirmed by histological diagnosis. Histological classification of OLGIM stages was applied by using the criteria of severity and topography of intestinal metaplasia (IM).
   RESULTS: The highest discrimination capacity for distinguishing ACAG from other groups of patients was the gastrin G17 test. The lowest mean for PG1 and PG2 serum levels was found in ACAG. In multivariate analysis by age, PG1 and PG1/PG2 were independent prognostic factors for metaplasia, and PG2 also for the presence of a histological H. pylori infection. The serum PG1 level was significantly lower in individuals with IM at OLGIM stage >2 than in those with IM at OLGIM stage <2, resulting in a useful method for the prediction of OLGIM stage. With the inclusion of patient age at diagnosis in the prediction of >= 2 vs. 0-1 OLGIM stages, the receiver operating characteristic (ROC) curve at 47.9 ng/ml PG1 level reached a significant area under the curve (AUC) value (0.978, P<0.001). We also observed a slight difference in PG2 serum levels between histological H. pylori-positive and H. pylori-negative subjects (ROC AUC: 0.599).
   CONCLUSIONS: This study demonstrated an important increase in gastrin G17 serum level in autoimmune gastritis. PG1 serum level corrected by patient age can be used in the management of patients at risk for GC with a high predicted probability of having an OLGIM stage >= 2. Using a cutoff of 47.9 ng/ml, PG1 testing in FDR-GC and ACAG patients had a sensitivity of 95.83% and a specificity of 93.37. Although these results could be validated in a prospective study, the known importance of higher OLGIM stages in increasing the risk of GC development supports the rationale of proposing PG1 algorithm as a diagnostic tool for the selection of high-risk FDR-GC and ACAG patients at high-risk stages for subsequent detailed endoscopic examination to detect dysplasia and asymptomatic GC. In addition, serum PG1 and PG2 levels could stratify patients based on both H. pylori infection and OLGIM risk in consideration of the increased acknowledge regarding the role of H. pylori in the progression of gastritis to GC.
C1 [De Re, Valli] Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Bioimmunotherapy Bioprot, Aviano, Italy.
   [Orzes, Enrico; Maiero, Stefania; Fornasarig, Mara; Cannizzaro, Renato] Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Div Oncol Gastroenterol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
   [Canzonieri, Vincenzo; Alessandrini, Lara] Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Div Pathol, Aviano, Italy.
   [Cervo, Silvia; Steffan, Agostino] Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Clin Pathol, Aviano, Italy.
   [Zanette, Giorgio] Pordenone Hosp, Div Diabetol, Pordenone, Italy.
   [Mazzon, Cinzia] Pordenone Hosp, Div Endocrinol, Pordenone, Italy.
   [De Paoli, Paolo] Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Sci Direct, Aviano, Italy.
C3 IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano (CRO); IRCCS Aviano
   (CRO); IRCCS Aviano (CRO)
RP Cannizzaro, R (corresponding author), Ctr Riferimento Oncol, IRCCS, Natl Canc Inst, Div Oncol Gastroenterol, Via Franco Gallini 2, I-33081 Aviano, PN, Italy.
EM rcannizzaro@cro.it
RI De Paoli, Paolo/AAG-2586-2021; De Re, Valli/K-4121-2016; Canzonieri,
   Vincenzo/AAA-7951-2019; Steffan, Agostino/ABE-5972-2020; Maiero,
   Stefania/ABD-6092-2020; DE RE, VALLI/AAA-1374-2019; Fornasarig,
   Mara/ABD-5093-2020; Canzonieri, Vincenzo/K-3141-2018; Cannizzaro,
   Renato/V-3804-2018
OI Emami, Mohammad Hassan/0000-0002-0318-0081; Steffan,
   Agostino/0000-0002-6320-3054; Maiero, Stefania/0000-0001-5085-1549; DE
   RE, VALLI/0000-0001-6100-9373; Fornasarig, Mara/0000-0003-3388-0676;
   Canzonieri, Vincenzo/0000-0001-6010-0976; Cannizzaro,
   Renato/0000-0002-2020-222X
FU CRO intramural 5x000 research grant
FX This study was funded by an CRO intramural 5x000 research grant. The
   study is independent of the funding.
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NR 50
TC 41
Z9 41
U1 0
U2 20
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2155-384X
J9 CLIN TRANSL GASTROEN
JI Clin. Transl. Gastroenterol.
PD JUL
PY 2016
VL 7
AR e183
DI 10.1038/ctg.2016.42
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA DU3CD
UT WOS:000382087500006
PM 27441820
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Bégueret, H
   Vergier, B
   Parrens, M
   Lehours, P
   Laurent, F
   Vernejoux, JM
   Dubus, P
   Velly, JF
   Mégraud, F
   Taytard, A
   Merlio, JP
   de Mascarel, A
AF Bégueret, H
   Vergier, B
   Parrens, M
   Lehours, P
   Laurent, F
   Vernejoux, JM
   Dubus, P
   Velly, JF
   Mégraud, F
   Taytard, A
   Merlio, JP
   de Mascarel, A
TI Primary lung small B-cell lymphoma versus lymphoid hyperplasia -:
   Evaluation of diagnostic criteria in 26 cases
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE pulmonary lymphoma; CD43; Helicobacter pylori
ID HEPATITIS-C VIRUS; HELICOBACTER-PYLORI; GASTRIC LYMPHOMA; MUCOSA;
   TISSUE; ADENOCARCINOMA; MALT; REGRESSION
AB Primary lung non-Hodgkin's lymphoma is a rare neoplasm mostly represented by low-grade B-cell lymphomas of mucosa-associated lymphoid tissue. Their diagnostic criteria are now well defined on surgical specimens, but pathologists may experience difficulties in distinguishing them on exiguous biopsies from benign lymphoid hyperplasia and other lymphomas. Therefore. we examined a series of 26 lung lymphoid lesions to further define the pathologic features of either lymphoma or lymphoid hyperplasia on small specimens. We observed 16 primary lung non-Hodgkin's lymphomas with a large predominance of low-grade mucosa-associated lymphoid tissue-type lymphomas (87.5%, n = 14). There were no autoimmune disorders, but three patients had a concomitant infectious disease (hepatitis C virus and Helicobacter pylori gastritis). One patient presented with a synchronous pulmonary adenocarcinoma. As well as the classical mucosa-associated lymphoid tissue cellular infiltrate, immunohistochemical characterization of the 14 mucosa-associated lymphoid tissue-type lymphomas revealed the CD20+/CD43+ centrocyte-like cell phenotype in 10 cases (71.5%). Although the lymphoepithelial lesions observed in all lymphomatous cases have been reported in lung lymphoid hyperplasia, the determination of B-cell CD20+/CD43+ phenotype of the intraepithelial lymphocytes highly increased the specificity of lymphoepithelial lesions, A monoclonal immunoglobulin heavy chain gene rearrangement was present in 71.4% of the mucosa-associated lymphoid tissue-type lymphoma specimens. Investigation of H. pylori by polymerase chain reaction detection was negative, even for the two cases associated with H. pylori gastritis.
C1 Univ Bordeaux, Dept Pathol & Mol Biol, Pessac, France.
   Hop Haut Leveque, Dept Radiol, Pessac, France.
   Hop Haut Leveque, Dept Pulm Pathol, Pessac, France.
   Hop Haut Leveque, Dept Thorac Surg, Pessac, France.
   Hop Pellegrin, Dept Bacteriol, F-33076 Bordeaux, France.
C3 Universite de Bordeaux; CHU Bordeaux; Universite de Bordeaux; CHU
   Bordeaux; Universite de Bordeaux; Universite de Bordeaux; CHU Bordeaux;
   Universite de Bordeaux; CHU Bordeaux
EM hugues.begueret@chu-bordeaux.fr
OI Dubus, Pierre/0000-0003-1803-4711
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NR 25
TC 41
Z9 51
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD JAN
PY 2002
VL 26
IS 1
BP 76
EP 81
DI 10.1097/00000478-200201000-00009
PG 6
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA 508PL
UT WOS:000173097600009
PM 11756772
DA 2025-06-01
ER

PT J
AU Nagai, H
   Muto, M
AF Nagai, Hiroki
   Muto, Manabu
TI Optimal management of immune-related adverse events resulting from
   treatment with immune checkpoint inhibitors: a review and update
SO INTERNATIONAL JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Review
DE Immune-related adverse events; Immune checkpoint inhibitor; Organ
   specialists; Corticosteroid; Immunomodulatory/immunosuppressive agents
ID CELL LUNG-CANCER; PROGRAMMED DEATH 1; METASTATIC MELANOMA; UNTREATED
   MELANOMA; PHASE-3 TRIAL; IPILIMUMAB; NIVOLUMAB; PEMBROLIZUMAB;
   ANTI-CTLA-4; AUTOIMMUNE
AB Over the last two decades, molecular-targeted agents have become mainstream treatment for many types of malignancies and have improved the overall survival of patients. However, most patients eventually develop resistance to these targeted therapies. Recently, immunotherapies such as immune checkpoint inhibitors have revolutionized the treatment paradigm for many types of malignancies. Immune checkpoint inhibitors have been approved for treatment of melanoma, non-small cell lung cancer, renal cell carcinoma, head and neck squamous cell carcinoma, Hodgkin's lymphoma, bladder cancer and gastric cancer. However, oncologists have been faced with immune-related adverse events caused by immune checkpoint inhibitors; these are generally mild but can be fatal in some cases. Because immune checkpoint inhibitors have distinct toxicity profiles from those of chemotherapy or targeted therapy, many oncologists are not familiar with the principles for optimal management of immune-related adverse events, which require early recognition and appropriate treatment without delay. To achieve this, oncologists must educate patients and health-care workers, develop checklists of appropriate tests for immune-related adverse events and collaborate closely with organ specialists. Clinical questions that remain include whether immune checkpoint inhibitors should be administered to patients with autoimmune disease and whether patients for whom immune-related adverse events lead to delays in immunotherapy should be retreated. In addition, the predicted use of combination immunotherapies in the near future means that oncologists will face a higher incidence and severity of immune-related adverse events. This review provides an overview of the optimal management of immune-related adverse events attributed to immune checkpoint inhibitors.
C1 [Nagai, Hiroki; Muto, Manabu] Kyoto Univ, Grad Sch Med, Dept Clin Oncol, Sakyo Ku, 54 Kawahara Cho, Kyoto, Kyoto 6068507, Japan.
C3 Kyoto University
RP Nagai, H (corresponding author), Kyoto Univ, Grad Sch Med, Dept Clin Oncol, Sakyo Ku, 54 Kawahara Cho, Kyoto, Kyoto 6068507, Japan.
EM hwithe@kuhp.kyoto-u.ac.jp
RI Nagai, Hiroki/GXZ-7815-2022
OI Nagai, Hiroki/0000-0003-1673-2647
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NR 61
TC 44
Z9 48
U1 5
U2 24
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
   JAPAN
SN 1341-9625
EI 1437-7772
J9 INT J CLIN ONCOL
JI Int. J. Clin. Oncol.
PD JUN
PY 2018
VL 23
IS 3
BP 410
EP 420
DI 10.1007/s10147-018-1259-6
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA GF8GQ
UT WOS:000432207900002
PM 29516216
DA 2025-06-01
ER

PT J
AU Auñón, C
   Sanvisens, A
   Turon, E
   Vidal-Vila, A
   Puigdemont, M
   Osca-Gelis, G
   Eraso, A
   Marcos-Gragera, R
AF Aunon, Carmen
   Sanvisens, Arantza
   Turon, Estel
   Vidal-Vila, Anna
   Puigdemont, Montse
   Osca-Gelis, Gemma
   Eraso, Arantxa
   Marcos-Gragera, Rafael
TI Time trends and survival of marginal zone lymphoma over 25 years in
   Girona, Spain (1994-2018)
SO CANCER MEDICINE
LA English
DT Article
DE cancer; epidemiology; hematology; marginal zone lymphoma;
   population-based
ID POPULATION-BASED INCIDENCE; NON-HODGKINS-LYMPHOMAS; B-CELL LYMPHOMA;
   HEMATOLOGICAL MALIGNANCY; AUTOIMMUNE-DISEASES; UNITED-STATES; SUB-TYPE;
   NEOPLASMS; EPIDEMIOLOGY; SUBTYPE
AB Objective To analyze the incidence, incidence trends, and survival of marginal zone lymphomas (MZLs) in Girona and to describe these indicators based on the location in the case of extranodal MZLs.Methods Population-based study of MZL collected in the Girona Cancer Registry, 1994-2018. Sociodemographic data, tumor location, and stage were obtained from clinical records. Crude (CR) and age-adjusted (ASR(E)) incidence rates expressed per 100,000 person-years (p-y) were calculated. Joinpoint regression models were used for the trend analysis according to the MZL group. Five-year observed and net survival were analyzed.Results A total of 472 MZLs were included, 44 (9.3%) were nodal, 288 (61.0%) extranodal, 122 (25.9%) splenic, and the rest (n = 18) MZL, NOS. The CR for the MZL was 2.89 x 100,000 p-y (95% CI: 2.63-3.15), the ASR(E) was 3.26 x 100,000 p-y (95% CI: 2.97-3.57), and the annual percentage change (APC) was 1.6 (95% CI: 0.5-2.7). The ASR(E) for nodal MZL was 0.30 x 100,000 p-y (95% CI: 0.22-0.41) and showed an APC of 2.9% (95% CI: -16.4-26.6). For extranodal MZL, the ASR(E) was 1.98 x 100,000 p-y (95% CI: 1.76-2.23) and the APC was -0.4 (95% CI: -2.0-1.2). The most frequent locations of this type of MZL were the gastric (35.4%), skin (13.2%), and respiratory system (11.8%). The ASR(E) of the splenic MZL was 0.85 (95% CI: 0.71-1.02) with an APC of 12.8 (95% CI: 2.5-24.0). The 5-year net survival of MZL was 82.1% (95% CI: 76.3-86.5).Conclusions This study reveals differences in the incidence and trend of the incidence of MZL according to the subgroup, showing a significant increase in the overall MZL mainly due to splenic MZL type.
C1 [Aunon, Carmen; Eraso, Arantxa] Inst Invest Biomed Girona Dr Josep Trueta IDIBGI, Inst Catala Oncol, Radiat Oncol Dept, Girona, Spain.
   [Aunon, Carmen; Eraso, Arantxa] Univ Girona, Dept Med Sci, Girona, Spain.
   [Sanvisens, Arantza; Turon, Estel; Vidal-Vila, Anna; Puigdemont, Montse; Marcos-Gragera, Rafael] Inst Invest Biomed Girona Dr Josep Trueta IDIBGI, Epidemiol Unit, Girona, Spain.
   [Sanvisens, Arantza; Turon, Estel; Vidal-Vila, Anna; Puigdemont, Montse; Marcos-Gragera, Rafael] Inst Invest Biomed Girona Dr Josep Trueta IDIBGI, Girona Cancer Registry, Inst Catala Oncol, Oncol, Girona, Spain.
   [Sanvisens, Arantza; Vidal-Vila, Anna; Puigdemont, Montse; Osca-Gelis, Gemma; Marcos-Gragera, Rafael] Inst Recerca Contra Leucemia Josep Carreras, Girona, Spain.
   [Osca-Gelis, Gemma] Hosp Univ Dr Josep Trueta, Inst Catala Oncol, Inst Invest Biomed Girona Dr Josep Trueta IDIBGI, Registre Tumors Hosp RTH ICO ICS, Girona, Spain.
   [Osca-Gelis, Gemma] Univ Girona, Dept Econ, Res Grp Stat Econometr & Hlth GRECS, Girona, Spain.
   [Marcos-Gragera, Rafael] CIBER Epidemiol & Publ Hlth CIBERESP, Girona, Spain.
   [Marcos-Gragera, Rafael] Univ Girona, Dept Nursing, Girona, Spain.
C3 Universitat de Girona; Girona University Hospital Dr. Josep Trueta;
   Institut d'Investigacio Biomedica de Girona (IDIBGI); Institut Catala
   d'Oncologia; Universitat de Girona; Universitat de Girona; Girona
   University Hospital Dr. Josep Trueta; Institut d'Investigacio Biomedica
   de Girona (IDIBGI); Institut Catala d'Oncologia; Universitat de Girona;
   Girona University Hospital Dr. Josep Trueta; Institut d'Investigacio
   Biomedica de Girona (IDIBGI); Institut de Recerca Contra la Leucemia
   Josep Carreras (IJC); Universitat de Girona; Girona University Hospital
   Dr. Josep Trueta; Institut d'Investigacio Biomedica de Girona (IDIBGI);
   Institut Catala d'Oncologia; Universitat de Girona; CIBER - Centro de
   Investigacion Biomedica en Red; CIBERESP; Universitat de Girona
RP Marcos-Gragera, R (corresponding author), Inst Catala Oncol, Unitat Epidemiol, C Sol 15, Girona 17004, Spain.; Marcos-Gragera, R (corresponding author), Inst Catala Oncol, Canc Girona, Oncol, C Sol 15, Girona 17004, Spain.
EM rmarcos@iconcologia.net
RI Marcos-Gragera, Rafael/A-1437-2017
OI Marcos-Gragera, Rafael/0000-0001-9824-3657; Turon i Pulido,
   Estel/0009-0002-8446-4648
FU Agencia de Gestio d'Ajuts Universitaris i de Recerca [2021 SGR 01511];
   Josep Carreras Leukaemia Research Institute [FIJC1100]
FX Agencia de Gestio d'Ajuts Universitaris i de Recerca, Grant/Award
   Number: 2021 SGR 01511; Josep Carreras Leukaemia Research Institute,
   Grant/Award Number: FIJC1100
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NR 51
TC 0
Z9 0
U1 0
U2 0
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD JUN
PY 2023
VL 12
IS 11
BP 12343
EP 12353
DI 10.1002/cam4.5935
EA APR 2023
PG 11
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA J6TM3
UT WOS:000975103500001
PM 37076996
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Grant, WB
AF Grant, WB
TI Lower vitamin-D production from solar ultraviolet-B irradiance may
   explain some differences in cancer survival rates
SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION
LA English
DT Review
DE lung cancer; tobacco; prostate cancer; vitamin D; ultraviolet B
ID PROSTATE-CANCER; BREAST-CANCER; RACIAL-DIFFERENCES; ETHNIC-DIFFERENCES;
   AFRICAN-AMERICAN; COLON-CANCER; SOCIOECONOMIC-FACTORS;
   AUTOIMMUNE-DISEASES; COLORECTAL-CANCER; ESOPHAGEAL CANCER
AB Black Americans diagnosed with cancer generally have lower survival rates than white Americans, even after adjustment for stage of cancer at time of discovery and level of treatment received. The hypothesis developed in this work is that these lower cancer survival rates may be due to lower serum 25-hydroxyvitamin D (25(OH)D] for black Americans attributed to lower production rates of vitamin D from solar ultraviolet-B (UVB) irradiance due to darker skin. Black Americans generally hove 50-75% as much serum 25(OH)D as white Americans, and vitamin D is now thought to reduce the risk of incidence and mortality for 18 types of cancer. To explore this hypothesis, data for mortality rates for various types of cancer for the period 1970-1994 for black Americans were used with indices for solar UVB levels for July, smoking, alcohol consumption, urban residence and poverty level, all averaged by state, in multiple linear regression analyses using the ecologic approach. Solar UVB was found significantly inversely correlated with mortality rates for breast, colon, esophageal, gastric and rectal cancers for black Americans, albeit with lower associations than for white Americans. Smoking and alcohol consumption were also significantly correlated with several cancers. Based on these results, it seems worthwhile to conduct observational, prevention and intervention studies to further test the hypothesis that vitamin D can reduce the risk of cancer incidence and death.
C1 SUNARC, San Francisco, CA 94109 USA.
RP SUNARC, 2107 Van Ness Ave,Suite 403B, San Francisco, CA 94109 USA.
EM wgrant@sunarc.org
RI Grant, William/B-8311-2009
OI Grant, William/0000-0002-1439-3285
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NR 104
TC 84
Z9 87
U1 0
U2 7
PU NATL MED ASSOC
PI WASHINGON
PA 1012 10TH ST, N W, WASHINGON, DC 20001 USA
SN 0027-9684
EI 1943-4693
J9 J NATL MED ASSOC
JI J. Natl. Med. Assoc.
PD MAR
PY 2006
VL 98
IS 3
BP 357
EP 364
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA 020RP
UT WOS:000235928300006
PM 16573299
DA 2025-06-01
ER

PT J
AU Schirmer, B
   Neumann, D
AF Schirmer, Bastian
   Neumann, Detlef
TI The Function of the Histamine H4 Receptor in Inflammatory and
   Inflammation-Associated Diseases of the Gut
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE inflammation; cancer; colitis; mast cell; epithelial cell; gut
ID NATURAL-KILLER-CELLS; H-4 RECEPTOR; MAST-CELLS; HUMAN EOSINOPHILS;
   COLORECTAL-CANCER; HISTIDINE-DECARBOXYLASE; ULCERATIVE-COLITIS;
   BOWEL-DISEASE; PHARMACOLOGICAL CHARACTERIZATION; ALLERGIC INFLAMMATION
AB Histamine is a pleiotropic mediator involved in a broad spectrum of (patho)-physiological processes, one of which is the regulation of inflammation. Compounds acting on three out of the four known histamine receptors are approved for clinical use. These approved compounds comprise histamine H1-receptor (H1R) antagonists, which are used to control allergic inflammation, antagonists at H2R, which therapeutically decrease gastric acid release, and an antagonist at H3R, which is indicated to treat narcolepsy. Ligands at H4R are still being tested pre-clinically and in clinical trials of inflammatory diseases, including rheumatoid arthritis, asthma, dermatitis, and psoriasis. These trials, however, documented only moderate beneficial effects of H4R ligands so far. Nevertheless, pre-clinically, H4R still is subject of ongoing research, analyzing various inflammatory, allergic, and autoimmune diseases. During inflammatory reactions in gut tissues, histamine concentrations rise in affected areas, indicating its possible biological effect. Indeed, in histamine-deficient mice experimentally induced inflammation of the gut is reduced in comparison to that in histamine-competent mice. However, antagonists at H1R, H2R, and H3R do not provide an effect on inflammation, supporting the idea that H4R is responsible for the histamine effects. In the present review, we discuss the involvement of histamine and H4R in inflammatory and inflammation-associated diseases of the gut.
C1 [Schirmer, Bastian; Neumann, Detlef] Hannover Med Sch, Inst Pharmacol, D-30625 Hannover, Germany.
C3 Hannover Medical School
RP Neumann, D (corresponding author), Hannover Med Sch, Inst Pharmacol, D-30625 Hannover, Germany.
EM schirmer.bastian@mh-hannover.de; neumann.detlef@mh-hannover.de
RI Schirmer, Bastian/H-6729-2019; Neumann, Detlef/F-6182-2011
OI Schirmer, Bastian/0000-0002-4074-3584
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NR 176
TC 28
Z9 28
U1 4
U2 16
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD JUN
PY 2021
VL 22
IS 11
AR 6116
DI 10.3390/ijms22116116
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA SQ2GF
UT WOS:000660175500001
PM 34204101
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Miron, RJ
   Estrin, NE
   Sculean, A
   Zhang, YF
AF Miron, Richard J.
   Estrin, Nathan E.
   Sculean, Anton
   Zhang, Yufeng
TI Understanding exosomes: Part 2-Emerging leaders in regenerative medicine
SO PERIODONTOLOGY 2000
LA English
DT Review
DE dermasomes; exosomes; immunosomes; regenerative medicine;
   ultra-centrifugation
ID MESENCHYMAL STEM-CELLS; SPINAL-CORD-INJURY; PULMONARY
   ARTERIAL-HYPERTENSION; POSTTRAUMATIC-STRESS-DISORDER;
   ISCHEMIA-REPERFUSION INJURY; SMALL EXTRACELLULAR VESICLES; TYPE-2
   DIABETES-MELLITUS; MARROW STROMAL CELLS; MSC-DERIVED EXOSOMES;
   MICROGLIAL-MEDIATED NEUROINFLAMMATION
AB Exosomes are the smallest subset of extracellular signaling vesicles secreted by most cells with the ability to communicate with other tissues and cell types over long distances. Their use in regenerative medicine has gained tremendous momentum recently due to their ability to be utilized as therapeutic options for a wide array of diseases/conditions. Over 5000 publications are currently being published yearly on this topic, and this number is only expected to dramatically increase as novel therapeutic strategies continue to be developed. Today exosomes have been applied in numerous contexts including neurodegenerative disorders (Alzheimer's disease, central nervous system, depression, multiple sclerosis, Parkinson's disease, post-traumatic stress disorders, traumatic brain injury, peripheral nerve injury), damaged organs (heart, kidney, liver, stroke, myocardial infarctions, myocardial infarctions, ovaries), degenerative processes (atherosclerosis, diabetes, hematology disorders, musculoskeletal degeneration, osteoradionecrosis, respiratory disease), infectious diseases (COVID-19, hepatitis), regenerative procedures (antiaging, bone regeneration, cartilage/joint regeneration, osteoarthritis, cutaneous wounds, dental regeneration, dermatology/skin regeneration, erectile dysfunction, hair regrowth, intervertebral disc repair, spinal cord injury, vascular regeneration), and cancer therapy (breast, colorectal, gastric cancer and osteosarcomas), immune function (allergy, autoimmune disorders, immune regulation, inflammatory diseases, lupus, rheumatoid arthritis). This scoping review is a first of its kind aimed at summarizing the extensive regenerative potential of exosomes over a broad range of diseases and disorders.
C1 [Miron, Richard J.; Sculean, Anton] Univ Bern, Dept Periodontol, Bern, Switzerland.
   [Estrin, Nathan E.] Adv PRF Educ, Venice, FL USA.
   [Estrin, Nathan E.] Lake Erie Coll Osteopath Med, Sch Dent Med, Bradenton, FL USA.
   [Zhang, Yufeng] Univ Wuhan, Dept Oral Implantol, Wuhan, Peoples R China.
C3 University of Bern; Wuhan University
RP Miron, RJ (corresponding author), Univ Bern, Dept Periodontol, Bern, Switzerland.
EM rick@themironlab.com
RI Miron, Richard/J-4995-2012; ZHANG, YAN/AAB-7383-2022
FU Universitat Bern
FX Open access funding provided by Universitat Bern.
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NR 1280
TC 16
Z9 16
U1 24
U2 50
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0906-6713
EI 1600-0757
J9 PERIODONTOL 2000
JI Periodontol. 2000
PD FEB
PY 2024
VL 94
IS 1
BP 257
EP 414
DI 10.1111/prd.12561
EA APR 2024
PG 158
WC Dentistry, Oral Surgery & Medicine
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dentistry, Oral Surgery & Medicine
GA RL4G8
UT WOS:001198670000001
PM 38591622
OA hybrid
HC Y
HP N
DA 2025-06-01
ER

PT J
AU DiCesare, E
   Previti, M
   Russo, F
   Brancatelli, S
   Ingemi, MC
   Scoglio, R
   Mazzu, N
   Cucinotta, D
   Raimondo, G
AF DiCesare, E
   Previti, M
   Russo, F
   Brancatelli, S
   Ingemi, MC
   Scoglio, R
   Mazzu, N
   Cucinotta, D
   Raimondo, G
TI Interferon-alpha therapy may induce insulin autoantibody development in
   patients with chronic viral hepatitis
SO DIGESTIVE DISEASES AND SCIENCES
LA English
DT Article
DE interferon-alpha; insulin autoantibody; chronic viral hepatitis
ID DEPENDENT DIABETES-MELLITUS; MALIGNANT CARCINOID-TUMORS; ISLET CELL
   ANTIBODIES; AUTOIMMUNE-DISEASE; ALFA THERAPY; HYPOTHYROIDISM; MICE;
   ONSET
AB Development of type 1 insulin-dependent diabetes mellitus has been recently reported in patients who underwent interferon-alpha (IFN-alpha) therapy because of chronic viral hepatitis. Furthermore IFN-alpha seems to be involved in the immunological events that lead to beta-cell destruction and development of type 1 diabetes. To evaluate whether IFN-alpha treatment could elicit an autoimmune response against beta-cell antigens, we determined the occurrence of islet cell antibodies and insulin auotantibodies in the sera of 60 patients with HCV- or HBV- related chronic hepatitis who had been treated with IFN-alpha for 6 or 12 months. The presence of antibodies against thyroglobulin, thyroid microsomal antigen, gastric parietal cells, and non-organ-specific antigens was also investigated. Insulin autoantibody positivity was observed in 2/60 (3.3%), 8/60 (13.3%), and 4/30(13.3%) patients, before IFN-alpha treatment, and after 6 months and 12 months of therapy, respectively. None of the studied patients developed islet cell antibodies of type 1 diabetes. Before IFN-alpha therapy four patients showed thyroid autoantibodies and four others developed antibodies against thyroglobulin and/or thyroid microsomal antigen during the treatment. Coexistence of insulin autoantibodies and thyroid autoantibodies was observed in only two patients. Our results showed that IFN-alpha therapy in patients with chronic viral hepatitis is capable of inducing development of autoantibodies against insulin. This event seems to be not related to other autoimmune disorders.
C1 UNIV MESSINA,DEPT INTERNAL MED,MESSINA,ITALY.
C3 University of Messina
RI cucinotta, domenico/F-4832-2014
OI CUCINOTTA, Domenico Maria/0000-0002-8159-5709
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NR 32
TC 45
Z9 46
U1 0
U2 0
PU PLENUM PUBL CORP
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013
SN 0163-2116
J9 DIGEST DIS SCI
JI Dig. Dis. Sci.
PD AUG
PY 1996
VL 41
IS 8
BP 1672
EP 1677
DI 10.1007/BF02087923
PG 6
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA VD696
UT WOS:A1996VD69600028
PM 8769300
DA 2025-06-01
ER

PT J
AU Zheng, ZZ
   Deng, WY
   Lou, XW
   Bai, Y
   Wang, JH
   Zeng, HS
   Gong, ST
   Liu, X
AF Zheng, Zengzhang
   Deng, Wanyan
   Lou, Xiwen
   Bai, Yang
   Wang, Junhong
   Zeng, Huasong
   Gong, Sitang
   Liu, Xing
TI Gasdermins: pore-forming activities and beyond
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Review
DE gasdermin; pore-forming protein; pyroptosis; deafness; tumorigenesis
ID SYNDROMIC HEARING-LOSS; DRUGS INDUCE PYROPTOSIS; SPLICE-SITE MUTATION;
   DFNA5 GENE; GASTRIC-CANCER; HAIR FOLLICLE; GASTROINTESTINAL-TRACT;
   PROMOTER METHYLATION; DUTCH FAMILY; IDENTIFICATION
AB Gasdermins (GSDMs) belong to a protein superfamily that is found only in vertebrates and consists of GSDMA, GSDMB, GSDMC, GSDMD, DFNA5 (a.k.a. GSDME) and DFNB59 (a.k.a. Pejvakin (PJVK)) in humans. Except for DFNB59, all members of the GSDM superfamily contain a conserved two-domain structure (N-terminal and C-terminal domains) and share an autoinhibitory mechanism. When the N-terminal domain of these GSDMs is released, it possesses pore-forming activity that causes inflammatory death associated with the loss of cell membrane integrity and release of inflammatory mediators. It has also been found that spontaneous mutations occurring in the genes of GSDMs have been associated with the development of certain autoimmune disorders, as well as cancers. Here, we review the current knowledge of the expression profile and regulation of GSDMs and the important roles of this protein family in inflammatory cell death, tumorigenesis and other related diseases.
C1 [Zheng, Zengzhang; Deng, Wanyan; Zeng, Huasong; Gong, Sitang; Liu, Xing] Guangzhou Women & Childrens Med Ctr, Joint Ctr Infect & Immun, Guangzhou Inst Pediat, Guangzhou 510623, Peoples R China.
   [Zheng, Zengzhang; Deng, Wanyan; Zeng, Huasong; Gong, Sitang; Liu, Xing] Chinese Acad Sci, Inst Pasteur Shanghai, Shanghai 200031, Peoples R China.
   [Zheng, Zengzhang; Deng, Wanyan; Lou, Xiwen; Bai, Yang; Wang, Junhong; Liu, Xing] Chinese Acad Sci, Inst Pasteur Shanghai, Ctr Microbes Dev & Hlth, Key Lab Mol Virol & Immunol, Shanghai 200031, Peoples R China.
   [Bai, Yang] Chinese Acad Sci, Univ Chinese Acad Sci, Shanghai 200031, Peoples R China.
C3 Chinese Academy of Sciences; Shanghai Institute of Immunity and
   Infection, CAS; Pasteur Network; Pasteur Network; Chinese Academy of
   Sciences; Shanghai Institute of Immunity and Infection, CAS; Chinese
   Academy of Sciences; University of Chinese Academy of Sciences, CAS
RP Gong, ST; Liu, X (corresponding author), Guangzhou Women & Childrens Med Ctr, Joint Ctr Infect & Immun, Guangzhou Inst Pediat, Guangzhou 510623, Peoples R China.; Gong, ST; Liu, X (corresponding author), Chinese Acad Sci, Inst Pasteur Shanghai, Shanghai 200031, Peoples R China.; Liu, X (corresponding author), Chinese Acad Sci, Inst Pasteur Shanghai, Ctr Microbes Dev & Hlth, Key Lab Mol Virol & Immunol, Shanghai 200031, Peoples R China.
EM sitangg@126.com; xingliu@ips.ac.cn
RI Zeng, Huasong/GOV-4872-2022; Wang, JunHong/HKE-0286-2023
FU China National Youth Thousand Talents Program; National Natural Science
   Foundation of China [31972897]; Key Research Program of the Chinese
   Academy of Sciences [ZDBS-LY-SM008]; Strategic Priority Research Program
   of Chinese Academy of Sciences [XDB29030300]; National Key R&D Program
   of China [2016YFC1100204]; Rising-Star Program of Shanghai Science and
   Technology Committee [19QA1409800]; Shanghai Municipal Natural Science
   Foundation [18ZR1443900]; Shanghai Municipal Science and Technology
   Major Project [2019SHZDZX02]; National Natural Science Foundation of
   China for the Youth [31900456]; China Postdoctoral Research Program
FX This work was supported in part by the grants from the China National
   Youth Thousand Talents Program, the National Natural Science Foundation
   of China (No. 31972897), the Key Research Program of the Chinese Academy
   of Sciences (No. ZDBS-LY-SM008), the Strategic Priority Research Program
   of Chinese Academy of Sciences (No. XDB29030300), the National Key R&D
   Program of China (No. 2016YFC1100204), the Rising-Star Program of
   Shanghai Science and Technology Committee (No. 19QA1409800), the
   Shanghai Municipal Natural Science Foundation (No. 18ZR1443900), the
   Shanghai Municipal Science and Technology Major Project (No.
   2019SHZDZX02) to X.L., and the National Natural Science Foundation of
   China for the Youth (No. 31900456) to Z.Z. W.D. is sponsored by the
   China Postdoctoral Research Program.
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NR 101
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U2 25
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1672-9145
EI 1745-7270
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD MAY
PY 2020
VL 52
IS 5
BP 467
EP 474
DI 10.1093/abbs/gmaa016
PG 8
WC Biochemistry & Molecular Biology; Biophysics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biophysics
GA ME9QU
UT WOS:000544989800001
PM 32294153
OA Bronze
DA 2025-06-01
ER

PT J
AU OGAWA, H
   SAKUMA, M
   MORIOKA, S
   KITAMURA, K
   SASAI, Y
   IMAMURA, S
   INABA, Y
AF OGAWA, H
   SAKUMA, M
   MORIOKA, S
   KITAMURA, K
   SASAI, Y
   IMAMURA, S
   INABA, Y
TI THE INCIDENCE OF INTERNAL MALIGNANCIES IN PEMPHIGUS AND BULLOUS
   PEMPHIGOID IN JAPAN
SO JOURNAL OF DERMATOLOGICAL SCIENCE
LA English
DT Article
DE PEMPHIGUS; BULLOUS PEMPHIGOID; INTERNAL MALIGNANCY
ID PARANEOPLASTIC PEMPHIGUS; CARCINOMA; COEXISTENCE; DISEASE
AB To evaluate the significance of the association of malignancy with autoimmune blistering diseases, we studied the incidence of internal malignancies in pemphigus and bullous pemphigoid based upon 496 cases of pemphigus and 1113 cases of bullous pemphigoid in Japan, Results showed that (1) an association between internal malignancies and pemphigus was observed in 25 out of 496 cases (5.0%), while that with bullous pemphigoid was seen in 64 out of 1113 cases (5.8%). Such association ratios were significantly higher than that of the controls aged over 70 years old (0.61%); (2) The average ages of pemphigus/bullous pemphigoid with malignancy were 64.7 and 69.2 years, respectively. The association ratio of malignancy with pemphigus increased by age, while that with pemphigoid was not correlated with aging; (3) Lung cancer was most common in pemphigus and gastric cancer in bullous pemphigoid; (4) There were no significant differences in the titers of circulating antibody, the presence or extent of mucous involvement or annular erythema between bullous pemphigoid patients with malignancy and without malignancy, Our results indicated that detailed examination for internal malignancy is essential for those patients with pemphigus or bullous pemphigoid.
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   KURUME UNIV,DEPT DERMATOL,KURUME,FUKUOKA 830,JAPAN.
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C3 Kurume University; Kyoto University; Juntendo University
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NR 24
TC 114
Z9 118
U1 0
U2 0
PU ELSEVIER SCI PUBL IRELAND LTD
PI CLARE
PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE,
   IRELAND
SN 0923-1811
J9 J DERMATOL SCI
JI J. Dermatol. Sci.
PD MAR
PY 1995
VL 9
IS 2
BP 136
EP 141
DI 10.1016/0923-1811(94)00371-K
PG 6
WC Dermatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Dermatology
GA QR207
UT WOS:A1995QR20700009
PM 7772576
DA 2025-06-01
ER

PT J
AU Wynne, A
   Kanwar, RK
   Khanna, R
   Kanwar, JR
AF Wynne, Alicia
   Kanwar, Rupinder K.
   Khanna, Rajiv
   Kanwar, Jagat R.
TI Recent Advances on the Possible Neuroprotective Activities of
   Epstein-Barr Virus Oncogene BARF1 Protein in Chronic Inflammatory
   Disorders of Central Nervous System
SO CURRENT NEUROPHARMACOLOGY
LA English
DT Article
DE Epstein-Barr Virus; neuroregeneration; chronic inflammatory disorders;
   multiple sclerosis
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; NORTH-AMERICAN OPOSSUM; RAT
   SPINAL-CORD; MULTIPLE-SCLEROSIS; STEM-CELLS; DIDELPHIS-VIRGINIANA;
   OXIDATIVE STRESS; CANCER CELLS; REGENERATION; TRANSPLANTATION
AB Multiple sclerosis and neurodegenerative diseases in which cells of the central nervous system (CNS) are lost or damaged are rapidly increasing in frequency, and there is neither effective treatment nor cure to impede or arrest their destructive course. The Epstein-Barr virus is a human gamma-herpesvirus that infects more than 90% of the human population worldwide and persisting for the lifetime of the host. It is associated with numerous epithelial cancers, principally undifferentiated nasopharyngeal carcinoma and gastric carcinoma. Individuals with a history of symptomatic primary EBV infection, called infectious mononucleosis, carry a moderately higher risk of developing multiple sclerosis (MS). It is not known how EBV infection potentially promotes autoimmunity and central nervous system (CNS) tissue damage in MS. Recently it has been found that EBV isolates from different geographic regions have highly conserved BARF1 epitopes. BARF1 protein has the neuroprotective and mitogenic activity, thus may be useful to combat and overcome neurodegenerative disease. BARF1 protein therapy can potentially be used to enhance the neuroprotective activities by combinational treatment with anti-inflammatory antagonists and neuroprotectors in neural disorders.
C1 [Wynne, Alicia; Kanwar, Rupinder K.; Kanwar, Jagat R.] Deakin Univ, Lab Immunol & Mol Biomed Res, Ctr Biotechnol & Interdisciplinary Biosci BioDeak, Inst Technol & Res Innovat, Geelong, Vic 3217, Australia.
   [Khanna, Rajiv] Queensland Inst Med Res, Australian Ctr Vaccine Dev NH & MRC, Herston, Qld 4006, Australia.
C3 Deakin University; QIMR Berghofer Medical Research Institute
RP Kanwar, JR (corresponding author), Deakin Univ, Lab Immunol & Mol Biomed Res, Ctr Biotechnol & Interdisciplinary Biosci BioDeak, Inst Technol & Res Innovat, Pigdons Rd, Geelong, Vic 3217, Australia.
EM jagat.kanwar@deakin.edu.au
RI Kanwar, Dr Rupinder Kaur/JBS-5937-2023; Kanwar, Jagat/JDO-1829-2023;
   Khanna, Rajiv/A-7691-2008
OI Khanna, Rajiv/0000-0003-2241-0353
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TC 7
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PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1570-159X
EI 1875-6190
J9 CURR NEUROPHARMACOL
JI Curr. Neuropharmacol.
PD SEP
PY 2010
VL 8
IS 3
BP 268
EP 275
DI 10.2174/157015910792246191
PG 8
WC Neurosciences; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 645FK
UT WOS:000281436200011
PM 21358976
OA Green Submitted, Green Published
DA 2025-06-01
ER

PT J
AU Darakhshan, S
   Pour, AB
AF Darakhshan, Sara
   Pour, Ali Bidmeshki
TI Tranilast: A review of its therapeutic applications
SO PHARMACOLOGICAL RESEARCH
LA English
DT Review
DE Tranilast; Anti-inflammatory agent; Fibrosis; Transforming growth
   factor-beta; Review
ID GROWTH-FACTOR-BETA; SMOOTH-MUSCLE-CELLS; PROSTAGLANDIN-D SYNTHETASE;
   SCIRRHOUS GASTRIC-CANCER; CHRONIC CYCLOSPORINE NEPHROTOXICITY;
   MATRIX-METALLOPROTEINASE PRODUCTION; UNILATERAL URETERAL OBSTRUCTION;
   INDUCED ENDOTHELIAL INJURY; OXIDE SYNTHASE EXPRESSION; ARYL-HYDROCARBON
   RECEPTOR
AB Tranilast (N-[3',4'-dimethoxycinnamoyl]-anthranilic acid) is an analog of a tryptophan metabolite. Initially, tranilast was identified as an anti-allergic agent, and used in the treatment of inflammatory diseases, such as bronchial asthma, atypical dermatitis, allergic conjunctivitis, keloids and hypertrophic scars. Subsequently, the results showed that it could be also effective in the management of a wide range of conditions. The beneficial effects of tranilast have also been seen in a variety of disease states, such as fibrosis, proliferative disorders, cancer, cardiovascular problems, autoimmune disorders, ocular diseases, diabetes and renal diseases. Moreover, several trials have shown that it has very low adverse effects and it is generally well tolerated by patients. In this review, we have attempted to accurately summarize previously published studies relating to the use of tranilast for a range of disorders and discuss the drug's possible mode of action. The major mode of the drug's efficacy appears to be the suppression of the expression and/or action of the TGF-beta pathway, but the drug affects other factors as well. The findings presented in this review demonstrate the potential of tranilast for the control of a vast array of pathological situations, furthermore, it is a prescribed drug without severe side effects. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Darakhshan, Sara; Pour, Ali Bidmeshki] Razi Univ, Fac Sci, Dept Biol, Kermanshah, Iran.
C3 Razi University
RP Pour, AB (corresponding author), Razi Univ, Fac Sci, Dept Biol, Kermanshah, Iran.
EM abidmeshki@razi.ac.ir
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NR 200
TC 252
Z9 260
U1 8
U2 78
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-6618
J9 PHARMACOL RES
JI Pharmacol. Res.
PD JAN
PY 2015
VL 91
BP 15
EP 28
DI 10.1016/j.phrs.2014.10.009
PG 14
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CA9VR
UT WOS:000349273400003
PM 25447595
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Fujisaka, S
   Watanabe, Y
   Tobe, K
AF Fujisaka, Shiho
   Watanabe, Yoshiyuki
   Tobe, Kazuyuki
TI The gut microbiome: a core regulator of metabolism
SO JOURNAL OF ENDOCRINOLOGY
LA English
DT Review
DE obesity; diabetes; metabolism
ID CHAIN FATTY-ACIDS; PROTEIN-COUPLED RECEPTOR; DIET-INDUCED OBESITY;
   BUTYRATE-PRODUCING BACTERIA; VITAMIN-A SUPPLEMENTATION; Y GASTRIC
   BYPASS; AKKERMANSIA-MUCINIPHILA; INTESTINAL MICROBIOTA;
   INSULIN-RESISTANCE; BILE-ACID
AB The human body is inhabited by numerous bacteria, fungi, and viruses, and each part has a unique microbial community structure. The gastrointestinal tract harbors approximately 100 trillion strains comprising more than 1000 bacterial species that maintain symbiotic relationships with the host. The gut microbiota consists mainly of the phyla Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria. Of these, Firmicutes and Bacteroidetes constitute 70-90% of the total abundance. Gut microbiota utilize nutrients ingested by the host, interact with other bacterial species, and help maintain healthy homeostasis in the host. In recent years, it has become increasingly clear that a breakdown of the microbial structure and its functions, known as dysbiosis, is associated with the development of allergies, autoimmune diseases, cancers, and arteriosclerosis, among others. Metabolic diseases, such as obesity and diabetes, also have a causal relationship with dysbiosis. The present review provides a brief overview of the general roles of the gut microbiota and their relationship with metabolic disorders.
C1 [Fujisaka, Shiho; Watanabe, Yoshiyuki; Tobe, Kazuyuki] Univ Toyama, Fac Med, Dept Internal Med 1, Toyama, Japan.
C3 University of Toyama
RP Fujisaka, S (corresponding author), Univ Toyama, Fac Med, Dept Internal Med 1, Toyama, Japan.
EM shihof@med.u-toyama.ac.jp
FU JSPS (Japan Society for the Promotion of Science), KAKENHI [17K09821,
   20K08882]; AMED PRIME [JP18gm6010023h0001]; AMED-FORCE
   [JP21gm4010014h0001]; Japan Diabetes Foundation; University of Toyama;
   Japan Society for the Study of Obesity (JASSO); Novo Nordisk Pharma
   Ltd.; Takeda Science Foundation; JSPS (Japan Society for the Promotion
   of Science) KAKENHI [21K20896, 22K16424]; Lotte Foundation; Yakult
   Bio-Science Foundation; Grants-in-Aid for Scientific Research [20K08882]
   Funding Source: KAKEN
FX Our lab is supported by grants from the JSPS (Japan Society for the
   Promotion of Science), KAKENHI grant numbers 17K09821 and 20K08882 to
   S.F., grants from AMED PRIME (JP18gm6010023h0001) to S.F., grants from
   AMED-FORCE (JP21gm4010014h0001) to K.T., and grants from the Japan
   Diabetes Foundation, Research Funding Granted by the President of the
   University of Toyama, Research Funding Granted by the Japan Society for
   the Study of Obesity (JASSO) and Novo Nordisk Pharma Ltd. and Takeda
   Science Foundation to S.F. Y.W. received grants from the JSPS (Japan
   Society for the Promotion of Science) KAKENHI grant numbers 21K20896 and
   22K16424, grants from the Lotte Foundation, and the Yakult Bio-Science
   Foundation.
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PI BRISTOL
PA STARLING HOUSE, 1600 BRISTOL PARKWAY N, BRISTOL, ENGLAND
SN 0022-0795
EI 1479-6805
J9 J ENDOCRINOL
JI J. Endocrinol.
PD MAR 1
PY 2023
VL 256
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DI 10.1530/JOE-22-0111
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WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 9L3DI
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PM 36458804
OA Green Published, hybrid
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HP N
DA 2025-06-01
ER

PT J
AU Tong, DM
   He, YQ
   Haile, SA
   Lee, Z
   Le, LHM
   Emery, J
   Wray-McCan, G
   Chonwerawong, M
   Philpott, DJ
   Hertzog, PJ
   Schneider, P
   Ferrero, RL
   Ying, L
AF Tong, Dongmei
   He, Yuqi
   Haile, Shambel Araya
   Lee, Zoe
   Le, Lena H. M.
   Emery, Jack
   Wray-McCan, Georgie
   Chonwerawong, Michelle
   Philpott, Dana J.
   Hertzog, Paul J.
   Schneider, Pascal
   Ferrero, Richard L.
   Ying, Le
TI BAFF Blockade Attenuates B Cell MALT Formation in Conditional
   Nlrc5-Deficient Mice With Helicobacter felis Infection
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE B cell; B cell-activating factor (BAFF); Helicobacter
   pylori; mucosa-associated lymphoid tissue (MALT) lymphoma;
   non-Hodgkin lymphoma
ID NECROSIS-FACTOR FAMILY; ACTIVATING-FACTOR; LYMPHOID-TISSUE; SPLICE
   ISOFORM; DELTA-BAFF; T-CELLS; EXPRESSION; BINDING; NLRC5; MACROPHAGES
AB Helicobacter infection is a key cause of gastric B cell mucosa-associated lymphoid tissue (MALT) lymphoma. This study examined the role of B cell-activating factor (BAFF), a major driver of B cell proliferation and many B cell disorders, in this malignancy using a model in which conditional knockout mice for NOD-like receptor family CARD domain-containing 5 (Nlrc5) are infected with Helicobacter felis. Gastric BAFF production was significantly increased in H. felis-infected Nlrc5m & oslash;-KO mice compared to wild-type. Blocking BAFF signalling, before or after the onset of Helicobacter-induced gastritis, significantly reduced MALT development, with fewer gastric B cell follicles and reduced gland hyperplasia. BAFF blockade also reshaped the immune cell landscape in the stomach, resulting in fewer CD4+ T cells, Tregs, macrophages and dendritic cells. Using a cell culture model, we identified the protein-coding BAFF transcripts that are upregulated in NLRC5-deficient macrophages stimulated with either H. felis or the NLRC5 agonist, lipopolysaccharide. Among the upregulated variants, TNFSF13B (BAFF)-206 acts as a transcription factor and is reported to enhance BAFF production in autoimmune diseases and cancer. Altogether, these findings implicate the NLRC5-BAFF signalling axis in Helicobacter-induced B cell MALT lymphoma, highlighting BAFF inhibition as a potential therapeutic approach.
C1 [Tong, Dongmei; He, Yuqi; Haile, Shambel Araya; Lee, Zoe; Le, Lena H. M.; Emery, Jack; Wray-McCan, Georgie; Chonwerawong, Michelle; Hertzog, Paul J.; Ferrero, Richard L.; Ying, Le] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
   [Tong, Dongmei; Haile, Shambel Araya; Chonwerawong, Michelle; Hertzog, Paul J.; Ferrero, Richard L.; Ying, Le] Monash Univ, Dept Mol & Translat Sci, Melbourne, Vic, Australia.
   [Philpott, Dana J.] Univ Toronto, Dept Immunol, Toronto, ON, Canada.
   [Schneider, Pascal] Univ Lausanne, Dept Immunobiol, Epalinges, Switzerland.
   [Ferrero, Richard L.] Monash Univ, Biomed Discovery Inst, Dept Microbiol, Melbourne, Vic, Australia.
   [Ying, Le] Monash Univ, Dept Med, Melbourne, Vic, Australia.
C3 Hudson Institute of Medical Research; Monash University; University of
   Toronto; University of Lausanne; Monash University; Monash University
RP Ferrero, RL; Ying, L (corresponding author), Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.; Ferrero, RL; Ying, L (corresponding author), Monash Univ, Dept Mol & Translat Sci, Melbourne, Vic, Australia.; Ferrero, RL (corresponding author), Monash Univ, Biomed Discovery Inst, Dept Microbiol, Melbourne, Vic, Australia.; Ying, L (corresponding author), Monash Univ, Dept Med, Melbourne, Vic, Australia.
EM richard.ferrero@hudson.org.au; le.ying@monash.edu
RI Hertzog, Paul/I-7053-2013; Ying, Le/C-2771-2018
FU U.S. Department of Defense; Monash Histology Platform (Monash
   University); Monash Micro Imaging platform at MHTP
FX We acknowledge the Monash Histology Platform (Monash University, Monash
   Health Translation Precinct) for assistance with tissue processing and
   scanning, and the Monash Micro Imaging platform at MHTP (MMI-MHTP) for
   access and assistance with microscopy and HALO analysis.
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NR 50
TC 0
Z9 0
U1 1
U2 1
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD FEB
PY 2025
VL 55
IS 2
DI 10.1002/eji.202451355
EA DEC 2024
PG 14
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA Y3H7E
UT WOS:001378420700001
PM 39686777
DA 2025-06-01
ER

PT J
AU Diver, WR
   Teras, LR
   Deubler, EL
   Turner, MC
AF Diver, W. Ryan
   Teras, Lauren R.
   Deubler, Emily L.
   Turner, Michelle C.
TI Outdoor air pollution and risk of incident adult haematologic cancer
   subtypes in a large US prospective cohort
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
ID GASTRIC-CANCER; PERNICIOUS-ANEMIA; AUTOIMMUNE; POPULATION; DIAGNOSIS;
   INFLAMMATION; PREVALENCE; MECHANISMS; DISEASE
AB Background Outdoor air pollution and particulate matter (PM) are classified as Group 1 human carcinogens for lung cancer. Pollutant associations with haematologic cancers are suggestive, but these cancers are aetiologically heterogeneous and sub-type examinations are lacking.Methods The American Cancer Society Cancer Prevention Study-II Nutrition Cohort was used to examine associations of outdoor air pollutants with adult haematologic cancers. Census block group level annual predictions of particulate matter (PM2.5, PM10, PM10-2.5), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and carbon monoxide (CO) were assigned with residential addresses. Hazard ratios (HR) and 95% confidence intervals (CI) between time-varying pollutants and haematologic subtypes were estimated.Results Among 108,002 participants, 2659 incident haematologic cancers were identified from 1992-2017. Higher PM10-2.5 concentrations were associated with mantle cell lymphoma (HR per 4.1 mu g/m3 = 1.43, 95% CI 1.08-1.90). NO2 was associated with Hodgkin lymphoma (HR per 7.2 ppb = 1.39; 95% CI 1.01-1.92) and marginal zone lymphoma (HR per 7.2 ppb = 1.30; 95% CI 1.01-1.67). CO was associated with marginal zone (HR per 0.21 ppm = 1.30; 95% CI 1.04-1.62) and T-cell (HR per 0.21 ppm = 1.27; 95% CI 1.00-1.61) lymphomas.Conclusions The role of air pollutants on haematologic cancers may have been underestimated previously because of sub-type heterogeneity.
C1 [Diver, W. Ryan; Turner, Michelle C.] Barcelona Inst Global Hlth ISGlobal, Barcelona, Spain.
   [Diver, W. Ryan; Turner, Michelle C.] Univ Pompeu Fabra UPF, Barcelona, Spain.
   [Diver, W. Ryan; Teras, Lauren R.; Deubler, Emily L.] Amer Canc Soc, Dept Populat Sci, Atlanta, GA 30303 USA.
   [Turner, Michelle C.] CIBER Epidemiol & Salud Publ CIBERESP, Madrid, Spain.
C3 ISGlobal; Pompeu Fabra University; American Cancer Society; CIBER -
   Centro de Investigacion Biomedica en Red; CIBERESP
RP Diver, WR (corresponding author), Barcelona Inst Global Hlth ISGlobal, Barcelona, Spain.; Diver, WR (corresponding author), Univ Pompeu Fabra UPF, Barcelona, Spain.; Diver, WR (corresponding author), Amer Canc Soc, Dept Populat Sci, Atlanta, GA 30303 USA.
EM ryan.diver@cancer.org
RI Teras, Lauren/JWG-5050-2024; Diver, Ryan/AAG-3469-2019; Turner, Michelle
   C/F-7659-2017
OI Diver, W. Ryan/0000-0002-5418-9000; Turner, Michelle
   C/0000-0002-6431-1997; Teras, Lauren/0000-0003-2419-8536
FU Generalitat de Catalunya (Government of Catalonia); Centres for Disease
   Control and Prevention's National Programme of Cancer Registries;
   National Cancer Institute's Surveillance Epidemiology and End Results
   Programme
FX The authors express sincere appreciation to all Cancer Prevention
   Study-II participants, and to each member of the study and biospecimen
   management group. The authors would like to acknowledge the contribution
   to this study from central cancer registries supported through the
   Centres for Disease Control and Prevention's National Programme of
   Cancer Registries and cancer registries supported by the National Cancer
   Institute's Surveillance Epidemiology and End Results Programme. The
   authors assume full responsibility for all analyses and interpretation
   of results. The views expressed here are those of the authors and do not
   necessarily represent the American Cancer Society or the American Cancer
   Society-Cancer Action Network.
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NR 42
TC 3
Z9 3
U1 4
U2 8
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD JUL 27
PY 2024
VL 131
IS 1
BP 149
EP 158
DI 10.1038/s41416-024-02718-3
EA MAY 2024
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA XZ4Y3
UT WOS:001232180300001
PM 38802672
OA hybrid
DA 2025-06-01
ER

PT J
AU Mo, CJ
   Peng, QL
   He, Y
   Wang, J
   Xie, L
   Li, TJ
   Li, S
   Qin, X
AF Mo, Cui-Ju
   Peng, Qi-Liu
   He, Yu
   Wang, Jian
   Xie, Li
   Li, Tai-Jie
   Li, Shan
   Qin, Xue
TI Positive Association Between IL-16 rs11556218 T/G Polymorphism
   and Cancer Risk: a Meta-analysis
SO ASIAN PACIFIC JOURNAL OF CANCER PREVENTION
LA English
DT Article
DE Interleukin-16; cancer; polymorphism; meta-analysis
ID CELL CARCINOMA ASSOCIATION; CHINESE POPULATION; PROSTATE-CANCER;
   SERUM-LEVELS; NASOPHARYNGEAL CARCINOMA; GENETIC-POLYMORPHISM;
   COLORECTAL-CANCER; GASTRIC-CANCER; INTERLEUKIN 16; TNF-ALPHA
AB Background: Interleukin-16 (IL-16) is a multifunctional cytokine which plays a key role in inflammatory and autoimmune diseases as well as in cancer. Genetic polymorphisms of IL-16 have been implicated in susceptibility to cancer. However, associations remain inconclusive. The present meta-analysis was therefore carried out to establish a more conclusive association of IL-16 polymorphisms with cancer risk. Materials and Methods: Relevant studies were searched through the PubMed, Embase, Web of Science, Google Scholar and Wan fang electronic databases updated in October 2013. Odds ratios (OR) and 95% confidence intervals (95% CI) were used to assess the association between IL-16 polymorphisms and cancer risk. Results: Eight eligible studies (rs4778889 T/C: 8, rs11556218 T/G: 7, rs4072111 C/T: 6) that met our selection criteria were included. The meta-analysis indicated that rs11556218 T/G was associated with a significant increased risk of cancer (G vs. T, OR=1.321, 95% CI=1.142-1.528, P<0.001; TG vs. TT, OR=1.665, 95% CI=1.448-1.915, P<0.001; GG+TG vs. TT, OR=1.622, 95% CI=1.416-1.858, P<0.001), as well as nasopharyngeal carcinoma and colorectal cancer. Furthermore, in the subgroup of Chinese, significant associations were found between rs11556218 polymorphism and cancer risk. There was no statistically significant association between the other two variants (rs4778889, rs4072111) and risk of cancer. Conclusions: This meta-analysis suggests that the IL-16 rs11556218 polymorphism is associated with increased cancer risk. Large well-designed studies involving various cancer types and different populations are now needed.
C1 [Mo, Cui-Ju; Peng, Qi-Liu; He, Yu; Wang, Jian; Xie, Li; Li, Tai-Jie; Li, Shan; Qin, Xue] Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
C3 Guangxi Medical University
RP Qin, X (corresponding author), Guangxi Med Univ, Affiliated Hosp 1, Dept Clin Lab, Nanning, Guangxi, Peoples R China.
EM qinxue919@126.com
RI qin, xue/KQV-3701-2024
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NR 39
TC 13
Z9 14
U1 0
U2 6
PU ASIAN PACIFIC ORGANIZATION CANCER PREVENTION
PI GYEONGGI-DO
PA APJCP HEAD OFFICE, KOREAN NATL CANCER CENTER, 323 ILAN -RO,
   ILSANDONG-GU, GOYANG-SI, GYEONGGI-DO, 410-769, SOUTH KOREA
SN 1513-7368
J9 ASIAN PAC J CANCER P
JI Asian Pac. J. Cancer Prev.
PY 2014
VL 15
IS 11
BP 4697
EP 4703
DI 10.7314/APJCP.2014.15.11.4697
PG 7
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA AK7VD
UT WOS:000338634900051
PM 24969906
OA gold
DA 2025-06-01
ER

PT J
AU Spitzweg, C
   Joba, W
   Schriever, K
   Goellner, JR
   Morris, JC
   Heufelder, AE
AF Spitzweg, C
   Joba, W
   Schriever, K
   Goellner, JR
   Morris, JC
   Heufelder, AE
TI Analysis of human sodium iodide symporter immunoreactivity in human
   exocrine glands
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID AUTOIMMUNE THYROID-DISEASE; NA+/I-SYMPORTER; SALIVARY-GLAND; INCREASED
   EXPRESSION; CANCER PATIENTS; MAMMARY-GLAND; RADIOIODINE; TRANSPORTER;
   TISSUES; CLONING
AB The human sodium iodide symporter (hNIS) is an intrinsic transmembrane protein that mediates the active transport of iodide across the basolateral membrane of thyroid follicular cells. In addition to normally functioning thyroid tissue, various extrathyroidal tissues, including salivary gland, lacrimal gland, gastric mucosa, choroid plexus, and lactating mammary gland, have been demonstrated to accumulate iodide. After cloning and molecular characterization of the sodium iodide symporter, expression of hNIS messenger ribonucleic acid has been detected in a broad range of extrathyroidal tissues using Northern blot analysis and RT-PCR. In this study we used both monoclonal and polyclonal antibodies directed against different portions of hNIS protein together with a highly sensitive immunostaining technique to assess hNIS protein expression in tissue sections derived from normal human salivary and lacrimal glands, pancreas, as well as gastric and colonic mucosa. Immunohistochemical analysis of normal human salivary and lacrimal glands revealed marked hNIS immunoreactivity in ductal cells and less intense staining of acinar cells. Further, immunostaining of gastric and colonic mucosa showed marked hNIS immunoreactivity confined to chief and parietal cells in gastric mucosa and to epithelial cells lining mucosal crypts in colonic mucosa In normal human pancreas, hNIS immunoreactivity was located in ductal cells, exocrine parenchymal cells, and Langerhans islet cells. In conclusion, our study demonstrates the expression of hNIS protein by several human exocrine glands, suggesting that iodide transport in these glands is a specific property conferred by the expression of hNIS protein, which may serve important functions by concentrating iodine in glandular secretions.
C1 Mayo Clin, Dept Endocrinol, Rochester, MN 55905 USA.
   Mayo Clin, Dept Pathol, Rochester, MN 55905 USA.
   Univ Marburg, Zentrum Innere Med, Div Gastroenterol Endocrinol & Metab, D-35033 Marburg, Germany.
C3 Mayo Clinic; Mayo Clinic; Philipps University Marburg
RP Mayo Clin, Endocrine Res Unit, Guggenheim 625,200 1st St SW, Rochester, MN 55905 USA.
EM spitzweg.christine@mayo.edu
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NR 38
TC 104
Z9 109
U1 0
U2 2
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD NOV
PY 1999
VL 84
IS 11
BP 4178
EP 4184
DI 10.1210/jc.84.11.4178
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 253KM
UT WOS:000083555800052
PM 10566669
DA 2025-06-01
ER

PT J
AU Cindoruk, M
   Cirak, MY
   Unal, S
   Karakan, T
   Erkan, G
   Engin, D
   Dumlu, S
   Turet, S
AF Cindoruk, Mehmet
   Cirak, Meltem Yalinay
   Unal, Selahattin
   Karakan, Tarkan
   Erkan, Gulbanu
   Engin, Doruk
   Dumlu, Sukru
   Turet, Sevgi
TI Identification of Helicobacter species by 16S rDNA PCR and
   sequence analysis in human liver samples from patients with various
   etiologies of benign liver diseases
SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Article
DE benign liver disease; chronic hepatitis; Helicobacter pylori; hepatitis
   C; nonalcoholic fatty liver disease
ID HEPATITIS-C VIRUS; HEPATOCELLULAR-CARCINOMA; HEPATOBILIARY DISEASES;
   PYLORI INFECTION; CIRRHOSIS; DNA; ASSOCIATION; CANCER; HYBRIDIZATION;
   STOMACH
AB Background/Aims Several reports indicated an increased prevalence of the Helicobacter species in hepatocellular cancer tissue and in liver samples infected with hepatitis viruses. The frequency of Helicobacter spp. in benign liver diseases was, however, not thoroughly investigated.
   Methods Seventy-five consecutive patients with suspected liver disease were enrolled. The indications were hepatitis B virus (n = 30), C virus (n = 8), B and C dual infection (n = 1), nonalcoholic steatohepatitis (n = 27), autoimmune hepatitis (n = 3), primary biliary cirrhosis (n=l) and idiopathic elevation of liver enzymes (n = 5). PCR detection of 16S recombinant RNA gene of Helicobacter spp. was performed on liver samples. PCR products of positive samples were further identified by DNA sequencing. The patients also had upper gastrointestinal endoscopy and gastric biopsy for the detection of H. pylori using histopathology and PCR.
   Results Helicobacter spp. DNA was detected in two out of 75 liver biopsy samples (2.6%), which were typed as H. pylori by DNA sequencing. One of these patients had chronic hepatitis C infection (man, 51 years old) and the other had nonalcoholic steatohepatitis (woman, 44 years old). Fifty-two out of 75 of the patients (69.3%) had H. pylori infection in their stomachs.
   Conclusion We have found that H. pylori infection is much less prevalent in benign liver diseases. The presence of H. pylori in nonalcoholic steatohepatitis (NASH) patients is a novel finding and this finding should be confirmed in a larger series.
C1 [Cindoruk, Mehmet; Unal, Selahattin; Karakan, Tarkan; Erkan, Gulbanu; Dumlu, Sukru] Gazi Univ, Fac Med, Ankara, Turkey.
   [Cirak, Meltem Yalinay; Engin, Doruk; Turet, Sevgi] Dept Gastroenterol & Med Microbiol, Ankara, Turkey.
C3 Gazi University
RP Karakan, T (corresponding author), Gazi Hastanesi Gastroentrol & Med Microbiol, TR-06500 Ankara, Turkey.
EM tkarakan@gmail.com
RI Cindoruk, Mehmet/C-2104-2009; Engin, Doruk/O-3604-2014; Karakan,
   Tarkan/A-9875-2016
OI Engin, Doruk/0000-0001-9209-8858; Karakan, Tarkan/0000-0003-1561-8789
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NR 32
TC 38
Z9 42
U1 1
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0954-691X
EI 1473-5687
J9 EUR J GASTROEN HEPAT
JI Eur. J. Gastroenterol. Hepatol.
PD JAN
PY 2008
VL 20
IS 1
BP 33
EP 36
DI 10.1097/MEG.0b013e3282efa4f2
PG 4
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 325ZN
UT WOS:000257627800008
PM 18090988
DA 2025-06-01
ER

PT J
AU Shi, WJ
   Liu, W
   Zhou, XY
   Ye, F
   Zhang, GX
AF Shi, Wei-Jia
   Liu, Wei
   Zhou, Xiao-Ying
   Ye, Feng
   Zhang, Guo-Xin
TI Associations of Helicobacter pylori Infection and
   Cytotoxin-Associated Gene A Status with Autoimmune Thyroid Diseases: A
   Meta-Analysis
SO THYROID
LA English
DT Article
ID HASHIMOTOS-THYROIDITIS; IMMUNE-RESPONSES; GASTRIC-CANCER;
   GRAVES-DISEASE; PARIETAL-CELL; HEPATITIS-C; ERADICATION; ANTIBODIES;
   DISORDERS; CAGA
AB Background:Helicobacter pylori infection is reportedly associated with extradigestive diseases such as immune thrombocytopenic purpura and coronary heart disease. The risk factors for autoimmune thyroid diseases (ATDs) remain largely unknown, and whether H. pylori infection is associated with ATDs is still controversial. The aim of this meta-analysis was to determine the association between H. pylori infection and ATDs. Methods: Studies comparing the prevalence rate of H. pylori infection in patients with ATDs and healthy controls, published in English, were identified through a systematic search in MEDLINE and EMBAS up to June 2012. Serological or nonserological tests were used to confirm H. pylori infection and the presence of cytotoxin-associated gene A (CagA) antigens. The odds ratios (OR) and associated 95% confidence intervals [CI] were obtained. Results: Seven studies involving a total of 862 patients met the inclusion criteria and thus were included in our meta-analysis. Overall, H. pylori infection was associated with ATDs (OR 1.92 [CI 1.41-2.61]); the association was significant for Graves' disease (OR 4.35 [CI 2.48-7.64]) but not for Hashimoto's thyroiditis (OR 1.45 [CI 0.92-2.26], p=0.11). No association was observed in the subanalysis of studies using only enzyme-linked immunosorbent assay to detect H. pylori infection (OR 1.38 [CI 0.86-2.19], p=0.18). Five of the seven articles reported the association of CagA seroprevalence and ATDs. CagA seropositivity significantly increased the risk for ATDs by 2.24-fold [CI 1.06-4.75]. Conclusions: Both the prevalence of H. pylori infection and the seroprevalence of CagA-positive strains are associated with ATDs. These findings suggest that H. pylori infection potentially plays a part in the development of ATDs.
C1 [Shi, Wei-Jia; Liu, Wei; Zhou, Xiao-Ying; Ye, Feng; Zhang, Guo-Xin] Nanjing Med Univ, Affiliated Hosp 1, Dept Gastroenterol, Nanjing 210029, Jiangsu, Peoples R China.
   [Zhang, Guo-Xin] Nanjing Med Univ, Jiangsu Shengze Hosp, Dept Gastroenterol, Wujiang 210029, Jiangsu, Peoples R China.
C3 Nanjing Medical University; Nanjing Medical University
RP Zhang, GX (corresponding author), Nanjing Med Univ, Affiliated Hosp 1, Dept Gastroenterol, 300 Guangzhou Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM guoxinz@njmu.edu.cn
RI Zhang, Guoxin/S-7345-2017; Zhou, Xiaoying/I-5400-2016
FU National Natural Science Foundation of China [81072032, 81270476]
FX This work was supported by the National Natural Science Foundation of
   China (No. 81072032 and 81270476). The authors thank Medjaden Bioscience
   Limited for assisting in proofreading the manuscript.
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NR 43
TC 42
Z9 48
U1 1
U2 10
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
J9 THYROID
JI Thyroid
PD OCT 1
PY 2013
VL 23
IS 10
BP 1294
EP 1300
DI 10.1089/thy.2012.0630
PG 7
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA 223TE
UT WOS:000324832100016
PM 23544831
DA 2025-06-01
ER

PT J
AU Vyas, U
   Ranganathan, N
AF Vyas, Usha
   Ranganathan, Natarajan
TI Probiotics, Prebiotics, and Synbiotics: Gut and Beyond
SO GASTROENTEROLOGY RESEARCH AND PRACTICE
LA English
DT Review
ID SYSTEMIC INFLAMMATORY RESPONSE; MINIMAL HEPATIC-ENCEPHALOPATHY; BOWEL
   BACTERIAL OVERGROWTH; STAGE KIDNEY-DISEASE; ABERRANT CRYPT FOCI;
   REGULATORY T-CELLS; LACTOBACILLUS-ACIDOPHILUS; DOUBLE-BLIND; INTESTINAL
   MICROFLORA; DIETARY INULIN
AB The human intestinal tract has been colonized by thousands of species of bacteria during the coevolution of man and microbes. Gut-borne microbes outnumber the total number of body tissue cells by a factor of ten. Recent metagenomic analysis of the human gut microbiota has revealed the presence of some 3.3 million genes, as compared to the mere 23 thousand genes present in the cells of the tissues in the entire human body. Evidence for various beneficial roles of the intestinal microbiota in human health and disease is expanding rapidly. Perturbation of the intestinal microbiota may lead to chronic diseases such as autoimmune diseases, colon cancers, gastric ulcers, cardiovascular disease, functional bowel diseases, and obesity. Restoration of the gut microbiota may be difficult to accomplish, but the use of probiotics has led to promising results in a large number of well-designed (clinical) studies. Microbiomics has spurred a dramatic increase in scientific, industrial, and public interest in probiotics and prebiotics as possible agents for gut microbiota management and control. Genomics and bioinformatics tools may allow us to establish mechanistic relationships among gut microbiota, health status, and the effects of drugs in the individual. This will hopefully provide perspectives for personalized gut microbiota management.
C1 [Vyas, Usha; Ranganathan, Natarajan] Kibow Biotech Inc, Newtown Business Ctr, Newtown Sq, PA 19073 USA.
RP Vyas, U (corresponding author), Kibow Biotech Inc, Newtown Business Ctr, 4781 W Chester Pike, Newtown Sq, PA 19073 USA.
EM usha@kibowbiotech.com
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NR 171
TC 138
Z9 164
U1 1
U2 25
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 1687-6121
EI 1687-630X
J9 GASTROENT RES PRACT
JI Gastroenterol. Res. Pract.
PY 2012
VL 2012
AR 872716
DI 10.1155/2012/872716
PG 16
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 012ZT
UT WOS:000309276000001
PM 23049548
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Kopalli, SR
   Kang, TB
   Lee, KH
   Koppula, S
AF Kopalli, Spandana R.
   Kang, Tae-Bong
   Lee, Kwang-Ho
   Koppula, Sushruta
TI NLRP3 Inflammasome Activation Inhibitors in Inflammation-Associated
   Cancer Immunotherapy: An Update on the Recent Patents
SO RECENT PATENTS ON ANTI-CANCER DRUG DISCOVERY
LA English
DT Review
DE Caspase; colitis; inflammasome; interleukin; MCC950; melanoma; sulphonyl
   urea
ID PHENOLIC ANTIDIARRHEIC INGREDIENTS; CALORIE RESTRICTION; NALP3
   INFLAMMASOME; INNATE IMMUNITY; DISEASE; CELLS; SUSCEPTIBILITY;
   MECHANISMS; POLYKETIDES; RECOGNITION
AB Background: Inflammasomes are recognized as key regulators in innate immunity from the pathogenic to endogenous danger signals. Although controlled activation of inflammasome is highly beneficial, dysregulation of inflammasome activation plays central role in various autoimmune, inflammatory disorders and aid in promoting various forms of cancers in humans such as breast cancer, fibrosarcoma, gastric carcinoma, and lung metastasis. NLRP3 inflammasome activation has been emerged as a topic of interest and is under profound investigation for its involvement in multiple forms of cancers.
   Objective: This review emphasizes an overview of the recent patents on NLRP3 inflammasome activation inhibitors with their relevant biological/pharmacological properties for the prevention and treatment of inflammation-associated cancer disorders.
   Methods: Data were obtained from online patent searchers such as World Intellectual Property Organization (WIPO (R)), Free Patent Online (FPO), Espacenet (R) and Google Patents.
   Results: Several NLRP3 inflammasome activation inhibitors were recently patented from naturally derived and synthetic agents mainly by academic researchers. Most of the claimed patents have been validated and confined to cell lines and animal models limiting their entry into clinical settings.
   Conclusion: The vigorous effort to discover and develop agents to specifically inhibit NLRP3 inflammasome activation, may pave the way to therapeutic intervention targeting inflammasome-regulated pathways that are involved in the pathogenesis of various forms of cancer.
C1 [Kopalli, Spandana R.; Kang, Tae-Bong; Lee, Kwang-Ho; Koppula, Sushruta] Konkuk Univ, Coll Biomed & Hlth Sci, Chungju, South Korea.
   [Lee, Kwang-Ho] Konkuk Univ, Res Inst Inflammatory Dis, Dept Biotechnol, Chungju, South Korea.
C3 Konkuk University; Konkuk University
RP Koppula, S (corresponding author), Konkuk Univ, Coll Biomed & Hlth Sci, Chungju, South Korea.
EM sushrutak@gmail.com
RI Koppula, Sushruta/JRW-6571-2023; kang, Tae-bong/AAD-7950-2022; Koppula,
   Sushruta/F-2817-2013
OI Koppula, Sushruta/0000-0002-8597-7763; kang,
   tae-bong/0000-0003-1441-9470; Kopalli, Spandana
   Rajendra/0000-0003-0908-4178
FU Konkuk University
FX This work was supported by Konkuk University.
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   Zhu H, 2017, CELL MOL IMMUNOL, V14, P403, DOI 10.1038/cmi.2017.14
   Zhu ZW, 2011, CANCER BIOL THER, V12, P95, DOI 10.4161/cbt.12.2.15952
NR 86
TC 21
Z9 24
U1 1
U2 30
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1574-8928
EI 2212-3970
J9 RECENT PAT ANTI-CANC
JI Recent Patents Anti-Canc. Drug Discov.
PY 2018
VL 13
IS 1
BP 106
EP 117
DI 10.2174/1574892812666171027102627
PG 12
WC Oncology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Pharmacology & Pharmacy
GA FW5BI
UT WOS:000425330600006
PM 29076433
DA 2025-06-01
ER

PT J
AU Haedicke, W
   Greiner, A
   Seeberger, H
   Müller-Hermelink, HK
AF Haedicke, W
   Greiner, A
   Seeberger, H
   Müller-Hermelink, HK
TI Oligoclonal expansions of T-cell repertoire in gastric mucosa associated
   lymphoid tissue type B-cell lymphoma and adjacent gastritis
SO DIAGNOSTIC MOLECULAR PATHOLOGY
LA English
DT Article
DE tumor infiltrating T cells; T-cell repertoire; low grade MALT type
   B-cell lymphoma; chronic gastritis; TCR beta V family specific reverse
   transcriptase-; polymerase chain reaction; local activation
ID MALT-TYPE LYMPHOMA; BETA GENE USAGE; HELICOBACTER-PYLORI; IN-VIVO;
   RECEPTOR; LYMPHOCYTES; DISEASE; SUPERANTIGENS; AMPLIFICATION; CLONOTYPES
AB Local stimulation by Helicobacter pylori (HP), autoantigen: and a concurrent T-cell-mediated stimulation of B cells are believed to play an important role in gastric mucosa-associated lymphoid tissue (MALT) type B cell lymphomagenesis. Many autoimmune diseases have shown to lead to a skewed T-cell repertoire with autoantigen specific expansions and deletions. Characterization of lymphoma and gastritis areas of seven gastrectomy specimens using a T-cell receptor beta variable chain (TCR beta V) family-specific reverse transcriptase (RT)polymerase chain reaction (PCR) assay and fluorescence-activated cell sorter (FACS) analysis revealed a local chronic and acute activation of T cells in lymphoma and an oligoclonal T-cell repertoire in gastritis and in lymphoma, partially sharing the same clones. Local activation and a partial identity suggest that an antigenic challenge caused by a common local pathogen may still continue to take place in MALT type lymphoma as in gastritis, consistent with the view that gastritis may be a precursor lesion of MALT type lymphoma. Expansions that were found only in one of the compartments suggest that also an immune hyperstimulation may contribute to the T-cell repertoire, possibly because of certain tissue antigens. Deletions of TCR PV families found only in gastritis underline the view that autoantigen may play an important role in its pathogenesis.
C1 Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
C3 University of Wurzburg
RP Haedicke, W (corresponding author), Univ Wurzburg, Inst Pathol, Josef Schneider Str 2, D-97080 Wurzburg, Germany.
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NR 36
TC 7
Z9 7
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1052-9551
J9 DIAGN MOL PATHOL
JI Diagn. Mol. Pathol.
PD SEP
PY 1999
VL 8
IS 3
BP 138
EP 144
DI 10.1097/00019606-199909000-00006
PG 7
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
   Pathology
GA 253ED
UT WOS:000083542900006
PM 10565685
DA 2025-06-01
ER

PT J
AU Park, JK
   Choi, IA
   Lee, EY
   Song, YW
   Lee, EB
AF Park, Jin Kyun
   Choi, In Ah
   Lee, Eun Young
   Song, Yeong Wook
   Lee, Eun Bong
TI Incidence of malignancy in Takayasu arteritis in Korea
SO RHEUMATOLOGY INTERNATIONAL
LA English
DT Article
DE Takayasu arteritis; Malignancy; Incidence; Outcome; Vasculitis
ID GIANT-CELL ARTERITIS; RHEUMATOLOGY 1990 CRITERIA;
   POLYMYALGIA-RHEUMATICA; CANCER; RISK; CLASSIFICATION; VASCULITIS;
   FREQUENCY; MORTALITY; FEATURES
AB Cancer is associated with autoimmune diseases. This study aimed to estimate the incidence of cancer in a cohort of patients with Takayasu arteritis (TA) and to compare this incidence with the general population cancer rate in South Korea in a retrospective cohort study. The medical records of TA patients who underwent medical care at our institution between 1979 and 2009 were reviewed. The 2008 National Cancer Registry was used as the reference to calculate the standardized incidence ratio (SIR). The mean age of 180 patients was 48.6 +/- A 14.3 years, and 87.2 % of the patients were female. During the follow-up of 2,285 person years, 10 females developed cancer. Breast cancer was the most common malignancy with three cases, followed by two endometrial, one gastric, one colon, one pancreatic, one myelodysplastic syndrome (MDS) with refractory anemia with excess blasts, and one multiple myeloma. The SIR of cancer in TA was comparable with that of the general population at 1.3 [95 % confidence interval (CI) 0.6-2.3]; however, the risk of MDS was significantly increased (SIR 51.3; 95 % CI 1.3-285.7). While two patients with hematologic malignancies died, all TA patients with non-hematologic malignancies were still alive during the follow-up period. The overall risk of malignancy is not increased in TA. Further work is needed to determine if TA is associated with an increased risk of certain hematologic malignancies.
C1 [Park, Jin Kyun; Choi, In Ah; Lee, Eun Young; Song, Yeong Wook; Lee, Eun Bong] Seoul Natl Univ Coll Med, Div Rheumatol, Dept Internal Med, Seoul 110744, South Korea.
C3 Seoul National University (SNU)
RP Lee, EB (corresponding author), Seoul Natl Univ Coll Med, Div Rheumatol, Dept Internal Med, 101 Daehak Ro, Seoul 110744, South Korea.
EM leb7616@snu.ac.kr
RI Lee, Eun/J-5594-2012; Lee, Youngil/AAX-2787-2021; Park, Kyung
   Woo/AAX-3046-2020
OI Choi, In Ah/0000-0003-4662-4065; Lee, Eun Young/0000-0001-6975-8627
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NR 26
TC 11
Z9 11
U1 0
U2 2
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0172-8172
EI 1437-160X
J9 RHEUMATOL INT
JI Rheumatol. Int.
PD APR
PY 2014
VL 34
IS 4
BP 517
EP 521
DI 10.1007/s00296-013-2887-9
PG 5
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA AD2QN
UT WOS:000333080300011
PM 24166213
DA 2025-06-01
ER

PT J
AU Chatzikyriakidou, A
   Voulgari, PV
   Georgiou, I
   Drosos, AA
AF Chatzikyriakidou, Anthoula
   Voulgari, Paraskevi V.
   Georgiou, Ioannis
   Drosos, Alexandros A.
TI miRNAs and related polymorphisms in rheumatoid arthritis susceptibility
SO AUTOIMMUNITY REVIEWS
LA English
DT Review
DE Rheumatoid arthritis; microRNA; Single nucleotide polymorphism
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; GASTRIC-CANCER RISK; FUNCTIONAL
   POLYMORPHISM; SYNOVIAL FIBROBLASTS; MIR-146A EXPRESSION; ALTERED
   EXPRESSION; INNATE IMMUNITY; MESSENGER-RNAS; PRE-MICRORNAS;
   BINDING-SITES
AB The epigenetic mechanisms in regulation of genes' expression seem to be another field of research that gains land in genetic association studies of rheumatoid arthritis (RA) susceptibility factors. Recently, a new class of molecules has been discovered, the microRNAs (miRNAs). miRNAs are related to post-transcriptional regulation of genes' expression. Different expression patterns of mir-146a, miRNA-155, miRNA-124a, mir-203, mir-223, mir-346, mir-132, mir-363, mir-498, mir-15a, and mir-16 were documented in several tissue sample types of RA patients. The polymorphisms of these miRNAs and their gene targets, which previously have been associated with RA or other autoimmune diseases, are also reviewed. Finally, using web-based tools we propose polymorphisms of the discussed miRNAs and their gene-targets that worth to be studied for their role in RA predisposition. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Voulgari, Paraskevi V.; Drosos, Alexandros A.] Univ Ioannina, Sch Med, Dept Internal Med, Rheumatol Clin, GR-45110 Ioannina, Greece.
   [Chatzikyriakidou, Anthoula; Georgiou, Ioannis] Univ Ioannina, Sch Med, Genet Unit, Dept Obstet & Gynecol, GR-45110 Ioannina, Greece.
C3 University of Ioannina; University of Ioannina
RP Drosos, AA (corresponding author), Univ Ioannina, Sch Med, Dept Internal Med, Rheumatol Clin, GR-45110 Ioannina, Greece.
EM adrosos@cc.uoi.gr
RI Drosos, Alexandros/AAK-1115-2020; Chatzikyriakidou,
   Anthoula/GMX-3038-2022
OI Georgiou, Ioannis/0000-0002-0308-5703
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NR 78
TC 76
Z9 85
U1 0
U2 20
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 1568-9972
EI 1873-0183
J9 AUTOIMMUN REV
JI Autoimmun. Rev.
PD JUL
PY 2012
VL 11
IS 9
BP 636
EP 641
DI 10.1016/j.autrev.2011.11.004
PG 6
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA 967TU
UT WOS:000305931500005
PM 22100329
DA 2025-06-01
ER

PT J
AU Shaker, OG
   Mahmoud, RH
   Abdelaleem, OO
   Ibrahem, EG
   Mohamed, AA
   Zaki, OM
   Abdelghaffar, NK
   Ahmed, TI
   Hemeda, NF
   Ahmed, NA
   Mansour, DF
AF Shaker, Olfat G.
   Mahmoud, Rania H.
   Abdelaleem, Omayma O.
   Ibrahem, Enas G.
   Mohamed, Abdelrahmaan A.
   Zaki, Othman M.
   Abdelghaffar, Noha K.
   Ahmed, Tarek I.
   Hemeda, Nada F.
   Ahmed, Naglaa A.
   Mansour, Dina F.
TI LncRNAs, MALAT1 and lnc-DC as potential biomarkers for multiple
   sclerosis diagnosis
SO BIOSCIENCE REPORTS
LA English
DT Article
ID LONG NONCODING RNA; GASTRIC-CANCER; CELL APOPTOSIS; LUNG-CANCER;
   EXPRESSION; IMMUNOPATHOGENESIS; CONTRIBUTES; METASTASIS; REGULATOR;
   MIGRATION
AB Long non-coding RNAs (lncRNAs) play an important role in gene regulation and show greater tissue specificity and complexity of biological functions. There is on-going research in their contribution in autoimmune diseases like multiple sclerosis (MS). Our study aimed at the evaluation of serum levels of lncRNAs, MALAT1 and lnc-DC in MS patients and the investigation of the association between these lncRNAs and the disease activity. Serum from 45 MS patients and 45 healthy controls was separated. MALAT1 and lnc-DC expression levels were assayed by qRT-PCR. MALAT1 and lnc-DC were significantly increased in MS patients (P=0.004 and P=0.006, respectively) in comparison with controls. There was a significant increase in expression of MALAT1 in secondary progressive MS (SPMS) subgroup compared with controls (P<0.0001); however, significant elevation of lnc-DC was demonstrated in relapsing remitting MS (RRMS) subtype (P=0.003) compared with normal controls. A positive association between the expression levels of MALAT1 and lnc-DC (r=0.513, P < 0.0001) in MS patients was detected. Moreover, positive correlation was observed between MALAT1and lnc-DC in RRMS (r=0.569, P=0.001). Serum levels of MALAT1 and lnc-DC may serve as potential novel molecular biomarkers for MS diagnosis and may provide a new direction for its treatment.
C1 [Shaker, Olfat G.] Cairo Univ, Fac Med, Dept Med Biochem & Mol Biol, Cairo, Egypt.
   [Mahmoud, Rania H.; Abdelaleem, Omayma O.] Fayoum Univ, Dept Med Biochem & Mol Biol, Fac Med, Al Fayyum, Egypt.
   [Ibrahem, Enas G.; Mohamed, Abdelrahmaan A.] Fayoum Univ, Dept Med Microbiol & Immunol, Fac Med, Al Fayyum, Egypt.
   [Zaki, Othman M.; Abdelghaffar, Noha K.] Fayoum Univ, Dept Clin Pathol, Fac Med, Al Fayyum, Egypt.
   [Ahmed, Tarek I.] Fayoum Univ, Dept Internal Med, Fac Med, Al Fayyum, Egypt.
   [Hemeda, Nada F.] Fayoum Univ, Dept Genet, Fac Agr, Al Fayyum, Egypt.
   [Ahmed, Naglaa A.] Zagazig Univ, Dept Physiol, Fac Med, Zagazig, Sharkea, Egypt.
   [Mansour, Dina F.] Minia Univ, Dept Neurol, Fac Med, Al Minya, Egypt.
C3 Egyptian Knowledge Bank (EKB); Cairo University; Egyptian Knowledge Bank
   (EKB); Fayoum University; Egyptian Knowledge Bank (EKB); Fayoum
   University; Egyptian Knowledge Bank (EKB); Fayoum University; Egyptian
   Knowledge Bank (EKB); Fayoum University; Egyptian Knowledge Bank (EKB);
   Fayoum University; Egyptian Knowledge Bank (EKB); Zagazig University;
   Egyptian Knowledge Bank (EKB); Minia University
RP Mahmoud, RH (corresponding author), Fayoum Univ, Dept Med Biochem & Mol Biol, Fac Med, Al Fayyum, Egypt.
EM tsneeem@gmail.com
RI Mahmoud, Rania/AAN-4320-2021; O, Shaker/Y-6125-2019; Hemeda, Nada
   Fathi/AAN-1520-2021; Talaat, Randa/E-7144-2019
OI abdelmoktader, abdelrahman/0000-0002-8092-6086; Hemeda, Nada
   F./0000-0002-1570-7944; , Rania/0000-0002-6876-992X; Talaat,
   Randa/0000-0003-0619-1234; Shaker, Olfat G./0000-0002-3031-3599
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NR 42
TC 50
Z9 53
U1 0
U2 6
PU PORTLAND PRESS LTD
PI LONDON
PA 1ST FLR, 10 QUEEN STREET PLACE, LONDON, ENGLAND
SN 0144-8463
EI 1573-4935
J9 BIOSCIENCE REP
JI Biosci. Rep.
PD JAN 31
PY 2019
VL 39
AR BSR20181335
DI 10.1042/BSR20181335
PN 1
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA HI3QX
UT WOS:000456367300050
PM 30514825
OA gold, Green Published, Green Submitted
DA 2025-06-01
ER

PT J
AU Zhou, Y
   Deng, YH
   You, YJ
   Li, X
   Zhang, D
   Qi, HL
   Shi, RC
   Yao, L
   Tang, YY
   Li, XF
   Ma, LK
   Li, YL
   Liu, J
   Feng, YN
   Chen, XM
   Hao, Q
   Li, XM
   Li, YZ
   Niu, M
   Gao, HJ
   Bai, FH
   Hu, SJ
AF Zhou, Yan
   Deng, Yanhong
   You, Yanjie
   Li, Xue
   Zhang, Di
   Qi, Hailong
   Shi, Ruichun
   Yao, Li
   Tang, Yuanyuan
   Li, Xiaofei
   Ma, Linke
   Li, Yanlin
   Liu, Jun
   Feng, Yaning
   Chen, Xianmei
   Hao, Qian
   Li, Xuemei
   Li, Yuzhen
   Niu, Min
   Gao, Hengjun
   Bai, Feihu
   Hu, Shengjuan
TI Prevalence and risk factors of Helicobacter pylori infection in
   Ningxia, China: comparison of two cross-sectional studies from 2017 and
   2022
SO AMERICAN JOURNAL OF TRANSLATIONAL RESEARCH
LA English
DT Article
DE Helicobacter pylori; prevalence; risk factors; Ningxia
ID METAANALYSIS; ERADICATION; WORLDWIDE; GASTRITIS
AB Objectives: Helicobacter pylori (H. pylori) infection causes a variety of intragastric and extragastric diseases. Despite its decreasing global prevalence, it remains a major public health problem in many developing countries. This study aimed to understand the prevalence of H. pylori infection and its risk factors in five cities of the Ningxia Hui Autonomous Region, an area with high incidence of gastric cancer. Methods: Cross-sectional studies were conducted in Ningxia from 2017 and 2022, to detect the prevalence of H. pylori using the C-14 urea breath test. All participants completed a questionnaire that included demographics, personal habits, household economic characteristics, and previous health status. Multiple logistic regression analyses were used to identify independent factors for H. pylori infection. Results: Our findings demonstrated that the prevalence of H. pylori infection in Ningxia decreased significantly from 60.3% in 2017 to 43.6% in 2022, with an increase in public awareness rate from 35.9% in 2017 to 68.5% in 2022. The lowest infection rate was found in Zhongwei and highest in Guyuan. The prevalence of H. pylori infection was higher among Hui ethnicity, farmers, individuals living in rural areas, individuals with lower income, low education, and those who consumed less fruit. Gallbladder, respiratory, cardiovascular and autoimmune diseases were not associated with H. pylori infection. Conclusions: The prevalence of H. pylori in Ningxia decreased in the past five years. Ethnicity, location, occupation, income, education, and consumption of fruits were independent risk factors for H. pylori infection in Ningxia. It was not associated with extra-gastric disease.
C1 [Zhou, Yan] Ningxia Med Univ, Yinchuan, Peoples R China.
   [Deng, Yanhong; You, Yanjie; Li, Xue; Yao, Li; Tang, Yuanyuan; Li, Xiaofei; Ma, Linke; Li, Yanlin; Liu, Jun; Feng, Yaning; Chen, Xianmei; Hao, Qian; Li, Xuemei; Li, Yuzhen; Niu, Min; Hu, Shengjuan] Ningxia Med Univ, Peoples Hosp Ningxia Hui Autonomous Reg, Affiliated Peoples Hosp Autonomous Reg, Yinchuan, Peoples R China.
   [Zhang, Di] Peoples Hosp Jingyuan, Dept Gastroenterol, Guyuan, Peoples R China.
   [Qi, Hailong] Second Peoples Hosp Shizuishan, Dept Gastroenterol, Shizuishan, Peoples R China.
   [Shi, Ruichun] Peoples Hosp Wuzhong, Dept Gastroenterol, Wuzhong, Peoples R China.
   [Gao, Hengjun] Tongji Univ, Tongji Hosp, Sch Med, Shanghai, Peoples R China.
   [Gao, Hengjun] Tongji Univ, Inst Digest Dis, Sch Med, Shanghai, Peoples R China.
   [Gao, Hengjun] China Ctr Helicobacter Pylori Mol Med, Shanghai, Peoples R China.
   [Bai, Feihu] Hainan Med Coll, Affiliated Hosp 2, Dept Gastroenterol, Haikou, Peoples R China.
   [Bai, Feihu] Gastroenterol Clin Med Ctr Hainan Prov, Haikou, Peoples R China.
   [Hu, Shengjuan] Ningxia Med Univ, Peoples Hosp Ningxia Hui Autonomous Reg, Affiliated Peoples Hosp Autonomous Reg, 301 Zhengyuan North St, Yinchuan 750001, Ningxia Hui Aut, Peoples R China.
   [Bai, Feihu] Hainan Med Coll, Affiliated Hosp 2, Dept Gastroenterol, 368 Coconut Sea Ave, Haikou 571199, Peoples R China.
C3 Ningxia Medical University; Ningxia Medical University; Tongji
   University; Tongji University; Hainan Medical University; Ningxia
   Medical University; Hainan Medical University
RP Hu, SJ (corresponding author), Ningxia Med Univ, Peoples Hosp Ningxia Hui Autonomous Reg, Affiliated Peoples Hosp Autonomous Reg, 301 Zhengyuan North St, Yinchuan 750001, Ningxia Hui Aut, Peoples R China.; Bai, FH (corresponding author), Hainan Med Coll, Affiliated Hosp 2, Dept Gastroenterol, 368 Coconut Sea Ave, Haikou 571199, Peoples R China.
EM baifeihu@sohu.com; hsj.judy@163.com
RI Lu, Wang/JVO-0416-2024; Li, Xue/HPE-4649-2023; tang, yuan/MVU-4402-2025;
   Qi, Hailong/GPF-9359-2022
OI Zhou, Yan/0000-0003-3379-2369
FU Central Guide Local Science and Technology Development Special Project
   fund [YDZX20176400004650]; Ningxia Hui Autonomous Region Key Research
   and Development Program [2021BEG02025, 2019BFG02003]; Ningxia Hui
   Autonomous Region Science and Technology Special Project [2022CMG03039];
   Hainan Province Clinical Medical Center [2021818]
FX We thank the government departments county hospitals and community
   health centers of Ningxia Hui Autonomous Region for facilitating the
   study for the people of Ningxia region. This study is supported by the
   Central Guide Local Science and Technology Development Special Project
   fund (No. YDZX20176400004650), Ningxia Hui Autonomous Region Key
   Research and Development Program (No. 2019BFG02003), Ningxia Hui
   Autonomous Region Key Research and Development Program (No.
   2021BEG02025), Ningxia Hui Autonomous Region Science and Technology
   Special Project to Benefit the People (No. 2022CMG03039), and Hainan
   Province Clinical Medical Center (No. 2021818).
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NR 43
TC 3
Z9 4
U1 1
U2 6
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1943-8141
J9 AM J TRANSL RES
JI Am. J. Transl. Res.
PY 2022
VL 14
IS 9
BP 6647
EP +
PG 13
WC Oncology; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Research & Experimental Medicine
GA 5T7NP
UT WOS:000876048500013
PM 36247252
DA 2025-06-01
ER

PT J
AU Kim, J
   Kim, YS
   Lee, HJ
   Park, SG
AF Kim, Joa
   Kim, Yun Sung
   Lee, Hee Jeong
   Park, Sang Gon
TI Pulmonary amyloidosis and multiple myeloma mimicking lymphoma in a
   patient with Sjogren's syndrome: A case report
SO WORLD JOURNAL OF CLINICAL CASES
LA English
DT Article
DE Case report; Sjogren's syndrome; Amyloidosis; Multiple myeloma;
   Plasmacytoma
ID SOFT-TISSUE PLASMACYTOMAS; SECONDARY; CANCER
AB BACKGROUND Sjogren's syndrome (SS), which affect salivary gland function, is an autoimmune disease. SS may involve extraglandular organs. Approximately 10 to 20 percent of SS patients have clinically significant lung disease, but presentation of pulmonary amylodosis is extremly rare. The incidence of benign monoclonal gammopathy in SS patients is high, but multiple myeloma is rare. No case involving the simultaneous occurrence of two rare diseases, pulmonary amyloidosis and multiple myeloma, in the same patient with SS has been reported so far.
   CASE SUMMARY A 41-year-old male patient was referred to our hematology department due to incidentally detected gastric plasmacytoma. He had been diagnosed with SS four years earlier. Multiple miliary nodules, ground glass opacity in both lung fields, and enlargement of both inguinal lymph nodes was observed on chest and abdomen computer tomography. Based on the pathological findings of lung and lymph node biopsied specimens, the patient was diagnosed with pulmonary amyloidosis and multiple myeloma. Pulmonary amyloidosis and multiple myeloma associated with SS has rarely been reported.
   CONCLUSION This is an extremely rare case of simultaneous pulmonary amyloidosis and multiple myeloma in the same patient with SS.
C1 [Kim, Joa; Kim, Yun Sung] Chosun Univ Hosp, Dept Internal Med, Rheumatol, Gwangju 501717, South Korea.
   [Lee, Hee Jeong] Chosun Univ Hosp, Dept Internal Med, Gwangju 501717, South Korea.
   [Park, Sang Gon] Chosun Univ Hosp, Dept Internal Med, Hematooncol, Gwangju 501717, South Korea.
C3 Chosun University; Chosun University; Chosun University
RP Lee, HJ (corresponding author), Chosun Univ Hosp, Dept Internal Med, Gwangju 501717, South Korea.
EM hjangel21c@hanmail.net
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NR 26
TC 1
Z9 1
U1 0
U2 0
PU BAISHIDENG PUBLISHING GROUP INC
PI PLEASANTON
PA 7041 Koll Center Parkway, Suite 160, PLEASANTON, CA, UNITED STATES
SN 2307-8960
J9 WORLD J CLIN CASES
JI World J. Clin. Cases
PD JAN 21
PY 2022
VL 10
IS 3
BP 1016
EP 1023
DI 10.12998/wjcc.v10.i3.1016
PG 8
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA ZM1GF
UT WOS:000764112600024
PM 35127915
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Geng, LY
   Wang, X
AF Geng, Lingyun
   Wang, Xin
TI Epstein-Barr Virus-associated lymphoproliferative disorders:
   experimental and clinical developments
SO INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
LA English
DT Review
DE EBV; lymphoproliferative disorders; microRNA; oncogenisis; signaling
   pathway; targeted therapy
ID B-CELL LYMPHOMA; PRIMARY EFFUSION LYMPHOMA; REED-STERNBERG-CELLS;
   NATURAL-KILLER-CELL; MEMBRANE-PROTEIN 1; PLASMODIUM-FALCIPARUM MALARIA;
   POLYMERASE-CHAIN-REACTION; PERIPHERAL T-CELL; BURKITTS-LYMPHOMA;
   HODGKINS-DISEASE
AB Epstein-Barr Virus (EBV), the first human virus related to oncogenesis, was initially identified in a Burkitt lymphoma cell line in 1964. EBV infects over 90% of the world's population. Most infected people maintain an asymptomatic but persistent EBV infection lifelong. However, in some individuals, EBV infection has been involved in the development of cancer and autoimmune disease. Nowadays, oncogenic potential of EBV has been intensively studied in a wide range of human neoplasms, including Hodgkin's lymphoma (HL), non-Hodgkin's lymphoma (NHL), nasopharyngeal carcinoma (NPC), gastric carcinoma (GC), etc. EBV encodes a series of viral protein and miRNAs, promoting its persistent infection and the transformation of EBV-infected cells. Although the exact role of EBV in the oncogenesis remains to be clarified, novel diagnostic and targeted therapeutic approaches are encouraging for the management of EBV-related malignancies. This review mainly focuses on the experimental and clinical advances of EBV-associated lymphoproliferative disorders.
C1 [Geng, Lingyun; Wang, Xin] Shandong Univ, Shandong Prov Hosp, Dept Hematol, Jinan 250021, Shandong, Peoples R China.
   [Wang, Xin] Shandong Univ, Sch Med, Dept Diagnost, Jinan 250021, Shandong, Peoples R China.
C3 Shandong University; Shandong First Medical University & Shandong
   Academy of Medical Sciences; Shandong University
RP Wang, X (corresponding author), Shandong Univ, Shandong Prov Hosp, Dept Hematol, 324 Jingwu Rd, Jinan 250021, Shandong, Peoples R China.
EM xinw007@126.com
FU National Natural Science Foundation [81270598, 81473486]; National
   Public Health Grand Research Foundation [201202017]; Natural Science
   Foundations of Shandong Province [2009ZRB14176, ZR-2012HZ003];
   Technology Development Projects of Shandong Province [2008-GG2NS02018,
   2010GSF10250, 2014GSF118021]; Program of Shandong Medical Leading
   Talent, and Taishan Scholar Foundation of Shandong Province
FX This study was partly supported by: National Natural Science Foundation
   (No. 81270598 and No. 81473486), National Public Health Grand Research
   Foundation (No. 201202017), Natural Science Foundations of Shandong
   Province (No. 2009ZRB14176 and No. ZR-2012HZ003), Technology Development
   Projects of Shandong Province (No. 2008-GG2NS02018, No. 2010GSF10250,
   and No. 2014GSF118021), Program of Shandong Medical Leading Talent, and
   Taishan Scholar Foundation of Shandong Province.
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NR 177
TC 37
Z9 43
U1 0
U2 5
PU E-CENTURY PUBLISHING CORP
PI MADISON
PA 40 WHITE OAKS LN, MADISON, WI 53711 USA
SN 1940-5901
J9 INT J CLIN EXP MED
JI Int. J. Clin. Exp. Med.
PY 2015
VL 8
IS 9
BP 14656
EP 14671
PG 16
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CW8TX
UT WOS:000365273300009
PM 26628948
DA 2025-06-01
ER

EF
FN Clarivate Analytics Web of Science
VR 1.0
PT J
AU Di Rocco, A
   Petrucci, L
   Assanto, GM
   Martelli, M
   Pulsoni, A
AF Di Rocco, Alice
   Petrucci, Luigi
   Assanto, Giovanni Manfredi
   Martelli, Maurizio
   Pulsoni, Alessandro
TI Extranodal Marginal Zone Lymphoma: Pathogenesis, Diagnosis and Treatment
SO CANCERS
LA English
DT Review
DE non-Hodgkin lymphoma; marginal zone lymphoma; diagnosis; prognosis;
   treatment; immunotherapy; targeted-therapy; MALT; BALT; OAL
ID OCULAR ADNEXAL LYMPHOMA; B-CELL LYMPHOMA; TERM-FOLLOW-UP; NF-KAPPA-B;
   HEALTH-ORGANIZATION CLASSIFICATION; GASTRIC MALT LYMPHOMA; TISSUE
   LYMPHOMA; HELICOBACTER-PYLORI; LOW-GRADE; CHLAMYDIA-PSITTACI
AB Simple Summary Extranodal marginal zone lymphoma (EMZL) is an indolent lymphoproliferative disease morphologically composed of small heterogeneous B lymphocytes. It generally occurs with a localized stage and can arise in various organs, the most frequent being the stomach, lung, and ocular adnexa. Depending on the presentation and the possible association with infectious agents, different therapeutic approaches are to be undertaken. The purpose of this review is to describe the biology underlying this pathology, the diagnostic, and therapeutic approach. Extranodal Marginal Zone Lymphoma (EMZL lymphoma) is an indolent B-cell lymphoma with a median age at diagnosis of about 60 years. It accounts for 7-8% of all B-cell lymphomas. It can occur in various extranodal sites, including stomach, lung, ocular adnexa, and skin; furthermore, the disseminated disease can be found in 25-50% of cases. Several infectious agents, such as Helicobacter pylori (H. Pylori) in the case of gastric Mucosa Associated Lymphoid Tissue (MALT) Lymphoma, can drive the pathogenesis of this cancer, through the autoantigenic stimulation of T cells, but there may also be other factors participating such autoimmune diseases. Initial staging should include total body computed tomography, bone marrow aspirate, and endoscopic investigation if indicated. Fluorescence in situ hybridization (FISH), should be performed to detect the presence of specific chromosomal translocations involving the MALT1 and BCL10 genes, which leads to the activation of the NF-kappa B signaling pathway. Depending on the location and dissemination of the disease, different therapeutic choices may include targeted therapy against the etiopathogenetic agent, radiotherapy, immunochemotherapy, and biological drugs. The purpose of this review is to illustrate the complex biology and the diagnosis of this disease and to better define new treatment strategies.
C1 [Di Rocco, Alice; Petrucci, Luigi; Assanto, Giovanni Manfredi; Martelli, Maurizio; Pulsoni, Alessandro] Sapienza Univ Rome, Dept Traslat & Precis Med, Hematol, I-00161 Rome, Italy.
C3 Sapienza University Rome
RP Pulsoni, A (corresponding author), Sapienza Univ Rome, Dept Traslat & Precis Med, Hematol, I-00161 Rome, Italy.
EM dirocco@bce.uniroma1.it; l.petrucci@bce.uniroma1.it;
   assanto@bce.uniroma1.it; martelli@bce.uniroma1.it;
   alessandro.pulsoni@uniroma1.it
RI Assanto, Giovanni Manfredi/HPF-0890-2023; Martelli, Maria
   Paola/ABH-3300-2021; Di Rocco, Alice/ISA-8582-2023
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   Alessandro/0000-0001-7429-8004
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NR 93
TC 38
Z9 37
U1 0
U2 11
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6694
J9 CANCERS
JI Cancers
PD APR
PY 2022
VL 14
IS 7
AR 1742
DI 10.3390/cancers14071742
PG 18
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA 0M1CC
UT WOS:000781899300001
PM 35406516
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Malecka, KA
   Dheekollu, J
   Deakyne, JS
   Wiedmer, A
   Ramirez, UD
   Lieberman, PM
   Messick, TE
AF Malecka, Kimberly A.
   Dheekollu, Jayaraju
   Deakyne, Julianna S.
   Wiedmer, Andreas
   Ramirez, Ursula D.
   Lieberman, Paul M.
   Messick, Troy E.
TI Structural Basis for Cooperative Binding of EBNA1 to the Epstein-Barr
   Virus Dyad Symmetry Minimal Origin of Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
DE DNA replication; dyad symmetry; EBNA-1; EBNA1; EBV; Epstein-Barr virus;
   OriP; X-ray crystallography
ID NUCLEAR ANTIGEN EBNA-1; DNA-BINDING; LATENT ORIGIN; SEQUENCE
   REQUIREMENTS; STABLE REPLICATION; CRYSTAL-STRUCTURE; PROTEIN; ORIP;
   DOMAIN; PLASMIDS
AB Epstein-Barr virus is associated with several human malignancies, including nasopharyngeal carcinoma, gastric cancer, and lymphoma. Latently infected cells carry a circularized EBV episome where the origin of replication (oriP) is comprised of two elements: the family of repeats (FR) and dyad symmetry (DS). The viral protein Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA1) binds to FR and DS to promote EBV episome maintenance and DNA replication during latent infection in proliferating cells. EBNA1 binding to the DS constitutes a minimal origin of DNA replication. Here we report the crystal structure of two EBNA1 DNA-binding domain dimers bound to a DS half-site. This structure shows that the DNA is smoothly bent, allowing for stabilizing interactions between the dimers. The dimer-dimer interface requires an intricate hydrogen bonding network involving residues R491 and D581. When this interface is disrupted, we note loss of stable dimer-dimer complex formation on the DNA, compromised oriP-containing plasmid replication in cells, and impaired recruitment of the MCM3 complex to the oriP. Surface conservation analysis reveals that these residues are part of a larger conserved surface that may be critical for recruitment of replication machinery to the oriP. Our results reveal a new region of EBNA1 critical for its activity and one that may be exploited by targeted small molecules to treat EBV-associated disease.
   IMPORTANCE Epstein-Barr virus (EBV) is a causative agent of various malignancies and may also contribute to autoimmune disease. The latent and episomal form of the virus is known to drive EBV-associated oncogenesis. Persistence of the viral episome in proliferating tumor cells requires the interaction of Epstein-Barr virus nuclear antigen 1 (EBNA1) with the viral origin of plasmid replication (oriP). The dyad symmetry (DS) element in oriP is the essential minimal replicator of oriP. Here we report the X-ray crystal structure of EBNA1 bound to DS. The structure reveals a previous unrecognized interface formed between dimers of EBNA1 necessary for cooperative DNA binding, recruitment of cellular replication machinery, and replication function. These findings provide new insights into the mechanism of EBNA1 function at the replication origin and new opportunities to inhibit EBV latent infection and pathogenesis.
C1 [Malecka, Kimberly A.; Dheekollu, Jayaraju; Deakyne, Julianna S.; Wiedmer, Andreas; Lieberman, Paul M.; Messick, Troy E.] Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA.
   [Ramirez, Ursula D.] Vironika LLC, Wynnewood, PA USA.
C3 The Wistar Institute
RP Lieberman, PM; Messick, TE (corresponding author), Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA.
EM troymessick@gmail.com
OI Messick, Troy/0000-0001-7914-1524
FU NIH [RO1 CA093606, RO1 DE017336, P30 CA010815]; Wellcome Trust seeding
   drug discovery grant [WT096496]; Wistar training grant [T32 CA09171]
FX This work was supported by NIH grants RO1 CA093606, RO1 DE017336, and
   P30 CA010815, a Wellcome Trust seeding drug discovery grant (WT096496),
   and a Wistar training grant to J.S.D. (T32 CA09171).
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NR 50
TC 14
Z9 17
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD OCT
PY 2019
VL 93
IS 20
AR e00487-19
DI 10.1128/JVI.00487-19
PG 16
WC Virology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Virology
GA JB0XG
UT WOS:000488281200002
PM 31142669
OA Green Submitted, Green Published
DA 2025-06-01
ER

PT J
AU Yano, S
   Ashida, K
   Sakamoto, R
   Sakaguchi, C
   Ogata, M
   Maruyama, K
   Sakamoto, S
   Ikeda, M
   Ohe, K
   Akasu, S
   Iwata, S
   Wada, N
   Matsuda, Y
   Nakanishi, Y
   Nomura, M
   Ogawa, Y
AF Yano, Seiichi
   Ashida, Kenji
   Sakamoto, Ryuichi
   Sakaguchi, Chihiro
   Ogata, Masatoshi
   Maruyama, Kengo
   Sakamoto, Shohei
   Ikeda, Munehiko
   Ohe, Kenji
   Akasu, Shoko
   Iwata, Shimpei
   Wada, Nobuhiko
   Matsuda, Yayoi
   Nakanishi, Yoichi
   Nomura, Masatoshi
   Ogawa, Yoshihiro
TI Human leucocyte antigen DR15, a possible predictive marker for immune
   checkpoint inhibitor-induced secondary adrenal insufficiency
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Article
DE ACTH deficiency; Adrenal insufficiency; CTLA4; Autoimmunity; HLA;
   Hypophysitis; IL-17; Immune checkpoint inhibitors; PD-1
ID BLOCKADE; HYPOPHYSITIS; SUSCEPTIBILITY; AUTOIMMUNITY; ANTIBODY; COLITIS;
   DISEASE
AB Background: Immune checkpoint inhibitors (ICPis) induce various immune-related adverse events (irAEs), despite their beneficial effects in treating various advanced cancers. ICPi-induced secondary adrenal insufficiency is described as a prevalent and serious 'pituitary irAE.' However, its precise mechanism remains unclear, and no definitive predictive markers have been reported.
   Patients and methods: We enrolled and studied 11 patients with advanced cancer (aged 39-70 years; 6 male patients) receiving nivolumab, pembrolizumab or ipilimumab who developed pituitary irAEs. Their clinical data, including endocrine functions, were retrospectively assessed and human leucocyte antigen (HLA) genotypes were determined to compare the HLA allele frequencies in these patients and healthy controls.
   Results: Among 11 patients, 7, 3 and 1 patients exhibited malignant melanoma, non-small-cell lung cancer and gastric cancer, respectively. HLA type screening results revealed that HLA-DR15, B52 and Cw12 were observed in 9, 7, and 7 patients with pituitary irAE, respectively. DR15, B52 and Cw12 were significantly more prevalent in our group than in the healthy control group from the Japanese HLA-haplotype database (this study vs healthy control group); DR15: 81.8% vs 33.5% (n = 11, P = 0.0014), B52: 63.6% vs 21.0% (n = 11, P = 0.0026) and Cw12: 70% vs 21.3% (n = 10, P = 0.0013).
   Conclusions: HLA-DR15, B52 and Cw12 are possible predisposing factors for pituitary ir AEs. HLA-DR15 is reportedly associated with autoimmune disease via interleukin-17 regulation, suggesting its involvement in pituitary ir AE development. Using HLA haplotypes as pituitary irAE predictive markers, we could provide safe ICPi treatment and understand irAE pathogenesis. (C) 2020 Elsevier Ltd. All rights reserved.
C1 [Yano, Seiichi; Ashida, Kenji; Sakamoto, Ryuichi; Sakaguchi, Chihiro; Ogata, Masatoshi; Maruyama, Kengo; Sakamoto, Shohei; Matsuda, Yayoi; Nomura, Masatoshi; Ogawa, Yoshihiro] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Fukuoka, Japan.
   [Ashida, Kenji; Akasu, Shoko; Iwata, Shimpei; Wada, Nobuhiko; Nomura, Masatoshi] Kurume Univ, Dept Internal Med, Div Endocrinol & Metab, Sch Med, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan.
   [Ikeda, Munehiko] Kyushu Univ Hosp, Dept Pharm, Fukuoka, Japan.
   [Ohe, Kenji] Fukuoka Univ, Fac Pharmaceut Sci, Fukuoka, Japan.
   [Nakanishi, Yoichi] Kyushu Univ, Grad Sch Med Sci, Res Inst Dis Chest, Fukuoka, Japan.
C3 Kyushu University; Kurume University; Kyushu University; Fukuoka
   University; Kyushu University
RP Ashida, K (corresponding author), Kurume Univ, Dept Internal Med, Div Endocrinol & Metab, Sch Med, 67 Asahi Machi, Kurume, Fukuoka 8300011, Japan.
EM ashida@med.kurume-u.ac.jp
RI Ashida, Kenji/AGG-8254-2022; Sakamoto, Ryuichi/HSI-0408-2023; Ashida,
   Kenji/P-2025-2018
OI Ogawa, Yoshihiro/0000-0002-0834-2836; Yano, Seiichi/0000-0001-7935-9654;
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NR 32
TC 69
Z9 72
U1 1
U2 15
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
EI 1879-0852
J9 EUR J CANCER
JI Eur. J. Cancer
PD MAY
PY 2020
VL 130
BP 198
EP 203
DI 10.1016/j.ejca.2020.02.049
PG 6
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA LR5BV
UT WOS:000535711100021
PM 32229416
DA 2025-06-01
ER

PT J
AU Schreuder, MI
   van den Brand, M
   Hebeda, KM
   Groenen, PJTA
   van Krieken, JH
   Scheijen, B
AF Schreuder, Max I.
   van den Brand, Michiel
   Hebeda, Konnie M.
   Groenen, Patricia J. T. A.
   van Krieken, J. Han
   Scheijen, Blanca
TI Novel developments in the pathogenesis and diagnosis of extranodal
   marginal zone lymphoma
SO JOURNAL OF HEMATOPATHOLOGY
LA English
DT Review
DE Lymphoid malignancies; Chromosomal rearrangements; Infections; MALT;
   EMZL
ID B-CELL LYMPHOMA; NF-KAPPA-B; GASTRIC MALT LYMPHOMA; HELICOBACTER-PYLORI
   CAGA; NON-HODGKIN-LYMPHOMA; OCULAR ADNEXAL LYMPHOMA; CONCERTED ACTION
   BHM4-CT98-3936; BORRELIA-BURGDORFERI INFECTION; ABERRANT SOMATIC
   HYPERMUTATION; CYTOTOXIN-ASSOCIATED GENE
AB Extranodal marginal zone lymphoma (EMZL), mostly represented by mucosa-associated lymphoid tissue (MALT) type, also referred to as MALT lymphoma, is a clinically heterogeneous entity within the group of low-grade B cell lymphomas that arises in a wide range of different extranodal sites, including the stomach, lung, ocular adnexa, and skin. It represents the third most common non-Hodgkin lymphoma in the Western world, and the median age of occurrence is around 60 years. One characteristic aspect in a subset of EMZL detectable in about 25% of the cases is the presence of specific chromosomal translocations involving the genes MALT1 and BCL10, which lead to activation of the NF-kappa B signaling pathway. Another unique aspect is that several infectious agents, such as Helicobacter pylori in the case of gastric EMZL, and autoimmune disorders, like Sjogren syndrome, have been implicated in the pathogenesis of this cancer. Recent findings as summarized in this review have further improved our understanding of the complex pathobiology of this disease and have been essential to better define novel treatment strategies. In addition, many of these specific features are currently being implemented for the diagnosis of EMZL.
C1 [Schreuder, Max I.; van den Brand, Michiel; Hebeda, Konnie M.; Groenen, Patricia J. T. A.; van Krieken, J. Han; Scheijen, Blanca] Radboud Univ Nijmegen, Med Ctr, Dept Pathol, Geert Grootepl Zuid 10, NL-6525 AG Nijmegen, Netherlands.
   [van den Brand, Michiel] Rijnstate Hosp, Pathol DNA, Arnhem, Netherlands.
   [van Krieken, J. Han; Scheijen, Blanca] Radboud Inst Mol Life Sci, Nijmegen, Netherlands.
C3 Radboud University Nijmegen; Rijnstate Hospital
RP Scheijen, B (corresponding author), Radboud Univ Nijmegen, Med Ctr, Dept Pathol, Geert Grootepl Zuid 10, NL-6525 AG Nijmegen, Netherlands.; Scheijen, B (corresponding author), Radboud Inst Mol Life Sci, Nijmegen, Netherlands.
EM blanca.scheijen@radboudumc.nl
RI Hebeda, K./L-4354-2015; van den Brand, Michiel/E-2900-2016; van Krieken,
   Joannes/D-4138-2009; Groenen, Patricia/L-4336-2015; Scheijen,
   Blanca/E-3523-2016
OI van Krieken, Joannes/0000-0002-8105-0450; Scheijen,
   Blanca/0000-0001-8029-9230
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NR 158
TC 42
Z9 45
U1 0
U2 10
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1868-9256
EI 1865-5785
J9 J HEMATOP
JI J. Hematop.
PD DEC
PY 2017
VL 10
IS 3-4
BP 91
EP 107
DI 10.1007/s12308-017-0302-2
PG 17
WC Hematology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Hematology; Pathology
GA FO5SB
UT WOS:000416919900002
PM 29225710
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Akram, M
   Daniyal, M
   Sultana, S
   Owais, A
   Akhtar, N
   Zahid, R
   Said, F
   Bouyahya, A
   Ponomarev, E
   Shariat, MA
   Thiruvengadam, M
AF Akram, Muhammad
   Daniyal, Muhammad
   Sultana, Sabira
   Owais, Aymen
   Akhtar, Naheed
   Zahid, Rabia
   Said, Fahad
   Bouyahya, Abdelhakim
   Ponomarev, Evgeny
   Shariat, Mohammad Ali
   Thiruvengadam, Muthu
TI Traditional and modern management strategies for rheumatoid arthritis
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Rheumatoid arthritis; Management of arthritis; Traditional medicines;
   Anti-arthritic potential
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; MODIFYING ANTIRHEUMATIC DRUGS;
   GINGER ZINGIBER-OFFICINALE; NECROSIS-FACTOR INHIBITORS; LONG-TERM
   IMPACT; DOUBLE-BLIND; DISEASE-ACTIVITY; RADIOGRAPHIC PROGRESSION;
   CARDIOVASCULAR-DISEASE; RECENT TRENDS
AB Rheumatoid arthritis (RA) is a serious disorder of the joints affecting 1 or 2% of the population aged between 20 and 50 years worldwide. RA is the foremost cause of disability in developing and Western populations. It is an autoimmune disease-causing inflammation and pain involving synovial joints. Pro-inflammatory markers, including cytokines, such as interleukin -1 (IL-1), IL-6, IL-7, IL-8, and tumor necrosis factor-alpha (TNF-alpha) are involved in RA. RA treatment involves TNF-alpha blockade, B cell therapy, IL-1 and IL-6 blockade, and angiogenesis inhibition. Synthetic drugs available for the treatment of RA include disease-modifying anti-rheumatic drugs (DMARD), such as cyclophosphamide, sulfasalazine, methotrexate, nonsteroidal anti-inflammatory drugs (NSAIDs), and intramuscular gold. These agents induce adverse hepatorenal effects, hypertension, and gastric ulcers. We found that patients diagnosed with chronic pain, as in RA, and those refractory to contemporary management are most likely to seek traditional medicine. Approximately 60-90% of patients with arthritis use traditional medicines. Therefore, the efficacy and safety of these traditional medicines need to be established. The treatment for RA entails a comprehensive multidisciplinary strategy to reduce pain and inflammation and to restore the activity of joints. The potential medicinal plants exhibiting anti-arthritic and anti-rheumatic pharmacological activity are reviewed here.
C1 [Akram, Muhammad; Sultana, Sabira; Zahid, Rabia] Govt Coll Univ Faisalabad, Dept Eastern Med, Directorate Med Sci, Faisalabad, Pakistan.
   [Daniyal, Muhammad] Hunan Univ Chinese Med, Sch Pharm, TCM & Ethnomed Innovat & Dev Int Lab, Changsha 410208, Peoples R China.
   [Owais, Aymen] Jinnah Univ Women, Dept Eastern Med, Karachi, Pakistan.
   [Akhtar, Naheed] Univ Poonch, Dept Pharm, Rawalakot Azad Kashmir, Pakistan.
   [Said, Fahad] Univ Poonch, Dept Eastern Med, Rawalakot Azad Kashmir, Pakistan.
   [Bouyahya, Abdelhakim] Mohammed V Univ, Fac Sci, Lab Human Pathol Biol, Rabat, Morocco.
   [Bouyahya, Abdelhakim] Mohammed V Univ, Genom Ctr Human Pathol, Rabat, Morocco.
   [Ponomarev, Evgeny; Shariat, Mohammad Ali] KG Razumovsky Moscow State Univ Technol & Managem, Cossack Univ 1, Moscow, Russia.
   [Thiruvengadam, Muthu] Konkuk Univ, Coll Sanghuh Life Sci, Dept Crop Sci, Seoul 05029, South Korea.
C3 Government College University Faisalabad; Hunan University of Chinese
   Medicine; Mohammed V University in Rabat; Mohammed V University in
   Rabat; K.G. Razumovsky Moscow State University of Technologies &
   Management the First Cossack University; Konkuk University
RP Akram, M (corresponding author), Govt Coll Univ Faisalabad, Dept Eastern Med, Directorate Med Sci, Faisalabad, Pakistan.; Thiruvengadam, M (corresponding author), Konkuk Univ, Coll Sanghuh Life Sci, Dept Crop Sci, Seoul 05029, South Korea.
EM makram_0451@hotmail.com; muthu@konkuk.ac.kr
RI Abdelhakim, BOUYAHYA/Y-5725-2019; Akram, Muhammad/A-5679-2018;
   Thiruvengadam, Muthu/AAP-8023-2021; Daniyal, Muhammad/A-1617-2015; Said
   Khan, Fahad/JLM-9998-2023; Zahid, Rabia/HTS-5264-2023
OI Ghauri, Aymen/0000-0003-4295-0496; Daniyal,
   Muhammad/0000-0002-5663-5211; Said Khan, Fahad/0000-0002-4497-9770;
   Zahid, Rabia/0000-0001-5069-4993
FU KU Research Professor Program of Konkuk University, Seoul, South Korea
FX This paper was supported by the KU Research Professor Program of Konkuk
   University, Seoul, South Korea.
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NR 183
TC 50
Z9 55
U1 4
U2 33
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0009-8981
EI 1873-3492
J9 CLIN CHIM ACTA
JI Clin. Chim. Acta
PD JAN
PY 2021
VL 512
BP 142
EP 155
DI 10.1016/j.cca.2020.11.003
PG 14
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA PI1BF
UT WOS:000600833300025
PM 33186593
DA 2025-06-01
ER

PT J
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   Yoshida, Akiko
   Mikawa, Akiko
TI Outcome of Nivolumab-Induced Vogt-Koyanagi-Harada Disease-Like Uveitis
   in a Patient Managed without Intravenous Methylprednisolone Therapy
SO CASE REPORTS IN OPHTHALMOLOGICAL MEDICINE
LA English
DT Article
ID ANTI-PD-1 ANTIBODY; ASSOCIATION
AB Background. In recent years, immune checkpoint inhibitors (ICI) have been often used for several types of cancers. Immune-related adverse events (irAEs) are autoimmune responses caused by ICI. Among the different types of irAEs, uveitis is common in ophthalmology. Moreover, there are reports on Vogt-Koyanagi-Harada (VKH) disease-like uveitis. In most cases, VKH, as in the usual VKH, is managed with intravenous methylprednisolone therapy. Case Report. A 72-year-old man was diagnosed with gastric cancer, and he was treated with nivolumab, a type of ICI. After eight cycles of nivolumab therapy, he developed fulminant type 1 diabetes mellitus and diabetic ketoacidosis. Thus, the treatment was discontinued. Subsequently, the patient was referred to our department due to bilateral blurry vision. He had decreased visual acuity in both eyes, and slit lamp examination revealed the presence of bilateral anterior chamber cells and keratic precipitates. Fundus examination showed bilateral serous retinal detachment (SRD), wavy retinal pigment epithelium (RPE), and choroidal thickening. Cerebrospinal fluid examination revealed prominent pleocytosis. Thus, we initiated eye drop therapy and subtenon injection of triamcinolone acetonide on the right eye only. After 1 month, SRD and wavy RPE disappeared, and the patient's visual acuity improved. Further, both eyes had similar improvements in visual acuity and abnormal findings. Oral prednisolone was subsequently administered for hearing loss. However, intravenous methylprednisolone was not used, and ophthalmologic findings and visual acuity did not change before and after systemic steroid therapy. One year after disease onset, SRD and wavy RPE did not relapse. Conclusion. Nivolumab-induced VKH disease-like uveitis can have good outcomes even in a patient managed without intravenous methylprednisolone therapy.
C1 [Nagai, Ryoji; Yoshida, Akiko; Mikawa, Akiko] Nishi Kobe Med Ctr, Dept Ophthalmol, Kobe, Japan.
   [Yamamoto, Akinari] Kyoto Univ, Dept Ophthalmol & Visual Sci, Grad Sch Med, Kyoto, Japan.
C3 Kobe City Medical Center General Hospital; Kyoto University
RP Nagai, R (corresponding author), Nishi Kobe Med Ctr, Dept Ophthalmol, Kobe, Japan.
EM r_n_2019@kuhp.kyoto-u.ac.jp; yamamotoyama@kuhp.kyoto-u.ac.jp;
   akiko_yoshida@kcho.jp; akiko_mikawa@kcho.jp
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NR 26
TC 7
Z9 7
U1 0
U2 0
PU HINDAWI LTD
PI LONDON
PA ADAM HOUSE, 3RD FLR, 1 FITZROY SQ, LONDON, W1T 5HF, ENGLAND
SN 2090-6722
EI 2090-6730
J9 CASE REP OPHTHAL MED
JI Case Rep. Ophthalmol. Med.
PD FEB 8
PY 2023
VL 2023
AR 9565205
DI 10.1155/2023/9565205
PG 8
WC Ophthalmology
WE Emerging Sources Citation Index (ESCI)
SC Ophthalmology
GA 9C3NL
UT WOS:000935328200001
PM 36818144
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Di Mario, F
   Rodriguez-Castro, KI
   Franceschi, M
   Landi, S
   Grillo, S
   Franzoni, L
   Russo, M
   Brandimarte, G
   Tursi, A
   Crafa, P
AF Di Mario, Francesco
   Rodriguez-Castro, Kryssia Isabel
   Franceschi, Marilisia
   Landi, Stefano
   Grillo, Simone
   Franzoni, Lorella
   Russo, Michele
   Brandimarte, Giovanni
   Tursi, Antonio
   Crafa, Pellegrino
TI Improvement of symptoms in patients affected by chronic atrophic
   gastritis using L-cysteine [Acetium®]
SO DIGESTIVE DISEASES
LA English
DT Article
ID GASTROESOPHAGEAL-REFLUX DISEASE; HELICOBACTER-PYLORI ANTIBODIES;
   IRRITABLE-BOWEL-SYNDROME; SERUM PEPSINOGEN-I; CARCINOGENIC ACETALDEHYDE;
   ALCOHOL-DEHYDROGENASE; AUTOIMMUNE GASTRITIS; CLINICAL-PRACTICE;
   PROTECTIVE ACTION; SULFUR-COMPOUNDS
AB Background:Chronic Atrophic Gastritis (CAG) alone is a precancerous condition for gastric cancer. Achlorhydria plays an important role in the formation of a class I carcinogen, acetaldehyde. L-cysteine has been claimed to bind acetaldehyde covalently. Symptoms are present in 55% of CAG patients, of whom 70% have upper gastrointestinal (GI) complaints. The aim of this study was to investigate the properties of L-cysteine in the modification of symptom patterns in CAG patients.Methods:Consecutive patients with histological diagnosis of CAG (OLGA >= 1 with gastric corpus involvement) were evaluated with serological determination of gastric function, clinical assessment of symptoms using the Visual Analogic Score (VAS) and the Global Score System (GSS), and considered for therapy with L-cysteine, 300 mg/daily. Data regarding symptoms were collected at enrollment and after 3, 6, 12, 18, 24 months, with an ultimate follow-up of 2 years.Results:A total of 330 patients with CAG were divided in group 1 (77 patients treated with L-cysteine) and group 2 (50 patients who received no specific treatment- control group). A statistically significant improvement both in the VAS score (7.8 at baseline vs 4.5 after 24 months; p<0.01) was observed in patients treated with L-cysteine, while no significant changes in symptom pattern/intensity were recorded in the two-year follow-up of untreated patients with CAG.Conclusions:Long-term treatment with L-cysteine provides symptom improvement in CAG patients and might be proposed as maintenance therapy in such patients.
C1 [Di Mario, Francesco; Landi, Stefano; Grillo, Simone; Franzoni, Lorella; Russo, Michele; Crafa, Pellegrino] Univ Parma, Dept Med & Surg, Parma, Italy.
   [Rodriguez-Castro, Kryssia Isabel; Franceschi, Marilisia] AltoVicentino Hosp, Dept Med, Endoscopy Unit, ULSS7 Pedemontana, Storso, VI, Italy.
   [Brandimarte, Giovanni] Cristo Re Hosp, Div Internal Med & Gastroenterol, Rome, Italy.
   [Tursi, Antonio] Azienda Sanit Locale Barletta Andria Trani, Terr Gastroenterol Serv, Andria, Italy.
   [Di Mario, Francesco] Univ Parma, Dept Med & Surg, Viale Gramsci n 14, I-43126 Parma, Italy.
C3 University of Parma; University of Parma
RP Di Mario, F (corresponding author), Univ Parma, Dept Med & Surg, Viale Gramsci n 14, I-43126 Parma, Italy.
EM francesco.dimario@unipr.it
RI Rodriguez-Castro, Kryssia/GZG-9769-2022; Grillo, Simone/AAA-4332-2021
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NR 48
TC 2
Z9 2
U1 0
U2 7
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0257-2753
EI 1421-9875
J9 DIGEST DIS
JI Dig. Dis.
PD MAR
PY 2023
VL 41
IS 2
BP 198
EP 205
DI 10.1159/000528168
EA NOV 2022
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 9U9AP
UT WOS:000892795700001
PM 36423587
DA 2025-06-01
ER

PT J
AU Kapadia, CR
AF Kapadia, CR
TI Gastric atrophy, metaplasia, and dysplasia - A clinical perspective
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE chronic atrophic gastritis; intestinal metaplasia; Helicobacter pylori;
   cobalamin deficiency
ID HELICOBACTER-PYLORI INFECTION; LASER-INDUCED FLUORESCENCE; HIGH-GRADE
   DYSPLASIA; INTESTINAL METAPLASIA; FOLLOW-UP; COBALAMIN DEFICIENCY;
   NATURAL-HISTORY; ACID-SECRETION; CANCER; ULCER
AB Gastric carcinoma of the intestinal type originates in dysplastic epithelium, which in turn develops in the milieu of atrophic gastritis and intestinal metaplasia. Cancers also may develop less often from gastric adenomatous polyps, which represent dysplastic epithelium arising in a raised lesion. The main causes of chronic atrophic gastritis and gastric atrophy are autoimmune due to pernicious anemia or chronic Helicobacter pylori infection. In the former condition, there is severe atrophy of the corpus (oxyntic mucosa), with the antrum being speared. In contrast, chronic atrophic gastritis consequent to H. pylori infection is a multifocal pangastritis, involving independent foci in the corpus and antrum of the stomach. For the most part, these clinical conditions are silent; the only manifestation of both these forms of chronic atrophic gastritis is cobalamin (vitamin B,,) deficiency. In the case of the autoimmume gastritis of pernicious anemia, cobalamin deficiency results form the absence of intrinsic factor. When cobalamin deficiency occurs in patients with H. pylori-related gastritis, for the most, part, it is because these patients have hypochlorhydria and are therefore unable to release cobalamin from its bound form in food. Patients may have advanced neuropsychiatric manifestations of cobalamin deficiency and yet not be anemic, have a normal blood smear, and even have serum cobalamin levels in the normal range. The condition may be identified by demonstrating elevated levels of homocysteine and methylmalonic acid. Intestinal metaplasia may be of the enteric (grade I), enterocolic (grade II), or colonic (grade III) type. Grade III intestinal metaplasia has traditionally been thought of as the most sinister variety, although the extent of atrophy and metaplasia may be a better marker for premalignancy than the mere identification of small areas of grade III intestinal metaplasia. Over the years, there has been much disagreement and a high degree of interrater variability, especially between Western and Japanese pathologists, as to the different grades of dysplasia and early gastric cancer. Recent consensus conferences at Vienna and Padova have resulted in better understanding of what constitutes these lesions, and it is hoped that in the near future agreement between pathologists will improve as a consequence. For the present, it is imperative that clinicians obtain second opinions from two or more expert pathologists on biopsy specimens before arriving at a diagnosis of either low- or high-grade dysplasia. The former histologic diagnosis is tantamount to subjecting the patient to endoscopic surveillance and the latter is tantamount to a decision regarding the resection of the lesion, both decisions being psychologically disturbing for patients. At this time, population screening for H. pylori is not recommended in Western countries, but most experts would agree that H. pylori should be eradicated if detected as part of the appropriate investigation of a clinical disorder such as dyspepsia. Certain other specific conditions may also be considered to be precancerous, such as the gastric remnant after a partial gastrectomy and the gastric mucosa in familial adenomatous polyposis syndrome and in familial Peutz-Jeghers syndrome and perhaps Menetrier disease.
C1 Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA.
C3 Yale University
RP Yale Univ, Sch Med, Dept Internal Med, LMP 1074,POB 208030, New Haven, CT 06520 USA.
EM cyrus.kapadia@yale.edu
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NR 44
TC 81
Z9 100
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD MAY-JUN
PY 2003
VL 36
IS 5
BP S29
EP S36
DI 10.1097/00004836-200305001-00006
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA 670XQ
UT WOS:000182435700006
PM 12702963
DA 2025-06-01
ER

PT J
AU de la Lastra, CA
   Barranco, MD
   Motilva, V
   Herrerías, JM
AF de la Lastra, CA
   Barranco, MD
   Motilva, V
   Herrerías, JM
TI Mediterranean diet and health:: Biological importance of olive oil
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
ID LOW-DENSITY-LIPOPROTEIN; POLYUNSATURATED FATTY-ACIDS; SERUM-LIPID
   LEVELS; FISH-OIL; PHENOLIC-COMPOUNDS; IN-VITRO; RHEUMATOID-ARTHRITIS;
   CYTOKINE PRODUCTION; STEROL COMPOSITION; CAFFEIC ACID
AB Olive oil, the main fatty component of the Mediterranean diet, is characterized by consisting of monounsaturated fatty acids as well as by its elevated content in antioxidant agents. This oil exhibits numerous biological functions which are beneficial for the state of health. A diet rich in monounsaturated fatty acids provides an adequate fluidity to the biological membranes, diminishing the hazard of lipid peroxidation which affects polyunsaturated fatty acids. Moreover, the antioxidants present in olive oil are able to scavenge free radicals and afford an adequate protection against peroxidation. Regarding the heart, olive oil decreases the plasmatic levels of LDL-cholesterol and increases those of HDL-cholesterol, hence diminishing the risk of suffering from heart complaints. In this context, it has been suggested that increased consumption of monounsaturated fatty acids in place of polyunsaturated fatty acids will render circulating lipoproteins less sensitive to peroxidation and thereby diminish the development of atherosclerosis. Olive oil has also been proven to contribute to a better control of the hypertriglyceridemia accompanying diabetes and may reduce the risk of breast cancer and colorectum. On the other hand, several investigations have suggested that olive oil can be beneficial in inflammatory and autoimmune diseases, such as rheumatoid arthritis. In this sense, some reports have indicated that olive oil modifies inflammatory cytokines production. As for the digestive system, olive oil enhances gallbladder emptying consequently reducing cholelithiasis risk, decreases the pancreatic exocrine secretion and gastric secretory function in response to food. Finally, it has been demonstrated that a diet rich in olive oil is associated with a high percentage of gastric ulcer healing and affords a higher resistance against non steroidal antiinflammatory drugs-induced gastric ulcerogenesis.
C1 Fac Farm, Dept Farmacol, Seville 41012, Spain.
C3 University of Sevilla
RP Fac Farm, Dept Farmacol, C Prof Garcia Gonzalez S-N, Seville 41012, Spain.
RI Alarcon-de-la-Lastra, Catalina/F-6282-2013
OI Alarcon-de-la-Lastra, Catalina/0000-0001-6625-3818; Motilva Sanchez,
   Virginia/0000-0001-5674-6969
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TC 162
Z9 169
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U2 36
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1381-6128
EI 1873-4286
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD JUL
PY 2001
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BP 933
EP 950
PG 18
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA 448WJ
UT WOS:000169652700004
PM 11472248
DA 2025-06-01
ER

PT J
AU Daniels, JA
   Lederman, HM
   Maitra, A
   Montgomery, EA
AF Daniels, Jason A.
   Lederman, Howard M.
   Maitra, Anirban
   Montgomery, Elizabeth A.
TI Gastrointestinal tract pathology in patients with common variable
   immunodeficiency (CVID) - A clinicopathologic study and review
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE common variable immunodeficiency; celiac disease; ulcerative colitis;
   Crohn disease; CVID; IBD; infectious colitis
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; COLLAGENOUS COLITIS; IGA
   DEFICIENCY; CYTOMEGALOVIRUS-INFECTION; MICROSCOPIC COLITIS;
   HELICOBACTER-PYLORI; DISEASE; LINKAGE; ENTEROPATHY; CANCER
AB Background: Common variable immunodeficiency (CVID) is characterized by a host of gastrointestinal (GI) lesions that can mimic other conditions.
   Methods: We reviewed clinical documentation and samples from 132 separate GI biopsy or resection sites on 20 CVID patients obtained over a 26-year period, including biopsies from the colon (34), esophagus (19), small intestine (38), and stomach (35), a partial gastrectomy, small bowel resection, colectomy, 2 cholecystectomies, and I appendectomy.
   Results: There were 13 males and 7 females. Nine patients were children (10 y and younger) and I I were adults. Age at diagnosis ranged from 6 months to 62 years (median, 35.5y), and age at biopsy ranged from 10 months to 67 years (median, 38y). Esophageal samples often showed intraepithelial neutrophils, accompanied by candida. Half of patients' esophageal biopsies had prominent intraepithelial lymphocytosis, one of which also had prominent apoptosis. The stomachs of 67% of patients lacked plasma cells. Most showed lymphoid aggregates. An increase in apoptosis was detected in biopsies from a third. About 20% had a lymphocytic gastritis pattern. Intraepithelial neutrophils were found in a subset, accompanied by various infections [cytornegalovirus (CMV), Helicobacter pylori, and Cryptosporidium]. Granulomas were found in I patient. Gastric adenocarcinoma was identified in one patient. There was a paucity of small bowel plasma cells in the majority of patients (68%). The small bowel showed prominent lymphoid aggregates in about half (47%). An increase in apoptosis was detected in specimens from about 20%. Increased intraepithelial lymphocytes (IELs) were found in samples from over half of patients (63%), most of whom (83%) also had villous blunting, mimicking celiac disease. Intraepithelial neutrophils were found in a subset (32%) and correlated with CMV and Cryptosporidium infections. Granulomas were seen in biopsies from 2 patients (11%). One patient had a collagenous enteritis pattern (accompanied by a collagenous colitis pattern). One patient had autoimmune enteritis; biopsies from this patient were initially relatively normal but later displayed prominent crypt apoptosis and loss of goblet cells. In colon samples, a paucity of plasma cells was seen in 10 patients (63%). The colon showed lymphoid aggregates in most patients (81 %). Apoptosis was prominent in samples from half of the patients (50%). Biopsies from 6 patients had a lymphocytic colitis pattern (38%) and 2 patients had a collagenous colitis pattern. Intraepithelial neutrophils were found in samples from most patients (88%). Crypt distortion was seen in 6 of these patients (43%), thereby mimicking ulcerative or Crohn colitis. Granulomas were found in 3 patients (19%). CMV was detected in I patient. The appendix from I patient showed Cryptosporidium and acute serositis with a paucity of plasma cells and an increase in apoptosis. The gallbladder from I patient showed acute cholecystitis, and another patient's gallbladder lacked plasma cells.
   Conclusions: GI tract CVID displays a wide spectrum of histologic patterns. Its features can mimic lymphocytic colitis, collagenous enterocolitis, celiac disease, lymphocytic gastritis, granulomatous disease, acute graft-versus-host disease, and inflammatory bowel disease. In fact, in our series, we found patients with a prior diagnosis of celiac disease (25%) and inflammatory bowel disease (35%). including Crohn disease (15 %). The diagnosis of CVID may be suspected on the basis of the lack of plasma cells in a GI biopsy, but because this feature is only present in about two-thirds of patients, the diagnosis cannot always be suggested in isolation of other clinical and laboratory findings.
C1 [Daniels, Jason A.; Maitra, Anirban; Montgomery, Elizabeth A.] Johns Hopkins Univ Hosp, Dept Pathol, Baltimore, MD 21231 USA.
   [Lederman, Howard M.] Johns Hopkins Univ Hosp, Dept Pediat, Baltimore, MD 21231 USA.
C3 Johns Hopkins University; Johns Hopkins Medicine; Johns Hopkins
   University; Johns Hopkins Medicine
RP Montgomery, EA (corresponding author), Johns Hopkins Univ Hosp, Dept Pathol, Weinberg 2242,401 N Broadway, Baltimore, MD 21231 USA.
EM emontgom@jhmi.edu
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0147-5185
EI 1532-0979
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD DEC
PY 2007
VL 31
IS 12
BP 1800
EP 1812
DI 10.1097/PAS.0b013e3180cab60c
PG 13
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA 241EA
UT WOS:000251638500003
PM 18043034
DA 2025-06-01
ER

PT J
AU García-García, E
   Staines-Boone, AT
   Vargas-Hernández, A
   González-Serrano, ME
   Carrillo-Tapia, E
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   Yamazaki-Nakashimada, MA
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AF Garcia-Garcia, E.
   Staines-Boone, A. T.
   Vargas-Hernandez, A.
   Gonzalez-Serrano, M. E.
   Carrillo-Tapia, E.
   Mogica-Martinez, D.
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   Espinosa-Rosales, F. J.
   Yamazaki-Nakashimada, M. A.
   Santos-Argumedo, L.
   Lopez-Herrera, G.
TI Clinical and mutational features of X-linked agammaglobulinemia in
   Mexico
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Btk; X-linked agammaglobulinemia; Splice site; Missense mutations
ID BRUTONS TYROSINE KINASE; MOLECULAR ANALYSIS; BTK; GENE; STIMULATION;
   EXPRESSION; PROTEIN
AB X-linked agammaglobulinemia (XLA) is caused by BTK mutations, patients typically show <2% of peripheral B cells and reduced levels of all immunoglobulins; they suffer from recurrent infections of bacterial origin; however, viral infections, autoimmune-like diseases, and an increased risk of developing gastric cancer are also reported. In this work, we report the BTK mutations and clinical features of 12 patients diagnosed with XLA. Furthermore, a clinical revision is also presented for an additional cohort of previously reported patients with XLA. Four novel mutations were identified, one of these located in the previously reported mutation refractory SH3 domain. Clinical data support previous reports accounting for frequent respiratory, gastrointestinal tract infections and other symptoms such as the occurrence of reactive arthritis in 19.2% of the patients. An equal proportion of patients developed septic arthritis; missense mutations and mutations in SH1, SH2 and PH domains predominated in patients who developed arthritis. (C) 2016 Elsevier Inc. All rights reserved.
C1 [Garcia-Garcia, E.; Gonzalez-Serrano, M. E.; Berron-Ruiz, L.; Espinosa-Rosales, F. J.; Lopez-Herrera, G.] SSA, Inst Nacl Pediat, Unidad Invest Inmunodeficiencias, Insurgentes Sur 3700-C, Mexico City, DF, Mexico.
   [Staines-Boone, A. T.] Unidad Alta Especialidad IMSS 25, Ctr Med Nacl Noreste, Dept Inmunol Clin, Monterrey, NL, Mexico.
   [Vargas-Hernandez, A.; Santos-Argumedo, L.] Ctr Invest & Estudios Avanzados, Biomed Mol, Mexico City, DF, Mexico.
   [Carrillo-Tapia, E.] Univ Autonoma Ciudad Mexico, Programa Ciencias Genom, Mexico City, DF, Mexico.
   [Mogica-Martinez, D.] IMSS, Ctr Med Nacl La Raza, Dept Alergia & Inmunol Clin, Mexico City, DF, Mexico.
   [Segura-Mendez, N. H.] IMSS, Hosp Especialidades, Ctr Med Nacl Siglo 21, Serv Alergia & Inmunol Clin, Mexico City, DF, Mexico.
   [Yamazaki-Nakashimada, M. A.] SSA, Inst Nacl Pediat, Serv Inmunol, Mexico City, DF, Mexico.
C3 CINVESTAV - Centro de Investigacion y de Estudios Avanzados del
   Instituto Politecnico Nacional; Instituto Mexicano del Seguro Social;
   Instituto Mexicano del Seguro Social
RP López-Herrera, G (corresponding author), SSA, Inst Nacl Pediat, Unidad Invest Inmunodeficiencias, Insurgentes Sur 3700-C, Mexico City, DF, Mexico.
RI Espinosa-Rosales, Francisco/B-9762-2014; LOPEZ HERRERA,
   GABRIELA/AAL-1781-2021; Yamazaki-Nakashimada, Marco Antonio/Y-7129-2019
OI segura, Nora Hilda/0000-0003-4958-6236; LOPEZ HERRERA,
   GABRIELA/0000-0002-5498-6739; Carrillo, Eduardo/0009-0004-4198-9078
FU Consejo Nacional de Ciencia y Tecnologia (CONACyT) [FOSISS
   2011-1-161089, CB-2010-01-154472]; PROBEI fellowship
FX This study was partially supported by grants from Consejo Nacional de
   Ciencia y Tecnologia (CONACyT), projects # FOSISS 2011-1-161089 and
   CB-2010-01-154472. Elizabeth Garcia-Garcia received a PROBEI fellowship
CR Al-Herz W, 2014, FRONT IMMUNOL, V5, DOI 10.3389/fimmu.2014.00162
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NR 31
TC 18
Z9 18
U1 1
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD APR
PY 2016
VL 165
BP 38
EP 44
DI 10.1016/j.clim.2016.02.010
PG 7
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA DK8KU
UT WOS:000375176400008
PM 26960951
DA 2025-06-01
ER

PT J
AU Bakulina, N
   Tikhonov, S
   Malkov, V
   Vorobyev, S
   Belyakov, I
   Peshkova, N
   Belko, E
   Syrjänen, K
AF Bakulina, Natalia
   Tikhonov, Sergey
   Malkov, Vladimir
   Vorobyev, Sergey
   Belyakov, Ilya
   Peshkova, Nataliya
   Belko, Elena
   Syrjanen, Kari
TI Non-invasive Screening of Autoimmune Atrophic Gastritis in Asymptomatic
   Subjects by Serological Biomarker Test (GastroPanel®)
SO ANTICANCER RESEARCH
LA English
DT Article
DE Atrophic gastritis; autoimmune; serological biomarker panel; GastroPanel
   (R); non-invasive test; updated Sydney System; Helicobacter pylori;
   pepsinogen; gastrin-17; Hp IgG antibody; parietal cell antibody;
   intrinsic factor antibody
ID HELICOBACTER-PYLORI INFECTION; IRON-DEFICIENCY ANEMIA;
   PERNICIOUS-ANEMIA; FOLLOW-UP; H+,K+-ADENOSINE TRIPHOSPHATASE;
   CARCINOID-TUMORS; THYROID-DISEASE; BODY GASTRITIS; DIAGNOSIS; CELL
AB Background/Aim: To estimate the prevalence of autoimmune atrophic gastritis (AAG) in the Russian Federation, a systematic screening of asymptomatic healthy adults by non-invasive biomarker testing was conducted. The aim was i) To test the validity of non-invasive serological screening for AAG; ii) to establish the prevalence of AAG among asymptomatic adults. Patients and Methods: Altogether, 1,283 asymptomatic, healthy . adults (mean age: 38 years) were screened by GastroPanel (R) test. Those with a biomarker profile indicating AG (n=46) were invited for fiirther examinations; 21 consented to gastroscopy with biopsies classified using the Updated Sydney System and Operative Link to Gastric Atrophy. Blood tests included parietal cell, intrinsic factor and thyroid peroxidase antibodies, and analysis of vitamin B12 and iron. Results: Gastroscopy and biopsies confirmed AG in 20 of the individuals. Parietal cell, intrinsic factor and thyroid peroxidase antibodies were present in five, one and eight individuals, respectively. AAG-associated co-morbidities (iron deficiency and pernicious anemia) were diagnosed in 10 out of 21. The final diagnosis of AAG was made in 15 out of 1,283 subjects (1.2%), of whom four were Helicobacter pylori-positive. When corrected fir verification bias (non-attendees in the confirmatory tests; n=25), the adjusted prevalence of AAG was 2.6% (33/1,283). Conclusion: AAG prevalence of 2.6% is among the highest reported using non-invasive tests. GastroPanel (R) is an optimal screening tool, providing the first link in the diagnostic protocol leading to the final diagnosis of this condition. The role of Helicobacter pylori as a trigger of AAG cannot be ruled out.
C1 [Bakulina, Natalia; Tikhonov, Sergey] State Med Univ II Mechnikov, Dept Internal Med Clin Pharmacol & Nephrol, St Petersburg, Russia.
   [Malkov, Vladimir] St Petersburg State Univ Hosp, St Petersburg, Russia.
   [Vorobyev, Sergey; Belyakov, Ilya] Natl Ctr Clin Morphol Diagnost, Dept Pathol, St Petersburg, Russia.
   [Peshkova, Nataliya; Belko, Elena] INVITRO SPb LLC, St Petersburg, Russia.
   [Syrjanen, Kari] Barretos Canc Hosp, Mol Oncol Res Ctr, Barretos, Brazil.
   [Syrjanen, Kari] SMW Consultants Ltd, Kaarina, Finland.
C3 Hospital de Cancer de Barretos
RP Syrjänen, K (corresponding author), SMW Consultants Ltd, Kylliaisentie 9, FI-21620 Kuusisto, Finland.
EM kasyrja@netti.fi
RI Bakulina, Natalia/GXA-0678-2022
OI Sergey, Tikhonov/0000-0001-5720-3528; Syrjanen,
   Kari/0000-0001-7180-7491; Vorob'ev, Sergei/0000-0002-7817-9069
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NR 67
TC 6
Z9 6
U1 1
U2 8
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
   ATHENS 19014, GREECE
SN 0250-7005
EI 1791-7530
J9 ANTICANCER RES
JI Anticancer Res.
PD MAR
PY 2022
VL 42
IS 3
BP 1517
EP 1526
DI 10.21873/anticames.15624
PG 10
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA ZQ8MR
UT WOS:000767352800016
PM 35220247
DA 2025-06-01
ER

PT J
AU Raderer, M
   Kiesewetter, B
   Ferreri, AJM
AF Raderer, Markus
   Kiesewetter, Barbara
   Ferreri, Andres J. M.
TI Clinicopathologic Characteristics and Treatment of Marginal Zone
   Lymphoma of Mucosa-Associated Lymphoid Tissue (MALT Lymphoma)
SO CA-A CANCER JOURNAL FOR CLINICIANS
LA English
DT Review
DE antigen-driven malignancy; Chlamydophila psittaci; extranodal;
   non-Hodgkin lymphoma; Helicobacter pylori
ID B-CELL LYMPHOMA; OCULAR ADNEXAL LYMPHOMA; HELICOBACTER-PYLORI INFECTION;
   NON-HODGKINS-LYMPHOMA; BENDAMUSTINE PLUS RITUXIMAB; PHASE-II;
   CHLAMYDOPHILA-PSITTACI; ANTIBIOTIC-TREATMENT; CHLAMYDIA-PSITTACI;
   CLINICAL ACTIVITY
AB Extranodal marginal zone lymphoma of the mucosa-associated lymphoid tissue (MALT lymphoma) accounts for 7% to 8% of newly diagnosed lymphomas. Because of its association with infectious causes, such as Helicobacter pylori (HP) or Chlamydophila psittaci (CP), and autoimmune diseases, it has become the paradigm of an antigen-driven malignancy. MALT lymphoma usually displays an indolent course, and watch-and-wait strategies are justified initially in a certain percentage of patients. In patients with gastric MALT lymphoma or ocular adnexal MALT lymphoma, antibiotic therapy against HP or CP, respectively, is the first-line management of choice, resulting in lymphoma response rates from 75% to 80% after HP eradication and from 33% to 65% after antibiotic therapy for CP. In patients who have localized disease that is refractory to antibiotics, radiation is widely applied in various centers with excellent local control, whereas systemic therapies are increasingly being applied, at least in Europe, because of the potentially systemic nature of the disease. Therefore, the objective of this review is to briefly summarize the clinicopathologic characteristics of this distinct type of lymphoma along with current data on management strategies. (C) 2015 American Cancer Society.
C1 [Raderer, Markus] Med Univ Vienna, Dept Internal Med 1, Div Oncol, Extranodal Lymphomas, Vienna, Austria.
   [Kiesewetter, Barbara] Med Univ Vienna, Dept Internal Med 1, Div Oncol, Vienna, Austria.
   [Ferreri, Andres J. M.] Ist Sci San Raffaele, Unit Lymphoid Malignancies, Div Oncohematol Med, Dept Oncohematol,Natl Inst Res & Treatment, I-20132 Milan, Italy.
C3 Medical University of Vienna; Medical University of Vienna; Vita-Salute
   San Raffaele University; IRCCS Ospedale San Raffaele
RP Raderer, M (corresponding author), Med Univ Vienna, Internal Med 1, Div Oncol, Waehringer Guertel 18-20, Vienna, Austria.
EM markus.raderer@meduniwien.ac.at
RI Ferreri, Andrés/A-6662-2013; Kiesewetter, Barbara/AGX-3260-2022
OI Kiesewetter, Barbara/0000-0002-5490-2371
FU Celgene; Roche; Novartis; Ipsen; Gilead; Mundipharma; SOBI Pharma;
   EISAI; Hospira
FX Markus Raderer reports personal fees from Celgene, Roche, Novartis,
   Ipsen, Gilead, Mundipharma, SOBI Pharma, and EISAI for work performed
   outside of the current study. Barbara Kiesewetter reports travel grants
   fromCelgene, Hospira, Ipsen, Novartis, and Roche for work performed
   outside of the current study. Andres J. M. Ferreri reports grants and
   personal fees from Celgene and Mundipharma and personal fees from Gilead
   for work performed outside of the current study.
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NR 147
TC 191
Z9 211
U1 0
U2 27
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-9235
EI 1542-4863
J9 CA-CANCER J CLIN
JI CA-Cancer J. Clin.
PD MAR-APR
PY 2016
VL 66
IS 2
BP 153
EP 171
DI 10.3322/caac.21330
PG 19
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA DG2HD
UT WOS:000371886900006
PM 26773441
OA gold
DA 2025-06-01
ER

PT J
AU Cheah, CY
   Opat, S
   Trotman, J
   Marlton, P
AF Cheah, Chan Y.
   Opat, Stephen
   Trotman, Judith
   Marlton, Paula
TI Front-line management of indolent non-Hodgkin lymphoma in Australia.
   Part 2: mantle cell lymphoma and marginal zone lymphoma
SO INTERNAL MEDICINE JOURNAL
LA English
DT Review
DE mantle cell lymphoma; marginal zone B-cell lymphoma; disease management;
   rituximab; bendamustine
ID BENDAMUSTINE PLUS RITUXIMAB; CLINICAL-PRACTICE GUIDELINES;
   PROGRESSION-FREE SURVIVAL; HIGH-DOSE CYTARABINE; 15-YEAR FOLLOW-UP;
   PHASE-II; TISSUE LYMPHOMA; MALT LYMPHOMA; OPEN-LABEL; ANTIVIRAL
   TREATMENT
AB Mantle cell lymphoma (MCL) and the marginal zone lymphoma (MZL) subtypes (nodal MZL, extra-nodal MZL of mucosa-associated lymphoid tissue (MALT lymphoma) and splenic MZL) are uncommon lymphoma subtypes, accounting for less than 5-10% of all non-Hodgkin lymphoma. The evidence base for therapy is therefore limited and enrolment into clinical trials is preferred. Outcomes for patients with MCL have been steadily improving mainly due to the adoption of more intense strategies in younger patients, the use of rituximab maintenance and the recent introduction of bendamustine in older patients. MZL is a more heterogeneous group of cancer with both nodal, extra-nodal and splenic subtypes. Extranodal MZL may be associated with autoimmune or infectious aetiologies, and can respond to eradication of the causative pathogen. Proton pump inhibitor plus dual antibiotics in Helicobacter pylori positive gastric MALT lymphoma is curative in many patients. Watchful waiting is appropriate in most patients with asymptomatic advanced stage disease, which tends to behave in a particularly indolent manner. Other options for symptomatic disease include splenectomy, chemoimmunotherapy with rituximab and, more recently, targeted therapies.
C1 [Cheah, Chan Y.] Sir Charles Gairdner Hosp, Dept Haematol, Nedlands, WA 6009, Australia.
   [Cheah, Chan Y.] Pathwest Lab Med, Dept Haematol, Nedlands, WA, Australia.
   [Cheah, Chan Y.] Univ Western Australia, Med Sch Pathol & Lab Med, Perth, WA, Australia.
   [Opat, Stephen] Monash Hlth, Clin Haematol & Sch Clin Sci, Melbourne, Vic, Australia.
   [Opat, Stephen] Monash Univ, Dept Med, Melbourne, Vic, Australia.
   [Trotman, Judith] Univ Sydney, Concord Hosp, Dept Haematol, Sydney, NSW, Australia.
   [Trotman, Judith] Univ Sydney, Dept Med, Sydney, NSW, Australia.
   [Marlton, Paula] Princess Alexandra Hosp, Div Canc Serv, Clin Haematol, 199 Ipswich Rd, Woolloongabba, Qld 4102, Australia.
   [Marlton, Paula] Univ Queensland, Sch Med, Brisbane, Qld, Australia.
C3 University of Western Australia; Sir Charles Gairdner Hospital;
   University of Western Australia; Pathwest Laboratory Medicine;
   University of Western Australia; Monash Health; Monash University;
   University of Sydney; Concord Repatriation General Hospital; University
   of Sydney; Princess Alexandra Hospital; University of Queensland
RP Marlton, P (corresponding author), Princess Alexandra Hosp, Div Canc Serv, Clin Haematol, 199 Ipswich Rd, Woolloongabba, Qld 4102, Australia.
EM paula.marlton@health.qld.gov.au
RI Opat, Stephen/AFR-0783-2022
OI Opat, Stephen/0000-0002-0308-6458; Cheah, Chan Yoon/0000-0001-7988-1565
FU Janssen-Cilag Australia; Janssen; Roche; Celgene; Pharmacyclics;
   Beigene; Gilead; Takeda Pharmaceuticals; Novartis; Abbvie
FX Janssen-Cilag Australia. J. Trotman reports research funding from
   Janssen, Roche, Celgene, Pharmacyclics and Beigene. C. Y. Cheah reports
   grants and advisory fees from Gilead, grants and speaker honoraria from
   Roche, advisory fees from Janssen and grants from Celgene. P. Marlton
   reports advisory fees, and/or speaker honoraria from Novartis, Roche,
   Janssen, Celgene, Abbvie, Gilead and Pfizer. S. Opat reports research
   funding, advisory fees, speaker fees, honoraria and provision of
   subsidised drugs from Roche, Janssen and Celgene, research funding,
   advisory fees, speaker fees and honoraria from Takeda Pharmaceuticals
   and Novartis, research funding, advisory fees and honoraria from Abbvie
   and Gilead, advisory fees and travel support from Bristol-Myers Squibb,
   research funding from BeiGene and advisory fees from Sanofi and
   Mundipharma.
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NR 80
TC 9
Z9 9
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1444-0903
EI 1445-5994
J9 INTERN MED J
JI Intern. Med. J.
PD SEP
PY 2019
VL 49
IS 9
BP 1070
EP 1080
DI 10.1111/imj.14268
PG 11
WC Medicine, General & Internal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC General & Internal Medicine
GA IY0IK
UT WOS:000486075700002
PM 30816618
DA 2025-06-01
ER

PT J
AU Seeberger, H
   Starostik, P
   Schwarz, S
   Knörr, C
   Kalla, J
   Ott, G
   Müller-Hermelink, HK
   Greiner, A
AF Seeberger, H
   Starostik, P
   Schwarz, S
   Knörr, C
   Kalla, J
   Ott, G
   Müller-Hermelink, HK
   Greiner, A
TI Loss of Fas (CD95/APO-1) regulatory function is an important step in
   early MALT-type lymphoma development
SO LABORATORY INVESTIGATION
LA English
DT Article
ID AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; NON-HODGKINS-LYMPHOMA; B-CELL
   LYMPHOMAS; LOW-GRADE; APO-1/CD95 GENE; SOLUBLE FAS; IN-VIVO; MEDIATED
   APOPTOSIS; SOMATIC MUTATIONS; ANTIGEN RECEPTOR
AB Fas(CD95, APO-1) mutations were found in autoimmune diseases and some lymphomas, suggesting impairment of Fas-mediated cell death signaling that may cause tumor development. Because mucosa-associated lymphoid tissue (MALT)-type lymphoma B cells recognize autoantigens and proliferate in response to antigen and T cell-mediated signals, it is suggestive that autoreactive B cell lymphoma precursor cells may have escaped the Fas-mediated checkpoint that normally operates in healthy individuals. Using different biochemical, molecular, and functional approaches, we analyzed the Fas signaling in malignant B cells from seven MALT-type lymphomas that were additionally characterized for the t(11;18)(q21;q21) and four gastric diffuse large B cell lymphomas (DLBL). All DLBLs and three of seven MALT-type lymphomas were resistant to Fas-mediated apoptosis in vitro. Moreover, four of five MALT-type lymphomas analyzed and one of three DLBLs analyzed showed mutations in Fas mRNA transcripts but no loss of heterozygosity in the Fas promotor region. Alternative mechanisms of resistance to apoptosis, such as decreased expression of fas or production of soluble Fas were not operative. Therefore. it is suggestive that a subgroup of MALT-type lymphoma B cells, irrespective of t(11;18)(q21:q21), escape the censoring Fas pathway by mutating and inactivating Fas. This identifies a key regulatory step in early MALT-type lymphomagenesis.
C1 Univ Wurzburg, Inst Pathol, D-97080 Wurzburg, Germany.
C3 University of Wurzburg
RP Univ Wurzburg, Inst Pathol, Josef Schneider Str 2, D-97080 Wurzburg, Germany.
EM path040@mail.uni-wuerzburg.de
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NR 56
TC 33
Z9 37
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
EI 1530-0307
J9 LAB INVEST
JI Lab. Invest.
PD JUL
PY 2001
VL 81
IS 7
BP 977
EP 986
DI 10.1038/labinvest.3780310
PG 10
WC Medicine, Research & Experimental; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine; Pathology
GA 453JR
UT WOS:000169913200009
PM 11454987
DA 2025-06-01
ER

PT J
AU McCarty, MF
AF McCarty, Mark F.
TI Potential ghrelin-mediated benefits and risks of hydrogen water
SO MEDICAL HYPOTHESES
LA English
DT Article
ID 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE MOUSE MODEL; EXPERIMENTAL
   AUTOIMMUNE ENCEPHALOMYELITIS; DETECTED CORONARY ATHEROSCLEROSIS; CHRONIC
   HEART-FAILURE; BLOOD-BRAIN-BARRIER; PARKINSONS-DISEASE; RICH WATER;
   OXIDATIVE STRESS; ALZHEIMERS-DISEASE; METABOLIC SYNDROME
AB Molecular hydrogen (H-2) can scavenge hydroxyl radical and diminish the toxicity of peroxynitrite; hence, it has interesting potential for antioxidant protection. Recently, a number of studies have explored the utility of inhaled hydrogen gas, or of hydrogen-saturated water, administered parenterally or orally, in rodent models of pathology and in clinical trials, oftentimes with very positive outcomes. The efficacy of orally ingested hydrogen-rich water (HW) has been particularly surprising, given that only transient and rather small increments in plasma hydrogen can be achieved by this method. A recent study in mice has discovered that orally administered MW provokes increased gastric production of the orexic hormone ghrelin, and that this ghrelin mediates the favorable impact of HW on a mouse model of Parkinson's disease. The possibility that most of the benefits observed with HW in experimental studies are mediated by ghrelin merits consideration. Ghrelin is well known to function as an appetite stimulant and secretagogue for growth hormone, but it influences physiological function throughout the body via interaction with the widely express GHS-R1a receptor. Rodent and, to a more limited extent, clinical studies establish that ghrelin has versatile neuroprotective and cognitive enhancing activity, favorably impacts vascular health, exerts anti-inflammatory activity useful in autoimmune disorders, and is markedly hepatoprotective. The stimulatory impact of ghrelin on GH-IGF-I activity, while potentially beneficial in sarcopenia or cachectic disorders, does raise concerns regarding the long-term impact of ghrelin up-regulation on cancer risk. The impact of ingesting MW water on ghrelin production in humans needs to be evaluated; if MW does up-regulate ghrelin in humans, it may have versatile potential for prevention and control of a number of health disorders. (c) 2015 Elsevier Ltd. All rights reserved.
C1 Catalyt Longev, Carlsbad, CA 92009 USA.
RP McCarty, MF (corresponding author), Catalyt Longev, 7831 Rush Rose Dr,Apt 316, Carlsbad, CA 92009 USA.
EM markfmccarty@gmail.com
FU Catalytic Longevity
FX Financial support provided by Catalytic Longevity, a non-profit
   organization.
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NR 122
TC 14
Z9 16
U1 0
U2 23
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PD APR
PY 2015
VL 84
IS 4
BP 350
EP 355
DI 10.1016/j.mehy.2015.01.018
PG 6
WC Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Research & Experimental Medicine
GA CE2PE
UT WOS:000351656700013
PM 25649854
DA 2025-06-01
ER

PT J
AU Bonella, F
   Long, XP
   Ohshimo, S
   Horimasu, Y
   Griese, M
   Guzman, J
   Kohno, N
   Costabel, U
AF Bonella, Francesco
   Long, Xiaoping
   Ohshimo, Shinichiro
   Horimasu, Yasushi
   Griese, Matthias
   Guzman, Josune
   Kohno, Nobuoki
   Costabel, Ulrich
TI MUC1 gene polymorphisms are associated with serum KL-6 levels and
   pulmonary dysfunction in pulmonary alveolar proteinosis
SO ORPHANET JOURNAL OF RARE DISEASES
LA English
DT Article
DE Pulmonary alveolar proteinosis; KL-6; MUC1 polymorphisms; Disease
   outcome
ID BRONCHOALVEOLAR LAVAGE; AUTOIMMUNE-DISEASE; GASTRIC-CANCER; PNEUMONITIS;
   DIAGNOSIS; ANTIGEN; MARKER; INDICATOR; PATIENT; COHORT
AB Background: KL-6, a human MUC1 mucin, is a sensitive biomarker for interstitial lung diseases including pulmonary alveolar proteinosis (PAP). A correlation between MUC1 gene single nucleotide polymorphism (SNP) rs4072037 genotype and serum KL-6 levels has been reported. This study was aimed at investigating the correlation between MUC1 SNP genotype, severity of disease and disease outcome in PAP.
   Methods: Twenty four patients with PAP and 30 healthy volunteers were studied. MUC1 rs4072037 was detected by using a real-time polymerase chain reaction (RT-PCR). Genotyping was performed by pyrosequencing. KL-6 levels were measured in serum by Nanopia KL-6 assay (SEKISUI Diagnostics).
   Results: The frequency of MUC1 rs4072037 alleles was significantly different between PAP patients and healthy volunteers (PAP, A/A 46 %, A/G 54 %, G/G 0 %; healthy controls, A/A 30 %, A/G 40 %, G/G 30 %; p = 0.013). Serum KL-6 levels were significantly higher in PAP patients than in controls (p < 0.0001), and significantly higher in PAP patients with A/A genotype than in those with A/G genotype (p = 0.007). Patients with A/A genotype had higher alveolar-arterial oxygen difference (A-aDO(2)) and lower DLco compared to those with A/G genotype (p = 0.027 and p = 0.012, respectively). Multivariate analysis, Kaplan-Meier analysis and C statistics showed that the rs4072037 A/A genotype was associated with higher rate of disease progression (HR: 5.557, p = 0.014).
   Conclusions: MUC1 rs4072037 A/A genotype is associated with more severe pulmonary dysfunction and a higher rate of disease progression in PAP patients.
C1 [Bonella, Francesco; Long, Xiaoping; Costabel, Ulrich] Univ Duisburg Essen, Interstitial & Rare Lung Dis Unit, Ruhrlandklin, D-45239 Essen, Germany.
   [Long, Xiaoping] Univ South China, Dept Resp Med, Affiliated Hosp 1, Hengyang, Hunan, Peoples R China.
   [Ohshimo, Shinichiro; Horimasu, Yasushi; Kohno, Nobuoki] Hiroshima Univ, Grad Sch Biomed Sci, Dept Emergency & Crit Care Med, Hiroshima, Japan.
   [Ohshimo, Shinichiro] Hiroshima Univ, Grad Sch Biomed Sci, Dept Mol & Internal Med, Hiroshima, Japan.
   [Griese, Matthias] Univ Munich, Dr Von Haunerschen Kinderspital, Lindwurmstr 4, D-80337 Munich, Germany.
   [Guzman, Josune] Ruhr Univ Bochum, Gen & Expt Pathol, Univ Str 150, Bochum, Germany.
C3 University of Duisburg Essen; University of South China; Hiroshima
   University; Hiroshima University; University of Munich; Ruhr University
   Bochum
RP Bonella, F (corresponding author), Univ Duisburg Essen, Interstitial & Rare Lung Dis Unit, Ruhrlandklin, D-45239 Essen, Germany.
EM francesco.bonella@ruhrlandklinik.uk-essen.de
RI Ohshimo, Shinichiro/B-4572-2018; Costabel, Ulrich/KGL-7781-2024;
   Horimasu, Yasushi/AAC-8800-2022; Bonella, Francesco/P-2390-2019
OI Bonella, Francesco/0000-0001-7579-9767
FU German Federal Ministry of Education and Research (EuPAPNet project
   inside ERARE) [01GM1011A]; Arbeitsgemeinschaft zur Forderung der
   Pneumologie an der Ruhrlandklinik (AFPR); Grants-in-Aid for Scientific
   Research [16K09541] Funding Source: KAKEN
FX This study was supported by the German Federal Ministry of Education and
   Research (EuPAPNet project inside ERARE, number 01GM1011A) and
   Arbeitsgemeinschaft zur Forderung der Pneumologie an der Ruhrlandklinik
   (AFPR).
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NR 39
TC 22
Z9 25
U1 0
U2 8
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1750-1172
J9 ORPHANET J RARE DIS
JI Orphanet J. Rare Dis.
PD APR 23
PY 2016
VL 11
AR 48
DI 10.1186/s13023-016-0430-2
PG 7
WC Genetics & Heredity; Medicine, Research & Experimental
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Genetics & Heredity; Research & Experimental Medicine
GA DK1DQ
UT WOS:000374653100001
PM 27108412
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Fagiolo, E
   Abenante, L
AF Fagiolo, E
   Abenante, L
TI Lymphocyte activation and cytokine production in autoimmune hemolytic
   anaemia (AIHA)
SO AUTOIMMUNITY
LA English
DT Article
DE lymphocyte activation; cytokines; autoimmune hemolytic anaemia
ID SYSTEMIC LUPUS-ERYTHEMATOSUS; TUMOR-NECROSIS-FACTOR; T-CELLS; B-CELLS;
   INTERLEUKIN-2; INVITRO; MICE; ABNORMALITIES; RECEPTOR; DISEASE
AB We studied 16 patients affected by autoimmune hemolytic anaemia (AIHA), both idiopathic and associated with other diseases (B and T lymphoma, B hepatitis, gastric carcinoma, systemic lupus erythematosus) or a-methyldopa therapy, in order to value T- and B-cell activation. We determined the count of T- and B-cell subsets in peripheral blood, the proliferative response of peripheral blood lymphocytes (PBL) to phytohemagglutinin (PHA) and to pokeweed mitogen (PWM), the percentage of CD25(+) cells in culture and interleukin (IL)-1 alpha, IL-2, IL-4, tumor necrosis factor (TNF)a and soluble IL-2 receptor (sIL-2R) levels in sera and in culture. Except for an increase in CD4(+) and CD8(+) T cell number in a case of AIHA associated with a T lymphoma and an increase in the percentage of CD5(+) and PCA1(+) B cells in two cases of AIHA associated with B lymphoma and with SLE, no further data showed a relationship with the disease possibly associated with AIHA, so both idiopathic and secondary AIHA cases mere analyzed together. CD4(+) T cells were reduced in number in 9 cases, while CD8(+) T cells were reduced in 6 cases. The percentage of CD5(+) B cells was increased in 5 cases. The percentage of PCA1(+) cells was increased in all cases (mean+/-sd: 18+/-22 vs 0,2+/-1 in controls). The average PBL proliferative response to PHA was reduced (S.I. 71 +/- 55 vs 138 +/- 45 in controls) as well as that to PWM (S.I. 27+/-21 vs 75+/-24 in controls), despite IL-2 high levels, in all cases, in both sera (mean+/-sd: 648+/-351 pg/ml vs 16+/-4 pg/ml in controls) and culture supernatants (mean+/-sd: 1045+/-677 pg/ml vs 195+/-51 pg/ml in controls). In PHA stimulated cultures the percentage of CD25(+) cells was reduced (mean+/-sd: 37+/-18 vs 63+/-14 in controls), sIL-2R levels were like controls in 7 cases. In sera sIL-2R levels mere increased in all cases (mean+/-sd: 1256+/-465 U/ml vs 256+/-114 U/ml in controls), IL-1 alpha was increased in all cases too, while IL-4 levels were increased only in 7 cases. Linear regression analysis generally showed a low relationship between S.I. and IL-2, IL-4 and sIL-2R levels in supernatants of PHA stimulated culture as well as between S.I. and the percentage of CD25(+) cells. Taken together these data suggest a state of B- and T-cell hyperactivation in AIHA. The lon PBL proliferative response in vitro, explained in previous studies as a temporary functional exhaustion, might be itself a sign of the complete lymphocyte activation occurring in vivo in AIHA.
RP Fagiolo, E (corresponding author), UNIV CATTOLICA SACRO CUORE,CATHOLIC SCH MED,LAB IMMUNOHEMATOL,ROME,ITALY.
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NR 27
TC 16
Z9 17
U1 0
U2 2
PU HARWOOD ACAD PUBL GMBH
PI READING
PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL
SN 0891-6934
J9 AUTOIMMUNITY
JI Autoimmunity
PY 1996
VL 24
IS 3
BP 147
EP 156
DI 10.3109/08916939608995360
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA VX789
UT WOS:A1996VX78900002
PM 9020407
DA 2025-06-01
ER

PT J
AU Douillard, C
   Jannin, A
   Vantyghem, MC
AF Douillard, Claire
   Jannin, Arnaud
   Vantyghem, Marie-Christine
TI Rare causes of hypoglycemia in adults
SO ANNALES D ENDOCRINOLOGIE
LA English
DT Review
DE Hypoglycemia; Inborn errors of metabolism; Glucokinase mutation;
   Anti-insulin receptor and insulin antibodies; Insulin receptor mutation;
   IGF2; NICTH; Type B insulin resistance; HIRATA syndrome; Glycogen
   synthesis disorder; Beta-oxidation disorders; Neoglucogenesis disorders;
   Hereditary fructose intolerance
ID CLINICAL-PRACTICE; HYPERINSULINEMIC HYPOGLYCEMIA; INSULIN; DIAGNOSIS;
   AUTOANTIBODIES; MANAGEMENT; CONSENSUS; MUTATION
AB Hypoglycemia is defined by a low blood glucose level associated to clinical symptoms. Hypoglycemia may be related to treatment of diabetes, but also to drugs, alcohol, critical illness, cortisol insufficiency including hypopituitarism, insulinoma, bariatric or gastric surgery, pancreas transplantation or glucagon deficiency, or may be surreptitious. Some hypoglycemic episodes remain unexplained, and genetic, paraneoplastic and immune causes should be considered. Genetic causes may be related to endogenous hyperinsulinism and to inborn errors of metabolism (IEM). Endogenous hyperinsulinism is related to monogenic congenital hyperinsulinism, and especially to mutations of the glucokinase-activating gene or of insulin receptors, both characterised by postprandial hypoglycemia with major hyperinsulinism. In adulthood, IEM-related hypoglycemia can persist in a previously diagnosed childhood disease or may be a presenting sign. It is suggested by systemic involvement (rhabdomyolysis after fasting or exercising, heart disease, hepatomegaly), sometimes associated to a family history of hypoglycemia. The timing of hypoglycemic episodes with respect to the last meal also helps to orientate diagnosis. Fasting hypoglycemia may be related to type 0, I or III glycogen synthesis disorder, fatty acid oxidation or gluconeogenesis disorder. Postprandial hypoglycemia may be related to inherited fructose intolerance. Exercise-induced hyperinsulinism is mainly related to activating mutation of the SLC16A1 gene. Besides exceptional ectopic insulin secretion, paraneoplastic causes involve NICTH (Non-Islet-Cell Tumour Hypoglycemia), caused by Big-IGF2 secretion by a large tumour, with low blood levels of insulin, C-peptide and IGF1. Autoimmune causes involve antibodies against insulin (HIRATA syndrome), especially in case of Graves' disease, or against the insulin receptor. Medical history, timing, and insulin level orientate the diagnosis. (C) 2020 Published by Elsevier Masson SAS.
C1 [Douillard, Claire; Jannin, Arnaud; Vantyghem, Marie-Christine] Lille Univ Hosp, Endocrinol Diabetol Metab Dept, Lille, France.
   [Douillard, Claire] Lille Reference Ctr Inborn Errors Metab, Lille, France.
   [Vantyghem, Marie-Christine] Inserm U1190 Translat Res Diabet, Lille, France.
   [Vantyghem, Marie-Christine] European Genom Inst Diabet EGID, Lille, France.
C3 Universite de Lille; CHU Lille; Universite de Lille; Institut National
   de la Sante et de la Recherche Medicale (Inserm); Universite de Lille
RP Vantyghem, MC (corresponding author), Lille Univ Hosp, Endocrinol Diabetol & Metab Dept, C Huriez Hosp, 1 Rue Polonovski, F-59037 Lille, France.
EM claire.douillard@chru-lille.fr; arnaud.jannin.aj@gmail.com;
   mc-vantyghem@chru-lille.fr
RI VANTYGHEM, Marie/T-8613-2019; JANNIN, Arnaud/KGM-5738-2024; VANTYGHEM,
   Marie-Christine/P-2939-2017
OI VANTYGHEM, Marie-Christine/0000-0002-9369-0463
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NR 40
TC 26
Z9 30
U1 0
U2 9
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
SN 0003-4266
EI 2213-3941
J9 ANN ENDOCRINOL-PARIS
JI Ann Endocrinol.
PD JUN
PY 2020
VL 81
IS 2-3
BP 110
EP 117
DI 10.1016/j.ando.2020.04.003
PG 8
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA LU2EH
UT WOS:000537572500008
PM 32409005
OA Green Published, Bronze
DA 2025-06-01
ER

PT J
AU Miceli, E
   Padula, D
   Lenti, MV
   Gallia, A
   Albertini, R
   Di Stefano, M
   Klersy, C
   Corazza, GR
AF Miceli, Emanuela
   Padula, Donatella
   Lenti, Marco V.
   Gallia, Alessandra
   Albertini, Riccardo
   Di Stefano, Michele
   Klersy, Catherine
   Corazza, Gino R.
TI A Laboratory Score in the Diagnosis of Autoimmune Atrophic Gastritis
   A Prospective Study
SO JOURNAL OF CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE gastric atrophy; score; gastrin; validation; stomach
ID PARIETAL-CELL ANTIBODIES; PERNICIOUS-ANEMIA; COBALAMIN DEFICIENCY;
   CARCINOID-TUMORS; INTRINSIC-FACTOR; PEPSINOGEN-I; SERUM-LEVELS;
   AUTOANTIBODIES; PREVALENCE; GASTRIN-17
AB Background: Several biomarkers have been proposed for the diagnosis of autoimmune atrophic gastritis (AAG), but at the present there is no appropriate testing strategy for the disease.
   Goals: The aim of this study was to develop and validate a laboratory score able to address the diagnosis of AAG in a general practice setting.
   Study: We prospectively evaluated a number of serum biomarkers (vitamin B-12, mean corpuscular volume, hemoglobin, gastrin, and chromogranin A levels) in a case-control population and built 2 biochemical scores, the first with all the parameters [Global Score (GS)], and the second as the best statistical combination of them [Simple Score (SS)]. In the second phase we validated the score that proved to be more efficient on a random population referred to our center (Gastroenterology Outpatient Clinic).
   Results: Both models turned out to be reliable in detecting patients with suspected AAG, showing excellent accuracy [area under the receiver operating curve (AUC-ROC) 0.94; 95% confidence interval (CI), 0.91-0.97 for GS and AUC-ROC 0.93; 95% CI, 0.89-0.86 for SS]. The SS proved to be more convenient because of its accessibility and availability in a general setting and its low cost. The validation of the SS showed a sensitivity of 85.7% (95% CI, 57.2-98.2) and a specificity of 83.7% (95% CI, 74.2-90.89).
   Conclusions: Herein, we describe 2 nonexpensive and reliable score models, particularly the SS, that can be applied in daily medical practice for identifying patients potentially affected by AAG.
C1 [Miceli, Emanuela; Padula, Donatella; Lenti, Marco V.; Gallia, Alessandra; Di Stefano, Michele; Corazza, Gino R.] Univ Pavia, Dept Internal Med 1, Fondazione IRCCS Policlinico San Matteo, I-27100 Pavia, Italy.
   [Albertini, Riccardo] Univ Pavia, Fondazione IRCCS Policlinico San Matteo, Clin Chem Lab, I-27100 Pavia, Italy.
   [Klersy, Catherine] Univ Pavia, Fondazione IRCCS Policlinico San Matteo, Serv Biometry & Stat, I-27100 Pavia, Italy.
C3 University of Pavia; IRCCS Fondazione San Matteo; University of Pavia;
   IRCCS Fondazione San Matteo; University of Pavia; IRCCS Fondazione San
   Matteo
RP Corazza, GR (corresponding author), Univ Pavia, Dept Internal Med 1, Fondazione IRCCS Policlinico San Matteo, Piazzale Golgi 19, I-27100 Pavia, Italy.
EM gr.corazza@smatteo.pv.it
RI di stefano, michele/AAC-2205-2019; albertini, riccardo/AAB-7779-2019;
   CORAZZA, GINO ROBERTO/K-8500-2016; Lenti, Marco Vincenzo/F-9044-2018;
   Klersy, Catherine/AAA-3003-2019
OI di stefano, michele/0000-0002-6971-6854; CORAZZA, GINO
   ROBERTO/0000-0001-9532-0573; Lenti, Marco Vincenzo/0000-0002-6654-4911;
   Klersy, Catherine/0000-0003-0314-8548
CR Andres E, 2012, J BLOOD MED, V3, P97, DOI 10.2147/JBM.S25620
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NR 34
TC 31
Z9 31
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0192-0790
EI 1539-2031
J9 J CLIN GASTROENTEROL
JI J. Clin. Gastroenterol.
PD JAN
PY 2015
VL 49
IS 1
BP E1
EP E5
PG 5
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA AW2XK
UT WOS:000346149800002
PM 24583750
DA 2025-06-01
ER

PT J
AU Silva, IN
   Marcal, LV
   Queiroz, DMM
AF Silva, Ivani Novato
   Marcal, Lara Vieira
   Queiroz, Dulciene Maria Magalhaes
TI Helicobacter pylori Infection Is Associated With Thyroid
   Dysfunction in Children With Congenital Hypothyroidism
SO FRONTIERS IN PEDIATRICS
LA English
DT Article
DE Helicobacter pylori; congenital hypothyroidism; thyroiditis autoimmune;
   primary hypothyroidism; childhood; triiodothyronine
ID TUMOR-NECROSIS-FACTOR; BREATH TEST
AB Helicobacter pylori (H. pylori) infection leads to a systemic low-grade inflammatory state and has been associated causally with a diverse spectrum of extra-gastric disorders. Among them, the infection has been involved in the pathogenesis of autoimmune thyroid disease (ATD), but only one study had evaluated children. Therefore, a cross-sectional study was conducted in a cohort of 142 children and adolescents, randomly assessed among those followed up for thyroid diseases in a university pediatric endocrinology service: 106 with congenital hypothyroidism (CH) and 36 with ATD. All children were asymptomatic, under strict control on levothyroxine replacement, and reported no other diseases or use of drugs. Helicobacter pylori status was evaluated by the C-13-Urea Breath Test (C-13-UBT). Antithyroid antibodies (ATPO, antiTg, and TRAb) and serum thyroid hormones (TSH, free T4, and T3) were assessed by standard assays. Data were analyzed in logistic models by the SPSS statistical software package, and a p-value <= 0.05 was considered statistically significant. The prevalence of H. pylori infection was 19.44% in children with ATD. Neither the gender nor the serum levels of thyroid hormones and antithyroid antibodies were associated with the H. pylori-positive status. Thirty-seven (34.90%) children with CH were infected with H. pylori. The mean T3 serum level (3.59 +/- 0.84) was significantly lower (p = 0.001) in the infected children than in those free from the infection (3.95 +/- 0.89), association that remained after adjustment for the other variables in the multivariate analysis. Because no difference was observed in the levels of TSH and T4, the results indicate that the infection may lead to impairment in the thyroid hormonal balance, but not in the hypothalamic-pituitary-thyroid axis function. In as much as H. pylori infection is highly widespread and the prevalence of CH is also not negligible, additional studies are required to confirm our results and to identify the involved mechanisms.
C1 [Silva, Ivani Novato; Marcal, Lara Vieira] Univ Fed Minas Gerais, Fac Med, Pediat Dept, Belo Horizonte, Brazil.
   [Queiroz, Dulciene Maria Magalhaes] Univ Fed Minas Gerais, Fac Med, Lab Res Bacteriol, Belo Horizonte, Brazil.
C3 Universidade Federal de Minas Gerais; Universidade Federal de Minas
   Gerais
RP Queiroz, DMM (corresponding author), Univ Fed Minas Gerais, Fac Med, Lab Res Bacteriol, Belo Horizonte, Brazil.
EM dqueiroz@medicina.ufmg.br
RI Queiroz, Dulciene/AAU-9386-2020
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NR 24
TC 1
Z9 3
U1 0
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 2296-2360
J9 FRONT PEDIATR
JI Front. Pediatr.
PD JUN 21
PY 2022
VL 10
AR 875232
DI 10.3389/fped.2022.875232
PG 5
WC Pediatrics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pediatrics
GA 2S4ZD
UT WOS:000821801100001
PM 35799701
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Fabiani, E
   Fianchi, L
   Falconi, G
   Boncompagni, R
   Criscuolo, M
   Guidi, F
   La Brocca, A
   Hohaus, S
   Leone, G
   Voso, MT
AF Fabiani, Emiliano
   Fianchi, Luana
   Falconi, Giulia
   Boncompagni, Riccardo
   Criscuolo, Marianna
   Guidi, Francesco
   La Brocca, Antonella
   Hohaus, Stefan
   Leone, Giuseppe
   Voso, Maria Teresa
TI The BCL2L10 Leu21Arg variant and risk of therapy-related myeloid
   neoplasms and de novo myelodysplastic syndromes
SO LEUKEMIA & LYMPHOMA
LA English
DT Article
DE BCL2L10; therapy-related myeloid neoplasms; myelodysplastic syndrome;
   polymorphisms; apoptosis
ID CHEMOTHERAPY-INDUCED LEUKEMIA; DNA-REPAIR ENZYMES; BCL-B;
   GASTRIC-CANCER; POLYMORPHISMS; PROTEIN; GENOME; DETOXIFICATION;
   AZACITIDINE; METHYLATION
AB Therapy-related myeloid neoplasms (t-MNs) are an increasingly recognized complication in patients previously treated with radiotherapy and/or chemotherapy for cancer or autoimmune disease. Single nucleotide variants (SNVs) in genes involved in the cellular pathways of detoxification, DNA repair and apoptosis may modify the individual risk of developing a t-MN. We studied the frequency of the SNVs of six genes involved in xenobiotic detoxification (CYP3A4, NQO1, GSTA1, GSTM1, GSTP1 and GSTT1), two DNA repair genes (RAD51 and XRCC3) and one key regulator of apoptosis (BCL2L10) in a case-control study including 111 cases of t-MN and 259 controls. This is the first report on the prevalence of BCL2L10 Leu21Arg polymorphism in myeloid malignancies. In this line, we also tested 146 cases of de novo myelodysplastic syndrome (MDS) and 109 cases of de novo acute myeloid leukemia (AML). Our results showed a significantly lower frequency of the BCL2L10-21Arg allele in patients with t-MN and de novo MDS compared to controls (Leu/Arg + Arg/Arg: 50.6% vs. 65.9%, p = 0.017 and 45.8% vs. 65.9%, p = 0.0003, respectively). Carriers of the BCL2L10-21Arg variant have a reduced risk of developing t-MN and de novo MDS.
C1 [Fabiani, Emiliano; Fianchi, Luana; Falconi, Giulia; Boncompagni, Riccardo; Criscuolo, Marianna; Guidi, Francesco; La Brocca, Antonella; Hohaus, Stefan; Leone, Giuseppe; Voso, Maria Teresa] Univ Cattolica S Cuore, Inst Hematol, I-00168 Rome, Italy.
C3 Catholic University of the Sacred Heart; IRCCS Policlinico Gemelli
RP Voso, MT (corresponding author), Univ Cattolica S Cuore, Inst Hematol, Largo A Gemelli 8, I-00168 Rome, Italy.
EM mtvoso@rm.unicatt.it
RI Hohaus, Stefan/K-9718-2016; Fabiani, Emiliano/AAP-7934-2020; FALCONI,
   giulia/AAB-7670-2019; Leone, Giuseppe/I-9166-2019; CRISCUOLO,
   Marianna/LNR-0511-2024; Boncompagni, Riccardo/GVU-1295-2022; Guidi,
   Francesco/AAS-9209-2021; VOSO, Maria Teresa/F-1172-2014
OI Leone, Giuseppe/0000-0002-7812-5300; VOSO, Maria
   Teresa/0000-0002-6164-4761; Fianchi, Luana/0000-0002-7113-7202; FABIANI,
   Emiliano/0000-0002-6209-8934; HOHAUS, Stefan/0000-0002-5534-7197;
   FALCONI, Giulia/0000-0001-7699-1427
FU Associazione Italiana Ricerca sul Cancro (A.I.R.C.); FIRB [RBAP11TF7Z]
FX This work was supported by grants from Associazione Italiana Ricerca sul
   Cancro (A.I.R.C.) and FIRB (RBAP11TF7Z).
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NR 30
TC 20
Z9 20
U1 0
U2 6
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
EI 1029-2403
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD JUL
PY 2014
VL 55
IS 7
BP 1538
EP 1543
DI 10.3109/10428194.2013.845885
PG 6
WC Oncology; Hematology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology; Hematology
GA AK1SL
UT WOS:000338196200017
PM 24047476
DA 2025-06-01
ER

PT J
AU Liu, XM
   Li, B
   Wang, WK
   Zhang, C
   Zhang, MX
   Zhang, Y
   Xia, YF
   Dong, Z
   Guo, Y
   An, FS
AF Liu, Xiaoman
   Li, Bo
   Wang, Wenke
   Zhang, Cheng
   Zhang, Mingxiang
   Zhang, Yun
   Xia, Yanfei
   Dong, Zhe
   Guo, Yuan
   An, Fengshuang
TI Effects of HMG-CoA Reductase Inhibitor on Experimental Autoimmune
   Myocarditis
SO CARDIOVASCULAR DRUGS AND THERAPY
LA English
DT Article
DE Rosuvastatin; EAM; Inflammation; Apoptosis
ID NITRIC-OXIDE SYNTHASE; CARDIOMYOCYTE APOPTOSIS; CARDIOVASCULAR-DISEASES;
   VENTRICULAR MYOCYTES; CARDIAC-FUNCTION; UP-REGULATION; IN-VITRO;
   ACTIVATION; STATINS; MICE
AB Myocarditis is an acute inflammatory disease of the heart and is often a precursor of dilated cardiomyopathy. Experimental autoimmune myocarditis (EAM) has been used as a model for human myocarditis. The purpose of this study was to investigate the therapeutic role of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor, rosuvastatin, on the development of EAM.
   Experimental autoimmune myocarditis was induced in BALB/c mice by immunization with murine cardiac alpha-myosin heavy chain (MyHc-alpha(614-629) [Ac-SLKLMATLFSTYASAD-OH]). High-dose (10 mg/kg/day) or low-dose (1 mg/kg/day) rosuvastatin or vehicle was administered orally by gastric gavage to mice with EAM from day 0 to day 21 after immunization. On day 21 after immunization, echocardiography was carried out and the severity of myocarditis was detected by histopathological evaluation. Levels of serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 were measured by ELISA. Histopathology was performed using haematoxylin and eosin. With apoptosis examined by Tunel, the expression of active caspase-3 in myocardium was investigated by immunohistochemistry.
   Rosuvastatin attenuated the histopathological severity of myocarditis. Cardiac function was improved in the two rosuvastatin-treated groups compared to the non-treated EAM group (LVFS: high-dose rosuvastatin group [group H], 0.38 +/- 0.10%; low-dose rosuvastatin group [group L], 0.34 +/- 0.06%; non-treated EAM group [group N], 0.29 +/- 0.07%. LVEF: group H, 0.80 +/- 0.09%; group L, 0.71 +/- 0.07%; group N, 0.68 +/- 0.07%). Furthermore, treatment with rosuvastatin decreased the expression levels of TNF-alpha (group H, 65.19 +/- 7.06 pg/ml; group L, 108.20 +/- 5.28 pg/ml; group N, 239.34 +/- 11.65 pg/ml) and IL-6 (group H, 14.33 +/- 2.15 pg/ml; group L, 19.67 +/- 3.04 pg/ml; group N, 40.39 +/- 7.17 pg/ml). The rates of expression of active Caspase-3 and myocardial apoptosis were positively correlated with the scores for myocardial pathology.
   These results demonstrate that administration of rosuvastatin can ameliorate EAM progression, inhibit apoptosis of cardiomyocytes, and preserve cardiac output, and they also suggest rosuvastatin may be a promising novel therapeutic strategy for the clinical treatment of myocarditis.
C1 [Liu, Xiaoman; Li, Bo; Wang, Wenke; Zhang, Cheng; Zhang, Mingxiang; Zhang, Yun; Xia, Yanfei; Dong, Zhe; Guo, Yuan; An, Fengshuang] Shandong Univ Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minist Educ, Jinan 250012, Shandong, Peoples R China.
   [Liu, Xiaoman; Li, Bo; Wang, Wenke; Zhang, Cheng; Zhang, Mingxiang; Zhang, Yun; Xia, Yanfei; Dong, Zhe; Guo, Yuan; An, Fengshuang] Shandong Univ Qilu Hosp, Chinese Minist Hlth, Jinan 250012, Shandong, Peoples R China.
C3 Shandong University; Ministry of Education - China; Shandong University
RP Guo, Y (corresponding author), Shandong Univ Qilu Hosp, Key Lab Cardiovasc Remodeling & Funct Res, Chinese Minist Educ, Jinan 250012, Shandong, Peoples R China.
EM yuanguo2011@126.com; fengshuangan@126.com
RI Yang, Haiou/U-6328-2019
FU National 973 Basic Research Program of China [2009CB521904]; Natural
   Science Foundation of Shandong Province [Y2007C074]
FX This work was supported by the National 973 Basic Research Program of
   China (No. 2009CB521904) and the grant of Natural Science Foundation of
   Shandong Province (Y2007C074). We greatly appreciate Doctor Shanying
   Huang and Hong Jiang for their excellent technical assistances.
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NR 36
TC 24
Z9 26
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0920-3206
J9 CARDIOVASC DRUG THER
JI Cardiovasc. Drugs Ther.
PD APR
PY 2012
VL 26
IS 2
BP 121
EP 130
DI 10.1007/s10557-012-6372-6
PG 10
WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy
GA 918XS
UT WOS:000302285500005
PM 22382902
DA 2025-06-01
ER

PT J
AU Tseng, LH
   Chen, PJ
   Lin, MT
   Shau, WY
   Chaung, SM
   Martin, PJ
   Hansen, JA
AF Tseng, LH
   Chen, PJ
   Lin, MT
   Shau, WY
   Chaung, SM
   Martin, PJ
   Hansen, JA
TI Single nucleotide polymorphisms in Intron 2 of the human interleukin-1
   receptor antagonist (IL-1Ra) gene:: further definition of the IL-1β and
   IL-1Ra polymorphisms in North American Caucasians and Taiwanese Chinese
SO TISSUE ANTIGENS
LA English
DT Article
DE Caucasian; IL-1 receptor antagonist; polymorphism; Taiwanese; VNTR
ID INFLAMMATORY BOWEL-DISEASE; SYSTEMIC LUPUS-ERYTHEMATOSUS; ASSOCIATION;
   ALLELE; SEVERITY; EXON
AB Previous studies have suggested that a variable number tandem repeat (VNTR) polymorphism in the second intron of the interleukin-l receptor antagonist (IL-1Ra) gene and the single nucleotide polymorphisms at positions -511 and +3954 of the IL-1 beta gene might be associated with increased risks of chronic inflammatory diseases, autoimmune diseases and gastric cancer. In the present study, IL-1 beta and IL-1Ra genotypes were analyzed among Asians in Taiwan and Caucasians in North America. We identified a novel polymorphism with 3 nucleotide substitutions in the IL-1Ra VNTR 2-repeat allele. One of the substitutions corresponds with the fourth 3' end nucleotide of the reverse primer that is often used for analysis of the IL-1Ra-associated VNTR locus. Mismatching between this primer and the 2-repeat allele can cause misleading amplification results when stringent conditions are used for annealing. The estimated haplotype frequencies of the variant IL-1 genes were significantly different between Taiwanese and Caucasians. The frequency of the pro-inflammatory IL-1Ra 2-repeat allele was significantly lower in Taiwanese than in Caucasians. In contrast, the frequencies of the pro-inflammatory IL-1 beta -511T allele and +3954C allele were significantly higher among Taiwanese compared with Caucasians.
C1 Fred Hutchinson Canc Res Ctr, Human Immunogenet Program, Div Clin Res, Seattle, WA 98109 USA.
   Univ Washington, Dept Med, Seattle, WA USA.
   Natl Taiwan Univ Hosp, Dept Med Genet Pathol & Oncol, Taipei, Taiwan.
   Natl Taiwan Univ, Grad Inst Clin Med, Taipei 10764, Taiwan.
   Natl Taiwan Univ, Ctr Canc Res, Taipei 10764, Taiwan.
C3 Fred Hutchinson Cancer Center; University of Washington; University of
   Washington Seattle; National Taiwan University; National Taiwan
   University Hospital; National Taiwan University; National Taiwan
   University
RP Hansen, JA (corresponding author), Fred Hutchinson Canc Res Ctr, Human Immunogenet Program, Div Clin Res, 1100 Fairview Ave N,D2-100, Seattle, WA 98109 USA.
RI Chen, Jiayi/GZM-5106-2022; shau, wen-yi/KPB-6470-2024
OI TSENG, LI-HUI/0000-0002-8308-6772; Chen, Pei-Jer/0000-0001-8316-3785;
   Shau, Wen-Yi/0000-0003-3977-1729
FU NCI NIH HHS [CA15704, CA18029] Funding Source: Medline; NIAID NIH HHS
   [AI33484] Funding Source: Medline
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Z9 46
U1 0
U2 0
PU MUNKSGAARD INT PUBL LTD
PI COPENHAGEN
PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK
SN 0001-2815
J9 TISSUE ANTIGENS
JI Tissue Antigens
PD APR
PY 2001
VL 57
IS 4
BP 318
EP 324
DI 10.1034/j.1399-0039.2001.057004318.x
PG 7
WC Cell Biology; Immunology; Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Cell Biology; Immunology; Pathology
GA 440RG
UT WOS:000169187600004
PM 11380940
DA 2025-06-01
ER

PT J
AU Grieb, G
   Kim, BS
   Simons, D
   Bernhagen, J
   Pallua, N
AF Grieb, Gerrit
   Kim, Bong-Sung
   Simons, David
   Bernhagen, Juregen
   Pallua, Norbert
TI MIF and CD74-Suitability as Clinical Biomarkers
SO MINI-REVIEWS IN MEDICINAL CHEMISTRY
LA English
DT Review
DE Biomarker; CD74; macrophage migration inhibitory factor (MIF);
   macrophage migration inhibitory factor receptor
ID MIGRATION-INHIBITORY FACTOR; GASTRIC EPITHELIAL-CELLS; CLASS-II
   MOLECULES; INVARIANT CHAIN; HELICOBACTER-PYLORI; DELAYED
   HYPERSENSITIVITY; PROINFLAMMATORY FUNCTION; MACROPHAGE FUNCTIONS;
   CYTOKINE PRODUCTION; INSULIN-RESISTANCE
AB Macrophage migration inhibitory factor (MIF) is a pleiotropic immunoregulatory cytokine whose effects on arresting `random' immune cell movement was already recognized decades ago. MIF is quasi-constitutively expressed by a variety of different cells and tissues, including immune cells such as T-cells and monocytes/macrophages, but also non-immune cells like certain endocrine cells and cells lining interior body cavities or contacting the exterior environment, such as endothelial cells (ECs), or epithelial cells in kidney, gut and skin. Contrary to its historic name, MIF has a direct chemokine-like function and promotes `directed' cell migration (i.e. chemotaxis) and plays a prominent role in inflammatory and atherogenic leukocyte recruitment. At the molecular level, these activities are based on a non-cognate interaction between MIF and the CXC chemokine receptors CXCR2 and CXCR4. Importantly, MIF also interacts with surface CD74, a type II transmembrane protein, inducing its phosphorylation and the recruitment of CD44, leading ultimately to ERK1/2 phosphorylation. Multiple studies have pointed to the utility of MIF as a biomarker for different diseases that have an inflammatory component; these include systemic infections and sepsis, cancer, autoimmune diseases as well as different metabolic disorders. In this Review, we highlight the suitability of MIF and CD74 as biomarkers for different disease applications.
C1 [Grieb, Gerrit; Kim, Bong-Sung; Simons, David; Pallua, Norbert] Rhein Westfal TH Aachen, Fac Med, Burn Ctr, Dept Plast Surg & Hand Surg, D-52074 Aachen, Germany.
   [Grieb, Gerrit; Kim, Bong-Sung; Simons, David; Bernhagen, Juregen] Rhein Westfal TH Aachen, Fac Med, Inst Biochem & Mol Cell Biol, D-52074 Aachen, Germany.
   [Simons, David] German Canc Res Ctr, D-69120 Heidelberg, Germany.
C3 RWTH Aachen University; RWTH Aachen University; Helmholtz Association;
   German Cancer Research Center (DKFZ)
RP Grieb, G (corresponding author), Rhein Westfal TH Aachen, Fac Med, Burn Ctr, Dept Plast Surg & Hand Surg, Pauwelsstr 30, D-52074 Aachen, Germany.
EM gerritgrieb@gmx.de
RI Kim, Bong-Sung/AAR-3802-2021
OI Kim, Bong-Sung/0000-0002-0493-3196
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NR 82
TC 33
Z9 38
U1 0
U2 12
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
   EMIRATES
SN 1389-5575
EI 1875-5607
J9 MINI-REV MED CHEM
JI Mini-Rev. Med. Chem.
PY 2014
VL 14
IS 14
BP 1125
EP 1131
PG 7
WC Chemistry, Medicinal
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA CB8GL
UT WOS:000349866900003
PM 25643609
DA 2025-06-01
ER

PT J
AU Tubau-Juni, N
   Bassaganya-Riera, J
   Leber, A
   Zoccoli-Rodriguez, V
   Kronsteiner, B
   Viladomiu, M
   Abedi, V
   Philipson, CW
   Hontecillas, R
AF Tubau-Juni, Nuria
   Bassaganya-Riera, Josep
   Leber, Andrew
   Zoccoli-Rodriguez, Victoria
   Kronsteiner, Barbara
   Viladomiu, Monica
   Abedi, Vida
   Philipson, Casandra W.
   Hontecillas, Raquel
TI Identification of new regulatory genes through expression pattern
   analysis of a global RNA-seq dataset from a Helicobacter pylori
   co-culture system
SO SCIENTIFIC REPORTS
LA English
DT Article
ID PPAR-GAMMA; PROTEIN PHOSPHATASE-1; GASTRIC-CANCER; MACROPHAGES;
   INFECTION; METABOLISM; INFLAMMATION; PATHOGENESIS; ACTIVATION; RESPONSES
AB Helicobacter pylori is a gram-negative bacterium that persistently colonizes the human stomach by inducing immunoregulatory responses. We have used a novel platform that integrates a bone marrow-derived macrophage and live H. pylori co-culture with global time-course transcriptomics analysis to identify new regulatory genes based on expression patterns resembling those of genes with known regulatory function. We have used filtering criteria based on cellular location and novelty parameters to select 5 top lead candidate targets. Of these, Plexin domain containing 2 (Plxdc2) was selected as the top lead immunoregulatory target. Loss of function studies with in vivo models of H. pylori infection as well as a chemically-induced model of colitis, confirmed its predicted regulatory function and significant impact on modulation of the host immune response. Our integrated bioinformatics analyses and experimental validation platform has enabled the discovery of new immunoregulatory genes. This pipeline can be used for the identification of genes with therapeutic applications for treating infectious, inflammatory, and autoimmune diseases.
C1 [Tubau-Juni, Nuria; Bassaganya-Riera, Josep; Leber, Andrew; Zoccoli-Rodriguez, Victoria; Kronsteiner, Barbara; Viladomiu, Monica; Abedi, Vida; Philipson, Casandra W.; Hontecillas, Raquel] NIMML Inst, Blacksburg, VA 24060 USA.
   [Tubau-Juni, Nuria; Bassaganya-Riera, Josep; Leber, Andrew; Zoccoli-Rodriguez, Victoria; Hontecillas, Raquel] BioTherapeut Inc, Blacksburg, VA 24060 USA.
RP Hontecillas, R (corresponding author), NIMML Inst, Blacksburg, VA 24060 USA.; Hontecillas, R (corresponding author), BioTherapeut Inc, Blacksburg, VA 24060 USA.
EM rmagarzo@nimml.org
RI Viladomiu, Monica/GNM-6447-2022; Abedi, Vida/AAU-3828-2021; Philipson,
   Casandra/AAY-5746-2021
OI Kronsteiner-Dobramysl, Barbara/0000-0003-0867-2867; Abedi,
   Vida/0000-0001-7689-933X; Zoccoli-Rodriguez,
   Victoria/0000-0002-5487-6521
FU Defense Threat Reduction Agency (DTRA) [HDTRA1-18-1-008]
FX This study was funded through funding from the NIMML Institute and grant
   HDTRA1-18-1-008 from the Defense Threat Reduction Agency (DTRA) to JBR
   and RH.
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NR 65
TC 10
Z9 11
U1 1
U2 8
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD JUL 13
PY 2020
VL 10
IS 1
AR 11506
DI 10.1038/s41598-020-68439-8
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA MN1BI
UT WOS:000550580900023
PM 32661418
OA Green Published, gold, Green Submitted
DA 2025-06-01
ER

PT J
AU Roy, AM
   Siddiqui, A
   Venkata, A
AF Roy, Arya Mariam
   Siddiqui, Aisha
   Venkata, Anand
TI Undiagnosed Acquired Hemophilia A: Presenting as Recurrent
   Gastrointestinal Bleeding
SO CUREUS JOURNAL OF MEDICAL SCIENCE
LA English
DT Article
DE acquired hemophilia a; gastro intestinal bleeding; bleeding disorders;
   gastroenterology and endoscopy; rituximab; feiba
AB Acute gastrointestinal bleeding (GIB) is a frequently encountered medical emergency and it can be life-threatening depending on the etiology and the clinical condition of the patient. The most common causes of GIB are peptic ulcer disease, aspirin-induced gastritis, variceal hemorrhage, esophagitis, neoplasms like gastric cancer. Acquired hemophilia causing acute gastrointestinal bleed is extremely rare and only a few cases are reported worldwide. Acquired hemophilia A (AHA) is a rare disorder caused by the production of autoantibodies that inactivates clotting factor VIII. We present a case of upper gastrointestinal bleed due to AHA which was undiagnosed for two years. A 74-year-old patient with a history of myasthenia gravis, presented with anemia, and GIB. She underwent multiple endoscopies without a clear bleeding source. Coagulation studies showed isolated activated partial thromboplastin time prolongation which was not corrected by mixing study. Factor VIII activity was low and Bethesda titer showed elevated inhibitor levels. Factor Eight Bypassing Agent, recombinant factor VIIa, and steroids were given to control bleeding. Her clinical condition worsened, and she passed away. Elderly patients presenting with an undiagnosed source of GIBS, inconclusive endoscopic studies should be evaluated for acquired coagulopathies, especially in those with a history of autoimmune diseases and malignancies. Prompt diagnosis and treatment are warranted as it carries a high mortality.
C1 [Roy, Arya Mariam] Univ Arkansas Med Sci, Internal Med, Little Rock, AR 72205 USA.
   [Siddiqui, Aisha] Amer Univ Antigua, Internal Med, New York, NY USA.
   [Venkata, Anand] Univ Arkansas Med Sci, Pulm & Crit Care Med, Little Rock, AR 72205 USA.
C3 University of Arkansas System; University of Arkansas Medical Sciences;
   University of Arkansas System; University of Arkansas Medical Sciences
RP Roy, AM (corresponding author), Univ Arkansas Med Sci, Internal Med, Little Rock, AR 72205 USA.
EM aryamariyamroy@gmail.com
RI siddiqui, aisha/GWC-2967-2022; Roy, Arya/AAW-2378-2020
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NR 15
TC 3
Z9 3
U1 0
U2 2
PU SPRINGERNATURE
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON, N1 9XW, ENGLAND
EI 2168-8184
J9 CUREUS J MED SCIENCE
JI Cureus J Med Sci
PD SEP 1
PY 2020
VL 12
IS 9
AR e10188
DI 10.7759/cureus.10188
PG 5
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA NH2BI
UT WOS:000564480400013
PM 33029467
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Knezevic, J
   Starchl, C
   Berisha, AT
   Amrein, K
AF Knezevic, Jovana
   Starchl, Christina
   Tmava Berisha, Adelina
   Amrein, Karin
TI Thyroid-Gut-Axis: How Does the Microbiota Influence Thyroid Function?
SO NUTRIENTS
LA English
DT Review
DE thyroid; gut microbiota; Hashimoto's thyroiditis; Grave ' s disease;
   celiac disease; Non-celiac wheat sensitivity; iodine; iron; probiotics;
   thyroid cancer
ID GASTRIC BYPASS-SURGERY; VITAMIN-D DEFICIENCY; CELIAC-DISEASE;
   HASHIMOTOS-THYROIDITIS; IRON-DEFICIENCY; SELENIUM DEFICIENCY; BARIATRIC
   SURGERY; HORMONE-LEVELS; OBESE-PATIENTS; IODINE
AB A healthy gut microbiota not only has beneficial effects on the activity of the immune system, but also on thyroid function. Thyroid and intestinal diseases prevalently coexist-Hashimoto's thyroiditis (HT) and Graves' disease (GD) are the most common autoimmune thyroid diseases (AITD) and often co-occur with Celiac Disease (CD) and Non-celiac wheat sensitivity (NCWS). This can be explained by the damaged intestinal barrier and the following increase of intestinal permeability, allowing antigens to pass more easily and activate the immune system or cross-react with extraintestinal tissues, respectively. Dysbiosis has not only been found in AITDs, but has also been reported in thyroid carcinoma, in which an increased number of carcinogenic and inflammatory bacterial strains were observed. Additionally, the composition of the gut microbiota has an influence on the availability of essential micronutrients for the thyroid gland. Iodine, iron, and copper are crucial for thyroid hormone synthesis, selenium and zinc are needed for converting T4 to T3, and vitamin D assists in regulating the immune response. Those micronutrients are often found to be deficient in AITDs, resulting in malfunctioning of the thyroid. Bariatric surgery can lead to an inadequate absorption of these nutrients and further implicates changes in thyroid stimulating hormone (TSH) and T3 levels. Supplementation of probiotics showed beneficial effects on thyroid hormones and thyroid function in general. A literature research was performed to examine the interplay between gut microbiota and thyroid disorders that should be considered when treating patients suffering from thyroid diseases. Multifactorial therapeutic and preventive management strategies could be established and more specifically adjusted to patients, depending on their gut bacteria composition. Future well-powered human studies are warranted to evaluate the impact of alterations in gut microbiota on thyroid function and diseases.
C1 [Knezevic, Jovana; Starchl, Christina; Amrein, Karin] Med Univ Graz, Dept Internal Med, Div Endocrinol & Diabetol, Auenbruggerpl 15, A-8036 Graz, Austria.
   [Tmava Berisha, Adelina] Med Univ Graz, Dept Psychiat & Psychotherapeut Med, A-8036 Graz, Austria.
C3 Medical University of Graz; Medical University of Graz
RP Starchl, C (corresponding author), Med Univ Graz, Dept Internal Med, Div Endocrinol & Diabetol, Auenbruggerpl 15, A-8036 Graz, Austria.
EM jovana.knezevic@stud.medunigraz.at;
   christina.starchl@stud.medunigraz.at; adelina.tmava@medunigraz.at;
   karin.amrein@medunigraz.at
OI Geiger, Christina/0000-0003-4918-1749
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NR 132
TC 205
Z9 225
U1 16
U2 167
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2072-6643
J9 NUTRIENTS
JI Nutrients
PD JUN
PY 2020
VL 12
IS 6
AR 1769
DI 10.3390/nu12061769
PG 16
WC Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Nutrition & Dietetics
GA ML1TM
UT WOS:000549257200001
PM 32545596
OA gold, Green Published
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Marginean, CM
   Pirscoveanu, D
   Popescu, M
   Docea, AO
   Radu, A
   Popescu, AIS
   Vasile, CM
   Mitrut, R
   Marginean, IC
   Iacob, GA
   Firu, DM
   Mitrut, P
AF Marginean, Cristina Maria
   Pirscoveanu, Denisa
   Popescu, Mihaela
   Docea, Anca Oana
   Radu, Antonia
   Popescu, Alin Iulian Silviu
   Vasile, Corina Maria
   Mitrut, Radu
   Marginean, Iulia Cristina
   Iacob, George Alexandru
   Firu, Dan Mihai
   Mitrut, Paul
TI Diagnostic Approach and Pathophysiological Mechanisms of Anemia in
   Chronic Liver Disease-An Overview
SO GASTROENTEROLOGY INSIGHTS
LA English
DT Review
DE chronic liver disease; anemia; hepcidin; chronic hepatitis; liver
   cirrhosis; gastrointestinal bleeding
ID ANTRAL VASCULAR ECTASIA; CHRONIC HEPATITIS-C; PORTAL-HYPERTENSION;
   CIRRHOTIC-PATIENTS; IRON-DEFICIENCY; HEPCIDIN EXPRESSION;
   HEMOLYTIC-ANEMIA; APLASTIC-ANEMIA; VIRUS-INFECTION; SPUR CELLS
AB Hematological abnormalities are frequently linked to chronic liver disease of any etiology. About 75% of patients with advanced chronic liver disease experience anemia. The causes of anemia are complex and multifactorial, particularly in cirrhotic patients. Acute and long-term blood loss from the upper gastrointestinal tract, malnutrition, an enlarged spleen brought on by portal hypertension, hemolysis, and coagulation issues are the main causes of anemia. Alcohol, a common cause of chronic liver disease, determines anemia through direct toxicity on the bone marrow, with the suppression of hematopoiesis, through vitamin B6, B12, and folate deficiency due to low intake and malabsorption. In patients with chronic hepatitis C virus infection, antiviral drugs such as pegylated interferon and ribavirin can also cause significant anemia. The use of interferon has been linked to bone marrow toxicity, and hemolytic anemia brought on by ribavirin is a well-known dose-dependent side effect. Within six months of the infection with hepatitis B, hepatitis C, and Epstein-Barr viruses, aplastic anemia associated with hepatitis is seen. This anemia is characterized by pancytopenia brought on by hypocellular bone marrow. Esophageal varices, portal hypertensive gastropathy, and gastric antral vascular ectasia can all cause acute and chronic blood loss. These conditions can progress to iron deficiency anemia, microcytic anemia, and hypochromic anemia. Another common hematologic abnormality in liver cirrhosis is macrocytosis, with multifactorial causes. Vitamin B12 and folate deficiency are frequent in liver cirrhosis, especially of alcoholic etiology, due to increased intestinal permeability, dysbiosis, and malnutrition. Many chronic liver diseases, like viral and autoimmune hepatitis, have a chronic inflammatory substrate. Proinflammatory cytokines, including tumor necrosis factor and interleukin 1, 6, and 10, are the main factors that diminish iron availability in progenitor erythrocytes and subsequent erythropoiesis, leading to the development of chronic inflammatory, normochromic, normocytic anemia.
C1 [Marginean, Cristina Maria; Mitrut, Paul] Univ Med & Pharm Craiova, Dept Internal Med, Craiova 200349, Romania.
   [Pirscoveanu, Denisa] Univ Med & Pharm Craiova, Dept Neurol, Craiova 200349, Romania.
   [Popescu, Mihaela] Univ Med & Pharm Craiova, Dept Endocrinol, Craiova 200349, Romania.
   [Docea, Anca Oana] Univ Med & Pharm Craiova, Dept Toxicol, Craiova 200349, Romania.
   [Radu, Antonia] Univ Med & Pharm Craiova, Dept Pharmaceut Bot, Craiova 200349, Romania.
   [Popescu, Alin Iulian Silviu] Univ Med & Pharm Craiova, Dept Pneumol, Craiova 200349, Romania.
   [Vasile, Corina Maria] Bordeaux Univ Hosp, Dept Pediat & Adult Congenital Cardiol, F-33600 Pessac, France.
   [Mitrut, Radu] Univ Emergency Hosp, Dept Cardiol, Bucharest 050098, Romania.
   [Marginean, Iulia Cristina; Iacob, George Alexandru] Univ Med & Pharm Craiova, Fac Med, Craiova 200349, Romania.
   [Firu, Dan Mihai] Univ Med & Pharm Craiova, Dept Med Semiol, Craiova 200349, Romania.
C3 University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova;
   University of Medicine & Pharmacy of Craiova; University of Medicine &
   Pharmacy of Craiova; University of Medicine & Pharmacy of Craiova; CHU
   Bordeaux; Universite de Bordeaux; University of Medicine & Pharmacy of
   Craiova; University of Medicine & Pharmacy of Craiova
RP Docea, AO (corresponding author), Univ Med & Pharm Craiova, Dept Toxicol, Craiova 200349, Romania.
EM marginean22@yahoo.com; pirscoveanudenisa@gmail.com;
   mihaela.n.popescu99@gmail.com; ancadocea@gmail.com;
   antonia.blendea@gmail.com; alinpope.09@gmail.com;
   corina.vasile93@gmail.com; radumitrut@yahoo.co.uk;
   iulia.cristina18@yahoo.com; georgeicb5@gmail.com;
   firu.danmihai@gmail.com; paulmitrut@yahoo.com
RI Radu (Blendea), Antonia/IQT-1348-2023; Mitrut, Radu/AAR-3344-2021;
   Mărginean, Cristina/GRX-4182-2022; Popescu, Sanda/B-9014-2011; Dan
   Mihai, Firu/ISA-2041-2023; Docea, Anca/P-5807-2019; Iacob, George
   Alexandru/HOH-8118-2023; Vasile, Corina/HJA-1313-2022
OI Radu, Antonia/0000-0002-3448-2736; Iacob, George
   Alexandru/0009-0000-4783-7420; Docea, Anca Oana/0000-0002-8162-5955;
   Mitrut, Radu/0000-0003-2207-6519; Marginean, Iulia
   Cristina/0009-0005-3968-255X; Vasile, Corina/0000-0002-4684-8213;
   Marginean, Cristina Maria/0009-0002-9956-4318
FU University of Medicine and Pharmacy of Craiova, Romania [26/510/2]
FX This study was supported by internal grant no. 26/510/2 May 2023 "Study
   of the effect of COVID-19 pandemic on quality of life in patients with
   chronic liver disease" of the University of Medicine and Pharmacy of
   Craiova, Romania.
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NR 100
TC 1
Z9 1
U1 4
U2 10
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
SN 2036-7414
EI 2036-7422
J9 GASTROENTEROL INSIGH
JI Gastroenterol. Insights
PD SEP
PY 2023
VL 14
IS 3
BP 327
EP 341
DI 10.3390/gastroent14030024
PG 15
WC Gastroenterology & Hepatology
WE Emerging Sources Citation Index (ESCI)
SC Gastroenterology & Hepatology
GA T0DJ7
UT WOS:001074777400001
OA gold
DA 2025-06-01
ER

PT J
AU Cornejo-Granados, F
   de la Barca, AMC
   Torres, N
   Martínez-Romero, E
   Torres, J
   López-Vidal, Y
   Soberón, X
   Partida-Martínez, LP
   Pinto-Cardoso, S
   Alcaraz, LD
   Pardo-López, L
   Canizales-Quinteros, S
   Puente, JL
   Ochoa-Leyva, A
AF Cornejo-Granados, Fernanda
   Calderon de la Barca, Ana Maria
   Torres, Nimbe
   Martinez-Romero, Esperanza
   Torres, Javier
   Lopez-Vidal, Yolanda
   Soberon, Xavier
   Partida-Martinez, Laila P.
   Pinto-Cardoso, Sandra
   David Alcaraz, Luis
   Pardo-Lopez, Liliana
   Canizales-Quinteros, Samuel
   Luis Puente, Jose
   Ochoa-Leyva, Adrian
TI Microbiome-MX 2018: microbiota and microbiome opportunities in Mexico, a
   megadiverse country
SO RESEARCH IN MICROBIOLOGY
LA English
DT Article
ID HEALTH; IMPACT; OBESE
AB A weekly conference series paired with lectures entitled "Microbiome-MX: exploring the Microbiota and Microbiome Research in Mexico" was organized to provide a multidisciplinary overview of the most recent research done in Mexico using high-throughput sequencing. Scientists and postgraduate students from several disciplines such as microbiology, bioinformatics, virology, immunology, nutrition, and medical genomics gathered to discuss state of the art in each of their respective subjects of expertise, as well as advances, applications and new opportunities on microbiota/microbiome research. In particular, high-throughput sequencing is a crucial tool to understand the challenges of a megadiverse developing country as Mexico, and moreover to know the scientific capital and capabilities available for collaboration. The conference series addressed three main topics important for Mexico: i) the complex role of microbiota in health and prevalent diseases such as obesity, diabetes, inflammatory bowel disease, tuberculosis, HIV, autoimmune diseases and gastric cancer; ii) the use of local, traditional and prehispanic products as pre/probiotics to modulate the microbiota and improve human health; and iii) the impact of the microbiota in shaping the biodiversity of economically important terrestrial and marine ecosystems. Herein, we summarize the contributions that Mexican microbiota/microbiome research is making to the global trends, describing the highlights of the conferences and lectures, rather than a review of the state-of-the-art of this research. This meeting report also presents the efforts of a multidisciplinary group of scientist to encourage collaborations and bringing this research field closer for younger generations. (C) 2019 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
C1 [Cornejo-Granados, Fernanda; Pardo-Lopez, Liliana; Luis Puente, Jose; Ochoa-Leyva, Adrian] Univ Nacl Autonoma Mexico, Dept Microbiol Mol, Inst Biotecnol, Ave Univ 2001, Cuernavaca 62210, Morelos, Mexico.
   [Calderon de la Barca, Ana Maria] Ctr Invest Alimentac & Desarrollo, Dept Nutr Humana, AC Astiazaran Rosas 46, Hermosillo 83304, Sonora, Mexico.
   [Torres, Nimbe] Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Dept Fisiol Nutr, Vasco de Quiroga 15, Ciudad De Mexico 14080, Cd De Mexico, Mexico.
   [Martinez-Romero, Esperanza] UNAM, CCG, Cuernavaca, Morelos, Mexico.
   [Torres, Javier] Inst Mexicano Seguro Social, Hosp Pediat, Unidad Invest Enfermedades Infecciosas & Parasita, Cd De Mexico, Mexico.
   [Lopez-Vidal, Yolanda] Univ Nacl Autonoma Mexico, Dept Microbiol & Parasitol, Fac Med, Cd Mexico, Mexico.
   [Soberon, Xavier] Inst Nacl Med Genom, Cd Mexico, Mexico.
   [Partida-Martinez, Laila P.] Ctr Invest & Estudios Avanzados CINVESTAV, Dept Ingn Genet, Km 9-6 Libramiento Norte Carr, Irapuato Leon 36824, Irapuato, Mexico.
   [Pinto-Cardoso, Sandra] Inst Nacl Enfermedades Resp Ismael Cosio Villegas, Dept Invest Enfermedades Infecciosas, Calzada de Tlalpan 4501,Colonia Secc 26, Ciudad De Mexico 14080, Mexico.
   [David Alcaraz, Luis] Ciudad Mexico, Fac Ciencias, Dept Biol Celular, Ciudad De Mexico 04510, Mexico.
   [David Alcaraz, Luis] Univ Nacl Autonoma Mexico, Inst Ecol, Lab Nacl Ciencias Sostenibilidad LANCIS, Ciudad De Mexico 04510, Mexico.
   [Canizales-Quinteros, Samuel] Univ Nacl Autonoma Mexico, Unidad Genom Poblac Aplicada Salud, Fac Quim, Inst Nacl Med Genom INMEGEN, Cd De Mexico, Mexico.
C3 Universidad Nacional Autonoma de Mexico; CIAD - Centro de Investigacion
   en Alimentacion y Desarrollo; Instituto Nacional de Ciencias Medicas y
   Nutricion Salvador Zubiran - Mexico; Universidad Nacional Autonoma de
   Mexico; Instituto Mexicano del Seguro Social; Universidad Nacional
   Autonoma de Mexico; Instituto Nacional de Medicina Genomica; Universidad
   Nacional Autonoma de Mexico; Instituto Nacional de Medicina Genomica;
   Universidad Nacional Autonoma de Mexico
RP Puente, JL; Ochoa-Leyva, A (corresponding author), Univ Nacl Autonoma Mexico, Dept Microbiol Mol, Inst Biotecnol, Ave Univ 2001, Cuernavaca 62210, Morelos, Mexico.
EM mafercg@ibt.unam.mx; amc@ciad.mx; nimbester@gmail.com;
   emartine@ccg.unam.mx; uimeip@gmail.com; lvidal@unam.mx;
   xsoberon@inmegen.gob.mx; laila.partida@cinvestav.mx;
   sandra.pinto@cieni.org.mx; lalcaraz@ciencias.unam.mx;
   liliana@ibt.unam.mx; scanizales@inmegen.gob.mx; puente@ibt.unam.mx;
   aochoa@ibt.unam.mx
RI López-Vidal, Yolanda/ABE-9501-2021; Soberon, Xavier/A-8826-2008; Torres,
   Nimbe/AAI-4340-2020; Calderon de la Barca, Ana-Maria/HPG-0991-2023;
   Puente, Jose/JBS-7468-2023; Ochoa-Leyva, Adrian/E-5540-2013;
   Partida-Martinez, Laila P./A-5935-2009; Alcaraz, Luis David/D-1352-2011
OI martinez-romero, esperanza/0000-0002-2295-2606; Ochoa-Leyva,
   Adrian/0000-0002-4701-2303; Pardo Lopez, Liliana/0000-0002-8927-1733;
   Puente Garcia, Jose Luis/0000-0002-8411-4974; Pinto-Cardoso,
   Sandra/0000-0001-8957-4972; soberon, xavier/0000-0002-4498-5628;
   Partida-Martinez, Laila P./0000-0001-8037-2856; Alcaraz, Luis
   David/0000-0003-3284-0605
FU Institute of Biotechnology of the National Autonomous University of
   Mexico (UNAM); Postgraduate Program in Biochemical Sciences of the
   National Autonomous University of Mexico (UNAM); National Council of
   Science and Technology (CONACyT) [SALUD-2014-C01-234188, CB-239659,
   FC-2015-2/950]; DGAPA PAPPIT UNAM [IA203118, IN213516]; CIC-UNAM
FX We wish to acknowledge and thank all the coauthors for their
   enthusiastic and enriching participation in this conference series, as
   well as to all the participating students. We gratefully acknowledged
   Dr. Marie Claire Arrieta from the University of Calgary for imparting
   the closing conference about the development of immune-mediated
   pediatric diseases such as asthma. We thank Dr. Sofia Moran-Ramos from
   National Institute of Genomic Medicine and Dr. Alejandra Escobar-Zepeda
   from the Institute of Biotechnology (UNAM) for their valuable academic
   support in the conferences and classrooms discussions during their
   session. We also thank Dr. Leonor Perez-Martinez for her academic
   support with a classroom discussion. Special thanks to Omar Arriaga for
   his expert audiovisual technical support and the Institute of
   Biotechnology and the Postgraduate Program in Biochemical Sciences of
   the National Autonomous University of Mexico (UNAM) for their kind and
   generous support. This work was supported by the National Council of
   Science and Technology (CONACyT) grant SALUD-2014-C01-234188 to AOL and
   CB-239659 and FC-2015-2/950 to JLP. The work was also supported by the
   DGAPA PAPPIT UNAM IA203118 to AOL and IN213516 to JLP and by the
   Programa Actividades de Intercambio Academico-2018 from CIC-UNAM to AOL.
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NR 61
TC 1
Z9 1
U1 1
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0923-2508
EI 1769-7123
J9 RES MICROBIOL
JI Res. Microbiol.
PD JUN-AUG
PY 2019
VL 170
IS 4-5
BP 235
EP 241
DI 10.1016/j.resmic.2019.03.001
PG 7
WC Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Microbiology
GA IK3EK
UT WOS:000476472100008
PM 30922683
OA Bronze
DA 2025-06-01
ER

PT S
AU Falkeis-Veits, C
   Vieth, M
AF Falkeis-Veits, Christina
   Vieth, Michael
BE Kamiya, S
   Backert, S
TI Non-malignant Helicobacter pylori-Associated Diseases
SO HELICOBACTER PYLORI IN HUMAN DISEASES: ADVANCES IN MICROBIOLOGY,
   INFECTIOUS DISEASES AND PUBLIC HEALTH. VOL 11
SE Advances in Experimental Medicine and Biology
LA English
DT Article; Book Chapter
DE Helicobacter pylori; Gastritis; Sydney system; Atrophic gastritis
ID UNIDENTIFIED CURVED BACILLI; INTESTINAL METAPLASIA; LYMPHOCYTIC
   GASTRITIS; GALLBLADDER MUCOSA; ERADICATION; INFECTION; STOMACH;
   ESOPHAGUS; ATROPHY; CANCER
AB Helicobacter pylori infection of the human stomach is associated with chronic gastritis, peptic ulcer disease or gastric carcinoma, and thus a high burden for the public health systems worldwide. Fortunately, only a small subfraction of up to 15-20% of infected individuals will develop serious complications. Unfortunately, it is not always known upfront, who will be affected by serious diesease outcome. For risk stratifications, it is therefore necessary to establish a common terminology and grading system, that can be applied worldwide to compare population data. The updated Sydney System for classification of gastritis with its semi-quantitative analogue scale is the system, that is currently used worldwide. Additionally, pathologists should always try to classify the etiology of the inflammatory infiltrates in the stomach to instruct the clinicians for choosing a proper treatment regime. Risk factors such as intestinal metaplasia, atrophy and scoring systems to classify these risk factors into a clinical context such as OLGA and OLGIM are discussed. Also, special forms of gastritis like lymphocytic gastritis, autoimmune gastritis and peptic ulcer disease are explained and discussed e.g. how to diagnose and how to treat. Extragastric sequelae of H. pylori infections inside and outside the stomach are shown in this chapter as well. Important host and bacterial risk factors such as pathogenicity islands are dicussed to draw a complete landscape around a H. pylori infection, that still can be diagnosed in patients. However, it needs to be noted that some countries have almost no H. pylori infection anymore, while others have still a very high frequency of infections with or without serious complications. The understanding and application of risk assessements may help to save money and quality of life. Extra-gastric H. pylori infections are rarely reported in the literature until today. The pathogenitiy is still under debate, but especially in the bile ducts and gallbladder, several pathological conditions may be also based on H. pylori infection, and will be also discussed.
C1 [Falkeis-Veits, Christina; Vieth, Michael] Klinikum Bayreuth, Inst Pathol, Bayreuth, Germany.
C3 Klinikum Bayreuth
RP Vieth, M (corresponding author), Klinikum Bayreuth, Inst Pathol, Bayreuth, Germany.
EM christina.falkeis@klinikum-bayreuth.de; vieth.lkpathol@uni-bayreuth.de
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NR 48
TC 7
Z9 7
U1 1
U2 3
PU SPRINGER INTERNATIONAL PUBLISHING AG
PI CHAM
PA GEWERBESTRASSE 11, CHAM, CH-6330, SWITZERLAND
SN 0065-2598
EI 2214-8019
BN 978-3-030-21916-1; 978-3-030-21915-4
J9 ADV EXP MED BIOL
JI Adv.Exp.Med.Biol.
PY 2019
VL 1149
BP 121
EP 134
DI 10.1007/5584_2019_362
D2 10.1007/978-3-030-21916-1
PG 14
WC Infectious Diseases; Medicine, Research & Experimental; Microbiology
WE Book Citation Index – Science (BKCI-S); Science Citation Index Expanded (SCI-EXPANDED)
SC Infectious Diseases; Research & Experimental Medicine; Microbiology
GA BP0SL
UT WOS:000536588000008
PM 31016630
DA 2025-06-01
ER

PT J
AU Langhans, W
   Hrupka, B
AF Langhans, W
   Hrupka, B
TI Interleukins and tumor necrosis factor as inhibitors of food intake
SO NEUROPEPTIDES
LA English
DT Review
ID CENTRAL-NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER; CORTICOTROPIN-RELEASING
   FACTOR; INDUCED INSULIN-RESISTANCE; IL-1 RECEPTOR ANTAGONIST; GASTRIC
   VAGAL AFFERENT; FACTOR-ALPHA ACTIVITY; FA/FA ZUCKER RATS; MESSENGER-RNA;
   GENE-EXPRESSION
AB Cytokines, such as interleukins and tumor necrosis factor-alpha (TNF alpha), are produced in response to immune stimulation and have systemic effects, mediated by the central nervous system (CNS). Interleukins, in particular interleukin [IL]-1 beta, and TNF alpha reduce food intake after peripheral and central administration, suggesting that they contribute to the anorexia during various infectious, neoplastic and autoimmune diseases. Because cytokines are mainly produced in the periphery during most of these diseases, IL-1 beta and TNF alpha may inhibit feeding indirectly through neural and humoral pathways activated by their peripheral actions. Activation of afferent nerve fibers by locally produced cytokines in the periphery is involved in several cytokine effects, but is not crucial for the anorectic effect of systemic immune stimulation. Cytokines increase OB protein (leptin) expression in the adipose tissue, and leptin may contribute to, but is also not essential for, the anorectic effects of cytokines. Finally, circulating IL-1 beta and TNF alpha may act directly on the brain or cytokine synthesis in the brain may contribute to the anorectic effect of systemic immune stimulation. Central mediators of the anorectic effects of cytokines appear to be neurochemicals involved in the normal control of feeding, such as serotonin, corticotropin releasing factor, histamine, a-melanocyte stimulating hormone, and neuropeptide Y. The well-documented cytokine production in the gut in relation to feeding and the expression of TNF alpha by adipocytes suggest that IL-1 beta and TNF alpha may also play a role in the control of normal feeding and energy balance. All in all, reciprocal, synergistic and antagonistic interactions between various pleiotropic cytokines and between cytokines and neurochemicals form a complex network that mediates the effects of cytokines on feeding and energy balance. (C) 1999 Harcourt Publishers Ltd.
C1 Swiss Fed Inst Technol, Inst Anim Sci, Zurich, Switzerland.
C3 Swiss Federal Institutes of Technology Domain; ETH Zurich
RP Langhans, W (corresponding author), ETH Zurich, Inst Nutztierwissensch, CH-8092 Zurich, Switzerland.
RI Langhans, Wolfgang/C-4073-2016
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NR 123
TC 110
Z9 120
U1 2
U2 10
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
   LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0143-4179
J9 NEUROPEPTIDES
JI Neuropeptides
PD OCT
PY 1999
VL 33
IS 5
BP 415
EP 424
DI 10.1054/npep.1999.0048
PG 10
WC Endocrinology & Metabolism; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 256UK
UT WOS:000083744600011
PM 10657519
DA 2025-06-01
ER

PT J
AU Annibale, B
   Marignani, M
   Azzoni, C
   DAmbra, G
   Caruana, P
   DAdda, T
   DelleFave, G
   Bordi, C
AF Annibale, B
   Marignani, M
   Azzoni, C
   DAmbra, G
   Caruana, P
   DAdda, T
   DelleFave, G
   Bordi, C
TI Atrophic body gastritis: Distinct features associated with Helicobacter
   pylori infection
SO HELICOBACTER
LA English
DT Article
ID PERNICIOUS-ANEMIA; CELL HYPERFUNCTION; DUODENAL-ULCER; ACID SECRETION;
   SYDNEY SYSTEM; FOLLOW-UP; MUCOSA; CLASSIFICATION; ANTIBODIES; BOMBESIN
AB Background. Usually, atrophic body gastritis has been considered an autoimmune disease characterized by the presence of parietal cell antibodies. Previous investigations into the role of Helicobacter pylori infection have obtained conflicting results. The aim of this study was to investigate the prevalence and role of H. pylori in a prospectively investigated population of patients with corpus-predominant atrophic gastritis.
   Patients and Methods. A consecutive series of 67 newly diagnosed cases of atrophic body gastritis was derived from a screening of 326 patients with unexplained anemia or dyspepsia. Criteria for diagnosis were fasting hypergastrinemia, pentagastrin-resistant achlorhydria, and histological confirmation of body atrophy. In all 67 patients, H. pylori infection was evaluated independently by histological assay and urease test. The gastritis status of both the fundic and antral mucosa were graded according to the Sydney system. Parietal cell and intrinsic factor antibodies also were determined.
   Results. Active H. pylori infection was present in 26.8% of our patients and allowed us to identify a patient's subpopulation with a significantly smaller degree of body mucosa damage as shown by functional parameters (gastrin, gastric acid secretion, pepsinogen I) and histological assessment. In this subpopulation, a higher prevalence of gastric cancer familial history was found. Presence elf parietal cell antibodies showed a similar prevalence in H. pylori-positive and H. pylori-negative patients (61.1% vs. 69.4%) and was not associated with significant functional and histological differences. Cure of infection determined an evident improvement of corporal atrophy as well as a reduction of hypergastrinemia.
   Conclusion. Active H. pylori infection, a potential cause of oxyntic gland atrophy, is found in one-fourth of patients with newly diagnosed atrophic body gastritis.
C1 UNIV ROMA LA SAPIENZA,GASTROENTEROL UNIT,ROME,ITALY.
   UNIV ROMA LA SAPIENZA,SEMEIOT CHIRURG 4,ROME,ITALY.
   UNIV PARMA,DEPT PATHOL,I-43100 PARMA,ITALY.
C3 Sapienza University Rome; Sapienza University Rome; University of Parma;
   University Hospital of Parma
RI Annibale, Bruno/A-5372-2008; Di Maio, Massimo/K-9990-2016
OI Marignani, Massimo/0000-0002-8912-9972; annibale,
   bruno/0000-0001-9120-5957
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NR 33
TC 90
Z9 90
U1 0
U2 1
PU BLACKWELL SCIENCE INC
PI MALDEN
PA 350 MAIN ST, MALDEN, MA 02148
SN 1083-4389
J9 HELICOBACTER
JI Helicobacter
PD JUN
PY 1997
VL 2
IS 2
BP 57
EP 64
DI 10.1111/j.1523-5378.1997.tb00060.x
PG 8
WC Gastroenterology & Hepatology; Microbiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology; Microbiology
GA XE194
UT WOS:A1997XE19400001
PM 9432330
DA 2025-06-01
ER

PT J
AU Jacob, PJ
   Manju, SL
   Ethiraj, KR
   Elias, G
AF Jacob, Jaismy P.
   Manju, S. L.
   Ethiraj, K. R.
   Elias, Geetha
TI Safer anti-inflammatory therapy through dual COX-2/5-LOX inhibitors: A
   structure-based approach
SO EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES
LA English
DT Review
DE Inflammation; Cyclooxygenase-2; 5-Lipoxygenase; Leukotrienes; Arthritis
ID PHARMACOPHORE BIOLOGICAL EVALUATION; ARACHIDONIC-ACID METABOLISM;
   CYCLOOXYGENASE-2/5-LIPOXYGENASE INHIBITORS;
   7-TERT-BUTYL-2,3-DIHYDRO-3,3-DIMETHYLBENZOFURAN DERIVATIVES;
   SELECTIVE-INHIBITION; 5-LOX INHIBITORS; ANALGESIC AGENTS; 5-LIPOXYGENASE
   INHIBITOR; PROSTAGLANDIN SYNTHESIS; MOLECULAR DOCKING
AB Inflammatory mediators of the arachidonic acid cascade from cyclooxygenase (COX) and lipoxygenase (LOX) pathways are primarily responsible for many diseases in human beings. Chronic inflammation is associated with the pathogenesis and progression of cancer, arthritis, autoimmune, cardiovascular and neurological diseases. Traditional non-steroidal anti-inflammatory agents (tNSAIDs) inhibit cyclooxygenase pathway non-selectively and produce gastric mucosal damage due to COX-1 inhibition and allergic reactions and bronchospasm resulting from increased leukotriene levels. 'Coxibs' which are selective COX-2 inhibitors cause adverse cardiovascular events. Inhibition of any of these biosynthetic pathways could switch the metabolism to the other, which can lead to fatal side effects. Hence, there is undoubtedly an urgent need for new anti-inflammatory agents having dual mechanism that prevent release of both prostaglandins and leukotrienes. Though several molecules have been synthesized with this objective, their unfavourable toxicity profile prevented them from being used in clinics. Here, this integrative review attempts to identify the promising pharmacophore that serves as dual inhibitors of COX-2/5-LOX enzymes with improved safety profile. A better acquaintance of structural features that balance safety and efficacy of dual inhibitors would be a different approach to the process of understanding and interpreting the designing of novel anti-inflammatory agents.
C1 [Jacob, Jaismy P.; Manju, S. L.; Ethiraj, K. R.] Vellore Inst Technol, Sch Adv Sci, Dept Chem, Vellore, Tamil Nadu, India.
   [Elias, Geetha] St James Coll Pharmaceut Sci, Dept Pharmaceut Chem, Chalakudy, Kerala, India.
C3 Vellore Institute of Technology (VIT); VIT Vellore
RP Manju, SL (corresponding author), Vellore Inst Technol, Sch Adv Sci, Dept Chem, Vellore, Tamil Nadu, India.
EM slmanju@vit.ac.in
RI RADHAKRISHNAN, ETHIRAJ/C-2902-2012
OI , Ethiraj kr/0000-0003-4637-7041
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NR 143
TC 134
Z9 137
U1 6
U2 55
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0928-0987
EI 1879-0720
J9 EUR J PHARM SCI
JI Eur. J. Pharm. Sci.
PD AUG 30
PY 2018
VL 121
BP 356
EP 381
DI 10.1016/j.ejps.2018.06.003
PG 26
WC Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pharmacology & Pharmacy
GA GL5QM
UT WOS:000437223600038
PM 29883727
DA 2025-06-01
ER

PT J
AU Colldén, G
   Tschöp, MH
   Müller, TD
AF Collden, Gustav
   Tschoep, Matthias H.
   Mueller, Timo D.
TI Therapeutic Potential of Targeting the Ghrelin Pathway
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE ghrelin; therapy; pathology; inflammation; anorexia
ID DES-ACYL GHRELIN; ACUTE LUNG INJURY; HORMONE SECRETAGOGUE RECEPTOR;
   DIET-INDUCED OBESITY; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; INDUCED
   PULMONARY-HYPERTENSION; ANOREXIA-CACHEXIA SYNDROME; SPINAL-CORD
   MOTONEURONS; VENTRAL TEGMENTAL AREA; STIMULATES FOOD-INTAKE
AB Ghrelin was discovered in 1999 as the endogenous ligand of the growth-hormone secretagogue receptor 1a (GHSR1a). Since then, ghrelin has been found to exert a plethora of physiological effects that go far beyond its initial characterization as a growth hormone (GH) secretagogue. Among the numerous well-established effects of ghrelin are the stimulation of appetite and lipid accumulation, the modulation of immunity and inflammation, the stimulation of gastric motility, the improvement of cardiac performance, the modulation of stress, anxiety, taste sensation and reward-seeking behavior, as well as the regulation of glucose metabolism and thermogenesis. Due to a variety of beneficial effects on systems' metabolism, pharmacological targeting of the endogenous ghrelin system is widely considered a valuable approach to treat metabolic complications, such as chronic inflammation, gastroparesis or cancer-associated anorexia and cachexia. The aim of this review is to discuss and highlight the broad pharmacological potential of ghrelin pathway modulation for the treatment of anorexia, cachexia, sarcopenia, cardiopathy, neurodegenerative disorders, renal and pulmonary disease, gastrointestinal (GI) disorders, inflammatory disorders and metabolic syndrome.
C1 [Collden, Gustav; Tschoep, Matthias H.; Mueller, Timo D.] German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Munchen, Inst Diabet & Obes, D-85764 Neuherberg, Germany.
   [Collden, Gustav; Tschoep, Matthias H.; Mueller, Timo D.] German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Munchen, Helmholtz Diabet Ctr, D-85764 Neuherberg, Germany.
   [Tschoep, Matthias H.] Tech Univ Munich, Div Metab Dis, Dept Med, D-80333 Munich, Germany.
   [Mueller, Timo D.] Inst Diabet & Obes, Business Campus Garching Hochbruck,Parkring 13, D-85748 Garching, Germany.
C3 Helmholtz Association; Helmholtz-Center Munich - German Research Center
   for Environmental Health; Helmholtz Association; Helmholtz-Center Munich
   - German Research Center for Environmental Health; Technical University
   of Munich
RP Müller, TD (corresponding author), German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Munchen, Inst Diabet & Obes, D-85764 Neuherberg, Germany.; Müller, TD (corresponding author), German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Munchen, Helmholtz Diabet Ctr, D-85764 Neuherberg, Germany.; Müller, TD (corresponding author), Inst Diabet & Obes, Business Campus Garching Hochbruck,Parkring 13, D-85748 Garching, Germany.
EM gustav.collden@helmholtz-muenchen.de;
   matthias.tschoep@helmholtz-muenchen.de;
   timo.mueller@helmholtz-muenchen.de
RI Tschoep, Matthias/I-5443-2014; Müller, Timo/AAZ-4445-2020
OI Muller, Timo/0000-0002-0624-9339
FU Alexander von Humboldt Foundation; Helmholtz Alliance Imaging and Curing
   Environmental Metabolic Diseases (ICEMED); Helmholtz Initiative on
   Personalized Medicine iMed by the Helmholtz Association; Helmholtz
   cross-program topic "Metabolic Dysfunction"; German Research Foundation
   [DFG-TS226/1-1, DFG-TS226/3-1, SFB1123]; European Research Council ERC
   AdG HypoFlam [695054]
FX This work was supported in part by funding from the Alexander von
   Humboldt Foundation, the Helmholtz Alliance Imaging and Curing
   Environmental Metabolic Diseases (ICEMED) and the Helmholtz Initiative
   on Personalized Medicine iMed by the Helmholtz Association and the
   Helmholtz cross-program topic "Metabolic Dysfunction". This work was
   further supported by grants from the German Research Foundation
   DFG-TS226/1-1, DFG-TS226/3-1, SFB1123, and the European Research Council
   ERC AdG HypoFlam No. 695054. The figures were made by using material
   from Servier Medical Art (Servier) under consideration of a Creative
   Commons Attribution 3.0 Unported License, as well as material from
   Wikimedia Commons. Timo D. Muller and Gustav Collden have no conflicts
   of interest, financial or otherwise. Matthias H. Tschop is a scientific
   advisor for Novo Nordisk, Bionorica SE and Erx Biotech.
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NR 300
TC 113
Z9 125
U1 2
U2 36
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD APR
PY 2017
VL 18
IS 4
AR 798
DI 10.3390/ijms18040798
PG 29
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA EW6SA
UT WOS:000402639400122
PM 28398233
OA Green Submitted, Green Published, gold
DA 2025-06-01
ER

PT J
AU Pikkarainen, S
   Martelius, T
   Ristimäki, A
   Siitonen, S
   Seppänen, MRJ
   Färkkilä, M
AF Pikkarainen, Sampsa
   Martelius, Timi
   Ristimaki, Ari
   Siitonen, Sanna
   Seppanen, Mikko R. J.
   Farkkila, Martti
TI A High Prevalence of Gastrointestinal Manifestations in Common Variable
   Immunodeficiency
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Article
ID DEFICIENCY; DISORDERS; PATHOLOGY
AB OBJECTIVES: Common variable immunodeficiency (CVID) is associated with a spectrum of autoimmune complications. We studied the prevalence of gastrointestinal (GI) manifestations and infections in patients with CVID.
   METHODS: Complete clinical data of 132 Finnish patients with CVID (106 probable and 26 possible CVID) followed up between 2007 and 2016 were collected to a structured database. Data on endoscopies, histology, and laboratory studies were retrieved from patient files.
   RESULTS: Most common referral indications were diarrhea and/or weight loss (47%-67%). Patients with probable CVID had higher fecal calprotectin and a1-antitrypsin and lower blood vitamin B12 than patients with possible CVID. Gastroscopy and colonoscopy were done to 71 (67%) and 63 (59%) patients with probable CVID, respectively. Endoscopies showed that 15% of them had chronic active gastritis and 17% atrophic gastritis and 3% had gastric adenocarcinoma. A celiac sprue-like condition was found in 7 patients (10%), of whom 3 responded to a gluten-free diet. Colonoscopies demonstrated unspecific colitis (14%), ulcerative colitis (8%), microscopic colitis (10%), and Crohn's disease (2%). Colonic polyps were noted in30% of patients, and3% had lower GI malignancies. Thirty-five patients with CVID had bacterial or parasitic gastroenteritis; chronic norovirus was detected in 4 patients with probable CVID. Patients with GI inflammation had higher levels of fecal calprotectin and blood CD81 T lymphocytes but lower counts of CD191CD271 memory B cells and/or CD191 B cells. Immunophenotype with low B-cell counts was associated with higher fecal calprotectin levels.
   DISCUSSION: Patients with CVID had a high prevalence of GI manifestations and infections of the GI tract. GI inflammation was associated with a distinct immunophenotype and elevated fecal calprotectin.
C1 [Pikkarainen, Sampsa; Farkkila, Martti] Univ Helsinki, Dept Gastroenterol, Helsinki, Finland.
   [Pikkarainen, Sampsa; Martelius, Timi; Siitonen, Sanna; Seppanen, Mikko R. J.; Farkkila, Martti] Helsinki Univ Hosp, Helsinki, Finland.
   [Martelius, Timi; Seppanen, Mikko R. J.] Univ Helsinki, Adult Immunodeficiency Unit, Infect Dis Inflammat Ctr, Helsinki, Finland.
   [Ristimaki, Ari] Hosp Dist Helsinki, Dept Pathol, Helsinki, Finland.
   [Ristimaki, Ari] Helsinki Univ Hosp, Uusimaa Lab, Helsinki, Finland.
   [Ristimaki, Ari] Univ Helsinki, Genome Scale Biol Res Program, Res Programs Unit, Helsinki, Finland.
   [Ristimaki, Ari] Univ Helsinki, Medicum, Helsinki, Finland.
   [Siitonen, Sanna] Hosp Dist Helsinki, Lab Serv, Helsinki, Finland.
   [Siitonen, Sanna] Univ Helsinki, Uusimaa Lab, Helsinki, Finland.
   [Seppanen, Mikko R. J.] Univ Helsinki, Rare Dis Ctr, Childrens Hosp, Helsinki, Finland.
   [Seppanen, Mikko R. J.] Univ Helsinki, Pediat Res Ctr, Childrens Hosp, Helsinki, Finland.
C3 University of Helsinki; University of Helsinki; Helsinki University
   Central Hospital; University of Helsinki; University of Helsinki;
   Helsinki University Central Hospital; University of Helsinki; University
   of Helsinki; University of Helsinki; University of Helsinki; University
   of Helsinki
RP Färkkilä, M (corresponding author), Univ Helsinki, Dept Gastroenterol, Helsinki, Finland.; Seppänen, MRJ; Färkkilä, M (corresponding author), Helsinki Univ Hosp, Helsinki, Finland.; Seppänen, MRJ (corresponding author), Univ Helsinki, Adult Immunodeficiency Unit, Infect Dis Inflammat Ctr, Helsinki, Finland.; Seppänen, MRJ (corresponding author), Univ Helsinki, Rare Dis Ctr, Childrens Hosp, Helsinki, Finland.; Seppänen, MRJ (corresponding author), Univ Helsinki, Pediat Res Ctr, Childrens Hosp, Helsinki, Finland.
EM mikko.seppanen@hus.fi; martti.farkkila@hus.fi
RI Seppänen, Mikko R J/HGU-4196-2022; Färkkilä, Martti/AAG-6970-2021
OI Farkkila, Martti/0000-0002-0250-8559; Pikkarainen,
   Sampsa/0000-0001-8506-0480; Seppanen, Mikko/0000-0001-9733-3650
FU Finnish Medical Foundation; Helsinki University Hospital Research Funds;
   Sigrid Juselius Foundation; Mary and Georg C. Ehrnrooth Foundation
FX M.S. and T.M. have received honoraria from the CSL Behring, but this
   work was independent of the honoraria. The remaining authors declare no
   competing financial interests. This work was supported by the Finnish
   Medical Foundation, the Helsinki University Hospital Research Funds, the
   Sigrid Juselius Foundation, and the Mary and Georg C. Ehrnrooth
   Foundation.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD APR
PY 2019
VL 114
IS 4
BP 648
EP 655
DI 10.14309/ajg.0000000000000140
PG 8
WC Gastroenterology & Hepatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Gastroenterology & Hepatology
GA HR8KA
UT WOS:000463404500018
PM 30747770
OA Green Published
DA 2025-06-01
ER

PT J
AU Rose-John, S
   Jenkins, BJ
   Garbers, C
   Moll, JM
   Scheller, J
AF Rose-John, Stefan
   Jenkins, Brendan J.
   Garbers, Christoph
   Moll, Jens M.
   Scheller, Juergen
TI Targeting IL-6 trans-signalling: past, present and future prospects
SO NATURE REVIEWS IMMUNOLOGY
LA English
DT Review
ID SOLUBLE INTERLEUKIN-6 RECEPTOR; MOLECULAR-CLONING; GASTRIC
   TUMORIGENESIS; PROTEOLYTIC CLEAVAGE; RHEUMATOID-ARTHRITIS;
   MONOCLONAL-ANTIBODY; SERUM INTERLEUKIN-6; DESIGNER CYTOKINE; STAT3
   ACTIVATION; EPITHELIAL-CELLS
AB This Review details the discovery of the interleukin-6 (IL-6) trans-signalling pathway and the subsequent development of biologics that specifically inhibit this pathway. Emerging evidence suggests that specifically targeting IL-6 trans-signalling can reduce pathological disease-promoting activities of IL-6 without blocking the protective actions of IL-6 in infection and tissue repair.
   Interleukin-6 (IL-6) is a key immunomodulatory cytokine that affects the pathogenesis of diverse diseases, including autoimmune diseases, chronic inflammatory conditions and cancer. Classical IL-6 signalling involves the binding of IL-6 to the membrane-bound IL-6 receptor alpha-subunit (hereafter termed 'mIL-6R') and glycoprotein 130 (gp130) signal-transducing subunit. By contrast, in IL-6 trans-signalling, complexes of IL-6 and the soluble form of IL-6 receptor (sIL-6R) signal via membrane-bound gp130. A third mode of IL-6 signalling - known as cluster signalling - involves preformed complexes of membrane-bound IL-6-mIL-6R on one cell activating gp130 subunits on target cells. Antibodies and small molecules have been developed that block all three forms of IL-6 signalling, but in the past decade, IL-6 trans-signalling has emerged as the predominant pathway by which IL-6 promotes disease pathogenesis. The first selective inhibitor of IL-6 trans-signalling, sgp130, has shown therapeutic potential in various preclinical models of disease and olamkicept, a sgp130Fc variant, had promising results in phase II clinical studies for inflammatory bowel disease. Technological developments have already led to next-generation sgp130 variants with increased affinity and selectivity towards IL-6 trans-signalling, along with indirect strategies to block IL-6 trans-signalling. Here, we summarize our current understanding of the biological outcomes of IL-6-mediated signalling and the potential for targeting this pathway in the clinic.
C1 [Rose-John, Stefan] Univ Kiel, Biochem Inst, Med Fac, Kiel, Germany.
   [Jenkins, Brendan J.] Hudson Inst Med Res, Ctr Innate Immun & Infect Dis, Clayton, Vic, Australia.
   [Jenkins, Brendan J.] Monash Univ, Fac Med Nursing & Hlth Sci, Dept Mol & Translat Sci, Clayton, Vic, Australia.
   [Garbers, Christoph] Otto von Guericke Univ, Med Fac, Dept Pathol, Magdeburg, Germany.
   [Garbers, Christoph] Otto von Guericke Univ, Hlth Campus Immunol Infectiol & Inflammat GC I3, Magdeburg, Germany.
   [Garbers, Christoph] Otto von Guericke Univ, Ctr Hlth & Med Prevent CHaMP, Magdeburg, Germany.
   [Moll, Jens M.; Scheller, Juergen] Heinrich Heine Univ, Inst Biochem & Mol Biol 2, Med Fac, Dusseldorf, Germany.
C3 University of Kiel; Hudson Institute of Medical Research; Monash
   University; Otto von Guericke University; Otto von Guericke University;
   Otto von Guericke University; Heinrich Heine University Dusseldorf
RP Scheller, J (corresponding author), Heinrich Heine Univ, Inst Biochem & Mol Biol 2, Med Fac, Dusseldorf, Germany.
EM jscheller@hhu.de
RI jenkins, brendan/J-7854-2012; Garbers, Christoph/D-9932-2015; Rose-John,
   Stefan/A-7998-2010
OI Garbers, Christoph/0000-0003-4939-6950; Rose-John,
   Stefan/0000-0002-7519-3279; Jenkins, Brendan/0000-0002-7552-4656
FU Deutsche Forschungsgemeinschaft [SCHE907/5-1, SCHE907/6-1, 125440785,
   SFB877]; Deutsche Forschungsgemeinschaft, Bonn, Germany [CRC877,
   CRC841]; German Cancer Aid (Deutsche Krebshilfe);
   German-Israeli-Foundation (GIF); Cluster of Excellence Precision
   Medicine in Chronic Inflammation'; United States Department of Defense
   Lung Cancer Research Program Idea Development Award [LC170062]
FX C.G. was supported by grants from the Deutsche Forschungsgemeinschaft
   (No. 125440785, SFB877, A10 and A14). J.S. was supported by grants from
   the Deutsche Forschungsgemeinschaft (SCHE907/5-1 and SCHE907/6-1).
   S.R.-J. was supported by the Deutsche Forschungsgemeinschaft, Bonn,
   Germany (CRC877 (Proteolysis as a Regulatory Event in Pathophysiology;
   project A1), CRC841 (Liver inflammation; project C1), German Cancer Aid
   (Deutsche Krebshilfe), German-Israeli-Foundation (GIF) and the Cluster
   of Excellence Precision Medicine in Chronic Inflammation'. B.J.J. was
   supported by a United States Department of Defense Lung Cancer Research
   Program Idea Development Award (LC170062)
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NR 209
TC 230
Z9 241
U1 47
U2 152
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 1474-1733
EI 1474-1741
J9 NAT REV IMMUNOL
JI Nat. Rev. Immunol.
PD OCT
PY 2023
VL 23
IS 10
BP 666
EP 681
DI 10.1038/s41577-023-00856-y
EA APR 2023
PG 16
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA S6YR6
UT WOS:000970705300001
PM 37069261
OA Bronze, Green Published
HC Y
HP Y
DA 2025-06-01
ER

PT J
AU Perceguetti, EIP
   Chiocchetti, GDE
   Baptista, DP
   Gigante, ML
   Macedo, JA
AF Perceguetti, Evelyn Ildefonso Press
   Chiocchetti, Gabriela de Matuoka e
   Baptista, Debora Parra
   Gigante, Mirna Lucia
   Macedo, Juliana Alves
TI Does milk prevent or promote inflammation? Insights from in
   vitro assays
SO FOOD BIOSCIENCE
LA English
DT Article
DE Milk; Intestinal inflammation; Thermal processing; Homogenization; In
   vitro digestion; Caco-2; Raw 264.7
ID MAILLARD REACTION-PRODUCTS; BETA-CASEIN; GASTRIC DIGESTION; BOVINE
   CASEINS; FAT GLOBULES; PROTEIN; IDENTIFICATION; COAGULATION;
   TEMPERATURE; CONSUMPTION
AB Milk is widely consumed worldwide due to its high nutritional value, having possible protection against infections and anti-inflammatory activity. Conversely, milk's vast microbiota reduces its shelf life and can pose risks to human health. Milk processing can introduce changes to its components, leading to speculation about its inflammatory potential. Chronic inflammation is associated with the development of a variety of metabolic, autoimmune, and degenerative diseases, being essential to understand the role of food in its etiology. This study aimed to investigate processed milk samples for their potential to modulate inflammatory responses in an intestinal in vitro model, contributing to the current debate about the effects of processed milk's consumption. Raw, pasteurized, and ultra -high temperature (UHT) homogenized milk were subjected to an in vitro simulated digestion process and human colorectal adenocarcinoma cells (Caco-2) and Abelson murine leukemia macrophages (Raw 264.7) were cultivated in vitro and challenged with milk samples from before and after digestion process. Post -digestion, pasteurized milk decreased the production of IL -8 in 59%, indicating an antiinflammatory activity. UHT homogenized milk increased the production of assessed cytokines up to 238%, showing a pro -inflammatory response. Raw milk presented a 321% increase in IL -6 production, indicating a proinflammatory effect, as observed in processed milk samples. These new findings suggest that consumption of raw milk can be potentially inflammatory due to its vast microbiota, in addition to the well-known risks of its consumption and, that processed milk can prevent or promote inflammation according to the type of processing to which it was submitted.
C1 [Perceguetti, Evelyn Ildefonso Press; Chiocchetti, Gabriela de Matuoka e; Macedo, Juliana Alves] State Univ Campinas UNICAMP, Fac Food Engn, Dept Food & Nutr, PC 6121, Campinas, SP, Brazil.
   [Baptista, Debora Parra; Gigante, Mirna Lucia] State Univ Campinas UNICAMP, Fac Food Engn, Dept Food Engn & Technol, PC 6121, Campinas, SP, Brazil.
C3 Universidade Estadual de Campinas; Universidade Estadual de Campinas
RP Perceguetti, EIP (corresponding author), State Univ Campinas UNICAMP, Fac Food Engn, Dept Food & Nutr, PC 6121, Campinas, SP, Brazil.
EM e263063@dac.unicamp.br
RI Macedo, Juliana/H-1961-2012; Parra Baptista, Debora/B-9686-2018; de
   Matuoka e Chiocchetti, Gabriela/S-5219-2018
OI Macedo, Juliana/0000-0001-7504-8111; Parra Baptista,
   Debora/0000-0002-4445-5643; de Matuoka e Chiocchetti,
   Gabriela/0000-0001-7942-3054
FU CNPq [130506/2020-6]; CAPES
FX This work was supported by CNPq [grant number 130506/2020-6, 2020] and
   CAPES.
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NR 62
TC 3
Z9 3
U1 5
U2 8
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 2212-4292
EI 2212-4306
J9 FOOD BIOSCI
JI Food Biosci.
PD FEB
PY 2024
VL 57
AR 103572
DI 10.1016/j.fbio.2024.103572
EA JAN 2024
PG 9
WC Food Science & Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology
GA GR1S9
UT WOS:001154312700001
DA 2025-06-01
ER

PT J
AU Saka, B
   Memis, B
   Seven, IE
   Pehlivanoglu, B
   Balci, S
   Bagci, P
   Reid, M
   Dursun, N
   Escalano, OT
   Roa, JC
   Araya, JC
   Kong, SY
   Basturk, O
   Koshiol, J
   Adsay, NV
AF Saka, Burcu
   Memis, Bahar
   Seven, Ipek Erbarut
   Pehlivanoglu, Burcin
   Balci, Serdar
   Bagci, Pelin
   Reid, Michelle
   Dursun, Nevra
   Tapia Escalano, Oscar
   Carlos Roa, Juan
   Carlos Araya, Juan
   Kong, So Yeon
   Basturk, Olca
   Koshiol, Jill
   Adsay, N. Volkan
TI Follicular Cholecystitis: Reappraisal of Incidence, Definition, and
   Clinicopathologic Associations in an Analysis of 2550 Cholecystectomies
SO INTERNATIONAL JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE cholecystectomy; follicular cholecystitis; histology
ID LYMPHOPLASMACYTIC CHRONIC CHOLECYSTITIS; BILIARY-TRACT DISEASE;
   HELICOBACTER-PYLORI; DISTINCTIVE FORM; GALLBLADDER; PANCREATITIS;
   AUTOIMMUNE; PREVALENCE; MUCOSA
AB Context.
   Follicular cholecystitis (FC) is a poorly characterized entity.
   Objective.
   To determine its frequency/clinicopathologic associations.
   Design.
   A total of 2550 cholecystectomy specimens were examined. Two hundred three of these were consecutive routine cholecystectomies submitted entirely for microscopic examination to determine the relative frequency of incidental pathologies in gallbladders (GBs). The remainder had representative sampling. Underlying conditions were nonobstructive pathologies (1270 nonspecific cholecystitis), obstructive (62 distal biliary tract tumors, 35 primary sclerosing cholangitis, and 31 autoimmune pancreatitis), and neoplastic (n = 949). FC was defined as 3 distinct lymphoid follicles (LFs)/centimeter.
   Results.
   In the GBs totally submitted for microscopic examination, the true frequency of FC was found to be 2.5% (5/203), and in the representatively sampled group, it was 1.9%, with similar frequencies in nonobstructive, obstructive, and neoplastic cases (2.3%, 3.1%, and 1.3%, respectively, P = .77). When the 39 FC in nonneoplastic GBs contrasted with ordinary chronic cholecystitis, they were associated with older age (68 vs 49 years, P < .0001), similar gallstone frequency (68 vs 81%), female/male ratio (2.7 vs 2.6), and wall thickness (4 mm for both). None had lymphoma/parasites/Salmonella infection. Of 17 cases who had undergone gastric biopsy, 5 had chronic gastritis (2 with Helicobacter pylori). Microscopically, the LFs were the main inflammatory process often with minimal intervening inflammation. IgG4-positive plasma cell density was low (<10/high-power field) in 21/24(87.5%) cases.
   Conclusions.
   Follicular cholecystitis is seen in 2% of cholecystectomies, typically in significantly older patients, suggesting a deranged immune response. A third of the patients reveal biopsy-proven gastritis. FC does not seem to be associated with autoimmunity, lymphoma, or obstructive pathologies.
C1 [Saka, Burcu] Istanbul Medipol Univ, Istanbul, Turkey.
   [Memis, Bahar; Pehlivanoglu, Burcin; Balci, Serdar; Reid, Michelle; Kong, So Yeon] Emory Univ, Atlanta, GA 30322 USA.
   [Seven, Ipek Erbarut; Bagci, Pelin] Marmara Univ, Istanbul, Turkey.
   [Dursun, Nevra] Istanbul Res & Training Hosp, Istanbul, Turkey.
   [Tapia Escalano, Oscar] Univ La Frontera, Temuco, Chile.
   [Carlos Roa, Juan] Pontificia Univ Catolica Chile, Santiago, Chile.
   [Carlos Araya, Juan] Hosp Dr Hernan Henriquez Aravena, Temuco, Chile.
   [Basturk, Olca] Mem Sloan Kettering Canc Ctr, 1275 York Ave, New York, NY 10021 USA.
   [Koshiol, Jill] NCI, NIH, Rockville, MD USA.
   [Adsay, N. Volkan] Koc Univ, Istanbul, Turkey.
C3 Istanbul Medipol University; Emory University; Marmara University;
   Istanbul Training & Research Hospital; Universidad de La Frontera;
   Pontificia Universidad Catolica de Chile; Memorial Sloan Kettering
   Cancer Center; National Institutes of Health (NIH) - USA; NIH National
   Cancer Institute (NCI); Koc University
RP Adsay, NV (corresponding author), Koc Univ, Dept Pathol, Sch Med, Davutpasa Caddesi 4, TR-34010 Istanbul, Turkey.
EM vadsay@kuh.ku.edu.tr
RI Pehlivanoglu, Burcin/AAZ-7405-2020; Adsay, Volkan/N-7130-2017; Basturk,
   Olca/N-7214-2017; MEMIS, BAHAR/JWA-5589-2024; Roa, Juan/K-4749-2014;
   Saka, Burcu/R-3487-2016; Koshiol, Jill/L-8686-2014; BALCI,
   Serdar/B-6401-2011; Araya-Orostica, Juan/Q-5575-2018
OI Memis, Bahar/0000-0002-8809-5846; Koshiol, Jill/0000-0002-3832-6204;
   BALCI, Serdar/0000-0002-7852-3851; Roa, Juan Carlos/0000-0001-8313-8774;
   Araya-Orostica, Juan/0000-0003-3501-8203
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NR 29
TC 7
Z9 7
U1 1
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1066-8969
EI 1940-2465
J9 INT J SURG PATHOL
JI Int. J. Surg. Pathol.
PD DEC
PY 2020
VL 28
IS 8
BP 826
EP 834
AR 1066896920924079
DI 10.1177/1066896920924079
EA MAY 2020
PG 9
WC Pathology; Surgery
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology; Surgery
GA OO4QC
UT WOS:000534596700001
PM 32423360
DA 2025-06-01
ER

PT J
AU Inagaki, H
   Chan, JKC
   Ng, JWM
   Okabe, M
   Yoshino, T
   Okamoto, M
   Ogawa, H
   Matsushita, H
   Yokose, T
   Matsuno, Y
   Nakamura, N
   Nagasaka, T
   Ueda, R
   Eimoto, T
   Nakamura, S
AF Inagaki, H
   Chan, JKC
   Ng, JWM
   Okabe, M
   Yoshino, T
   Okamoto, M
   Ogawa, H
   Matsushita, H
   Yokose, T
   Matsuno, Y
   Nakamura, N
   Nagasaka, T
   Ueda, R
   Eimoto, T
   Nakamura, S
TI Primary thymic extranodal marginal-zone B-Cell lymphoma of
   mucosa-associated lymphoid tissue type exhibits distinctive
   clinicopathological and molecular features
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID SMALL-INTESTINAL DISEASE; HELICOBACTER-PYLORI; SJOGRENS-SYNDROME;
   MALT-TYPE; MALIGNANT-LYMPHOMA; GASTRIC LYMPHOMA; T(11/18)(Q21,Q21);
   ERADICATION; PATIENT; GENE
AB Extranodal marginal-zone B-cell lymphoma (MZBL) of mucosa-associated lymphoid tissue (MALT) arising in the thymus is rare, with the largest series in the literature including only three cases. In the present study, we investigated 15 cases of thymic MALT lymphoma. to systematically characterize its clinical, histopathological, and molecular features. There was a marked female predilection (male:female = 1:4), with a mean age of 55 years at diagnosis. There was a strong association with autoimmune disease, especially Sjogren's syndrome. Histologically, the thymic lymphoma showed the characteristic morphological features of extranodal MZBL of MALT type. Cysts were common. Prominent lymphoepithelial lesions were formed by centrocyte-like cells infiltrating and expanding the Hassall's corpuscles and epithelium lining the cysts. Plasmacytic differentiation was apparent in all cases. Notably, 13 of 15 cases expressed immunoglobulin (Ig) A phenotype; IgA expression in thymic MALT lymphoma was in striking contrast with the IgM phenotype observed in most of the Sjogren's syndrome-associated MZBLs and MALT lymphomas at other sites. Epstein-Barr virus was absent, and AP12-MALT1 gene fusion, a recently reported MALT lymphoma-specific gene abnormality, was not detected in any case. Although one patient died of disease 85 months after the diagnosis, other patients were alive with overall 3-year and 5-year survival rates being 89% and 83%, respectively. Among the 22 patients reported previously and in the present series, at least 17 patients (77%) were Asians. These data indicate that thymic MALT lymphoma may represent a distinct subgroup of MALT lymphoma characterized by apparent predilection for Asians, a strong association with autoiminune disease, frequent presence of cysts, consistent plasma cell differentiation, tumor cells expressing IgA phenotype, and consistent lack of AP12-MALT1 gene fusion.
C1 Nagoya City Univ, Sch Med, Dept Pathol, Mizuho Ku, Nagoya, Aichi 4678601, Japan.
   Nagoya City Univ, Sch Med, Dept Med, Nagoya, Aichi 467, Japan.
   Okayama Univ, Sch Med, Dept Pathol, Okayama 700, Japan.
   Fujita Univ, Sch Med, Dept Hematol, Toyoake, Aichi, Japan.
   Seirei Mikatagahara Hosp, Dept Pathol, Hamamatsu, Shizuoka, Japan.
   Toranomon Gen Hosp, Dept Pathol, Tokyo, Japan.
   Natl Canc Ctr Res Inst E, Div Pathol, Kashiwa, Chiba, Japan.
   Natl Canc Ctr, Div Clin Lab, Tokyo, Japan.
   Fukushima Med Univ, Sch Med, Dept Pathol, Fukushima, Japan.
   Nagoya Univ Hosp, Div Pathol, Nagoya, Aichi, Japan.
   Aichi Canc Ctr Hosp, Dept Pathol, Nagoya, Aichi 464, Japan.
   Queen Elizabeth Hosp, Dept Pathol, Hong Kong, Hong Kong, Peoples R China.
   Queen Elizabeth Hosp, Dept Clin Oncol, Hong Kong, Hong Kong, Peoples R China.
C3 Nagoya City University; Nagoya City University; Okayama University;
   Fujita Health University; Toranomon Hospital; National Cancer Center -
   Japan; National Cancer Center - Japan; Fukushima Medical University;
   Nagoya University; Aichi Cancer Center
RP Nagoya City Univ, Sch Med, Dept Pathol, Mizuho Ku, 1 Kawasumi, Nagoya, Aichi 4678601, Japan.
EM hinagaki@med.nagoya-cu.ac.jp
RI Nakamura, Shigeo/I-1571-2012; Nagasaka, Takashi/MDT-9320-2025
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NR 48
TC 77
Z9 88
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA STE 800, 230 PARK AVE, NEW YORK, NY 10169 USA
SN 0002-9440
EI 1525-2191
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2002
VL 160
IS 4
BP 1435
EP 1443
DI 10.1016/S0002-9440(10)62569-2
PG 9
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 542FY
UT WOS:000175033900025
PM 11943727
OA Green Accepted, Bronze, Green Published
DA 2025-06-01
ER

PT J
AU Moradali, MF
   Mostafavi, H
   Ghods, S
   Hedjaroude, GA
AF Moradali, Mohammad-Fata
   Mostafavi, Hossein
   Ghods, Shirin
   Hedjaroude, Ghorban-Ali
TI Immunomodulating and anticancer agents in the realm of macromycetes
   fungi (macrofungi)
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Review
DE macrofungi; immunomodulating; antitumor; glycopeptide/protein complexes;
   Fips
ID PROTEIN-BOUND POLYSACCHARIDE; PATTERN-RECOGNITION RECEPTORS;
   AGARICUS-BLAZEI MURRILL; GASTRIC-CANCER PATIENTS; LING ZHI-8 LZ-8;
   GANODERMA-LUCIDUM; BETA-GLUCAN; CYTOKINE PRODUCTION; GRIFOLA-FRONDOSA;
   CORIOLUS-VERSICOLOR
AB Nowadays macrofungi are distinguished as important natural resources of immunomodulating and anticancer agents and with regard to the increase in diseases involving immune dysfunction, cancer, autoimmune conditions in recent years, applying such immunomodulator agents especially with the natural original is vital. These compounds belong mainly to polysaccharides especially P-D-glucan derivates, glycopeptide/protein complexes (polysaccharide-peptide/protein complexes), proteoglycans, proteins and triterpenoids. Among polysaccharides, beta(1 -> 3)-D-glucans and their peptide/protein derivates and among proteins, fungal immunomodulatory proteins (Fips) have more important role in immunomodulating and antitumor activities. Immunomodulating and antitumor activity of these metabolites related to their effects to act of immune effecter cells such as hematpoietic stem cells, lymphocytes, macrophages, T cells, dendritic cells (DCs), and natural killer (NK) cells involved in the innate and adaptive immunity, resulting in the production of biologic response modifiers. In this review we have introduced the medicinal mushrooms' metabolites with immunomoduling and antitumor activities according to immunological evidences and then demonstrated their effects on innate and adaptive immunity and also the mechanisms of activation of immune responses and signaling cascade. In addition, their molecular structure and their relation to these activities have been shown. The important instances of these metabolites along with their immunomodulating and/or antitumor activities isolated from putative medicinal mushrooms are also introduced. (C) 2007 Elsevier B.V. All rights reserved.
C1 Tabriz Univ, Fac Chem, Organ Chem & Biochem Dept, Tabriz, Iran.
   Univ Tehran, Fac Agr, Plant Protect Dept, Karaj, Iran.
C3 University of Tabriz; University of Tehran
RP Mostafavi, H (corresponding author), Tabriz Univ, Fac Chem, Organ Chem & Biochem Dept, Tabriz, Iran.
EM hmostafavi1@excite.com
RI mostafavi, hossein/ABH-1481-2020
OI Ghods, Shirin/0009-0006-5743-5883
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NR 132
TC 384
Z9 439
U1 2
U2 220
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD JUN
PY 2007
VL 7
IS 6
BP 701
EP 724
DI 10.1016/j.intimp.2007.01.008
PG 24
WC Immunology; Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology; Pharmacology & Pharmacy
GA 172QE
UT WOS:000246818200001
PM 17466905
DA 2025-06-01
ER

PT J
AU Kiesewetter, B
   Lukas, J
   Dolak, W
   Simonitsch-Klupp, I
   Mayerhoefer, ME
   Raderer, M
AF Kiesewetter, Barbara
   Lukas, Julius
   Dolak, Werner
   Simonitsch-Klupp, Ingrid
   Mayerhoefer, Marius E.
   Raderer, Markus
TI Gender Aspects in Extranodal Marginal Zone B-Cell Lymphoma of the
   Mucosa-Associated Lymphoid Tissue: Does Sex Matter?
SO ONCOLOGY
LA English
DT Article
DE Mucosa-associated lymphoid tissue lymphoma; Extranodal lymphoma;
   Indolent lymphoma; Gender aspects; Gender medicine
ID GASTRIC MALT LYMPHOMA; SINGLE-CENTER ANALYSIS; NON-HODGKIN-LYMPHOMA;
   REPRODUCTIVE FACTORS; RITUXIMAB; HELICOBACTER; DISEASE; RISK
AB Objectives: Gender-related aspects have been investigated in a variety of tumor entities including results on sex-specific differences in non-Hodgkin lymphoma. However, there are no data on gender differences in mucosa-associated lymphoid tissue (MALT) lymphoma. Methods: We have analyzed 327 patients treated between 1999 and 2015 with a median follow-up time of 55.2 months. Results: There was a female predominance, with 197 female (60.2%) and 130 male patients (39.8%, female-to-male ratio 1.5). The mean age was comparable between female and male patients (61.2 vs. 61.7 years, p = 0.777). Female patients less frequently had gastric MALT lymphoma (31.5 vs. 39.2%), but this was not statistically significant (p = 0.149). Extragastric manifestations were equally distributed, except for parotid (p = 0.003) and breast lymphoma (n = 8, 100% female) showing a female predominance. This was most likely related to a higher rate of active autoimmune disorders in women (35.6 vs. 11.0%, p < 0.001). beta(2)-Microglobulin elevation at diagnosis occurred more often in female patients (42.8 vs. 26.0%; p = 0.008). However, this did not translate into a worse progression-free survival for female (56.0 months, 95% CI 30.1-81.9) versus male patients (49.0 months, 95% CI 25.4-72.5, p = 0.433). Overall survival did not differ between groups. Conclusion: Our data show surprisingly little differences between female and male patients with MALT lymphoma. Both sexes appeared to have well-balanced clinical features and an identical prognosis. (C) 2016 S. Karger AG, Basel
C1 [Kiesewetter, Barbara; Raderer, Markus] Med Univ, Dept Med 1, Div Clin Oncol, Vienna, Austria.
   [Lukas, Julius] Med Univ, Dept Ophthalmol, Vienna, Austria.
   [Dolak, Werner] Med Univ, Dept Med 3, Clin Div Gastroenterol & Hepatol, Vienna, Austria.
   [Simonitsch-Klupp, Ingrid] Med Univ, Dept Pathol, Vienna, Austria.
   [Mayerhoefer, Marius E.] Med Univ, Dept Radiol, Vienna, Austria.
RP Raderer, M (corresponding author), Med Univ, Dept Internal Med 1, Div Oncol, Waehringer Guertel 18-20, AT-1090 Vienna, Austria.
EM markus.raderer@meduniwien.ac.at
RI Kiesewetter, Barbara/AGX-3260-2022; Mayerhoefer, Marius/AAD-2156-2021
OI Mayerhoefer, Marius/0000-0001-8786-8686; Kiesewetter,
   Barbara/0000-0002-5490-2371
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NR 37
TC 9
Z9 10
U1 0
U2 1
PU KARGER
PI BASEL
PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND
SN 0030-2414
EI 1423-0232
J9 ONCOLOGY-BASEL
JI Oncology
PY 2016
VL 91
IS 5
BP 243
EP 250
DI 10.1159/000448218
PG 8
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA EB7WI
UT WOS:000387601400002
PM 27548082
DA 2025-06-01
ER

PT J
AU Min, XZ
   Ma, Y
   Leng, YF
   Li, XX
   Zhang, JM
   Xu, SC
   Wang, XQ
   Lv, RJ
   Guo, J
   Xing, HX
AF Min, Xiangzhen
   Ma, Yan
   Leng, Yufang
   Li, Xiaoxi
   Zhang, Jianmin
   Xu, Shoucai
   Wang, Xiuqin
   Lv, Renjun
   Guo, Jie
   Xing, Huaixin
TI Effects of perioperative low-dose naloxone on the immune system in
   patients undergoing laparoscopic-assisted total gastrectomy: a
   randomized controlled trial
SO BMC ANESTHESIOLOGY
LA English
DT Article
DE Low-dose naloxone; Immune function; Laparoscopic-assisted total
   gastrectomy; Postoperative complications
ID NALTREXONE; EFFICACY; SAFETY; PAIN
AB Background Low immune function after laparoscopic total gastrectomy puts patients at risk of infection-related complications. Low-dose naloxone (LDN) can improve the prognosis of patients suffering from chronic inflammatory diseases or autoimmune diseases. The use of LDN during perioperative procedures may reduce perioperative complications. The purpose of this study was to examine the effects of LDN on endogenous immune function in gastric cancer patients and its specific mechanisms through a randomized controlled trial. Methods Fifty-five patients who underwent laparoscopic-assisted total gastrectomy were randomly assigned to either a naloxone group (n = 23) or a nonnaloxone group (n = 22). Patients in the naloxone group received 0.05 mu g/kg-1.h(- 1)naloxone from 3 days before surgery to 5 days after surgery via a patient-controlled intravenous injection (PCIA) pump, and patients in the nonnaloxone group did not receive special treatment. The primary outcomes were the rates of postoperative complications and immune function assessed by NK cell, CD3(+) T cell, CD4(+) T cell, CD8(+) T cell, WBC count, neutrophil percentage, and IL-6 and calcitonin levels. The secondary outcomes were the expression levels of TLR4 (Toll-like receptor), IL-6 and TNF-alpha in gastric cancer tissue. Results Compared with the nonnaloxone group, the naloxone group exhibited a lower incidence of infection (in the incision, abdomen, and lungs) (P < 0.05). The numbers of NK cells and CD8(+) T cells in the naloxone group were significantly greater than those in the nonnaloxone group at 24 h after surgery (P < 0.05) and at 96 h after surgery (P < 0.05). Compared with those in the nonnaloxone group, the CD3 (+) T-cell (P < 0.05) and CD4 T+ -cell (P < 0.01) counts were significantly lower in the naloxone group 24 h after surgery. At 24 h and 96 h after surgery, the WBC count (P < 0.05) and neutrophil percentage (P < 0.05) were significantly greater in the nonnaloxone group. The levels of IL-6 (P < 0.05) and calcitonin in the nonnaloxone group were significantly greater at 24 h after surgery. At 24 h following surgery, the nonnaloxone group had significantly greater levels of IL-6 (P < 0.05) and calcitonin than did the naloxone group. Compared with those in the naloxone group, the expression levels of TLR4 (P < 0.05) in gastric cancer tissue in the naloxone group were greater; however, the expression levels of IL-6 (P < 0.01) and TNF-alpha (P < 0.01) in the naloxone group were greater than those in the nonnaloxone group. Conclusion Laparoscopic total gastrectomy patients can benefit from 0.05 ug/kg(- 1). h(- 1) naloxone by reducing their risk of infection. It is possible that LDN alters the number of cells in lymphocyte subpopulations, such as NK cells, CD3 T+  cells, and CD4( + )T cells, and the CD4(+)/CD8 (+) T-cell ratio or alters TLR4 receptor expression in immune cells, thereby altering immune cell activity.
C1 [Min, Xiangzhen; Li, Xiaoxi; Zhang, Jianmin; Lv, Renjun] Lanzhou Univ, Sch Clin Med 1, Lanzhou, Gansu, Peoples R China.
   [Min, Xiangzhen; Xu, Shoucai; Wang, Xiuqin; Guo, Jie; Xing, Huaixin] Shandong First Med Univ, Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Anesthesiol, Jinan, Shandong, Peoples R China.
   [Ma, Yan] Shandong Univ Tradit Chinese Med, Dept Anesthesiol, Affiliated Hosp, Jinan, Shandong, Peoples R China.
   [Leng, Yufang] Lanzhou Univ, Hosp 1, Dept Anesthesiol, Lanzhou, Gansu, Peoples R China.
C3 Lanzhou University; Shandong First Medical University & Shandong Academy
   of Medical Sciences; University of Jinan; Shandong University of
   Traditional Chinese Medicine; Lanzhou University
RP Xing, HX (corresponding author), Shandong First Med Univ, Shandong Acad Med Sci, Shandong Canc Hosp & Inst, Dept Anesthesiol, Jinan, Shandong, Peoples R China.; Leng, YF (corresponding author), Lanzhou Univ, Hosp 1, Dept Anesthesiol, Lanzhou, Gansu, Peoples R China.
EM lengyf@lzu.edu.cn; xinghuaixin521@163.com
RI 李, 晓曦/AEG-7480-2022; Leng, Yufang/AAL-2786-2021
OI Xu, Shoucai/0009-0003-5359-2337
FU Beijing Medical Award Foundation
FX We would like to thank sincerely Professor Leng Yufang and Teacher Xing
   Huaixin for their efforts and performance during this study.
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NR 38
TC 1
Z9 1
U1 1
U2 2
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-2253
J9 BMC ANESTHESIOL
JI BMC Anesthesiol.
PD MAY 8
PY 2024
VL 24
IS 1
AR 172
DI 10.1186/s12871-024-02524-7
PG 11
WC Anesthesiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Anesthesiology
GA PT2C1
UT WOS:001216258800001
PM 38720250
OA Green Submitted, gold
DA 2025-06-01
ER

PT J
AU Nagpal, R
   Wang, S
   Ahmadi, S
   Hayes, J
   Gagliano, J
   Subashchandrabose, S
   Kitzman, DW
   Becton, T
   Read, R
   Yadav, H
AF Nagpal, Ravinder
   Wang, Shaohua
   Ahmadi, Shokouh
   Hayes, Joshua
   Gagliano, Jason
   Subashchandrabose, Sargurunathan
   Kitzman, Dalane W.
   Becton, Thomas
   Read, Russel
   Yadav, Hariom
TI Human-origin probiotic cocktail increases short-chain fatty acid
   production via modulation of mice and human gut microbiome
SO SCIENTIFIC REPORTS
LA English
DT Article
ID ASSOCIATION; BUTYRATE; STRAINS; CELLS; FERMENTATION; AUTOIMMUNITY;
   INHIBITION; BACTERIA; EXCHANGE
AB The gut bacteria producing metabolites like short-chain fatty acids (SCFAs; e.g., acetate, propionate and butyrate), are frequently reduced in Patients with diabetes, obesity, autoimmune disorders, and cancers. Hence, microbiome modulators such as probiotics may be helpful in maintaining or even restoring normal gut microbiome composition to benefit host health. Herein, we developed a human-origin probiotic cocktail with the ability to modulate gut microbiota to increase native SCFA production. Following a robust protocol of isolation, characterization and safety validation of infant gut-origin Lactobacillus and Enterococcus strains with probiotic attributes (tolerance to simulated gastric and intestinal conditions, adherence to intestinal epithelial cells, absence of potential virulence genes, cell-surface hydrophobicity, and susceptibility to common antibiotics), we select 10 strains (5 from each genera) out of total 321 isolates. A single dose (oral gavage) as well as 5 consecutive doses of this 10-strain probiotic cocktail in mice modulates gut microbiome and increases SCFA production (particularly propionate and butyrate). Inoculation of these probiotics in human feces also increases SCFA production along with microbiome modulation. Results indicate that human-origin probiotic lactobacilli and enterococci could ameliorate gut microbiome dysbiosis and hence may prove to be a potential therapy for diseases involving reduced SCFAs production in the gut.
C1 [Nagpal, Ravinder; Wang, Shaohua; Ahmadi, Shokouh; Hayes, Joshua; Yadav, Hariom] Wake Forest Sch Med, Dept Internal Med Mol Med, Winston Salem, NC 27101 USA.
   [Nagpal, Ravinder; Wang, Shaohua; Ahmadi, Shokouh; Hayes, Joshua; Subashchandrabose, Sargurunathan; Yadav, Hariom] Wake Forest Sch Med, Dept Microbiol & Immunol, Winston Salem, NC 27101 USA.
   [Gagliano, Jason; Read, Russel] Forsyth Tech Community Coll, Natl Ctr Biotechnol Workforce, Winston Salem, NC USA.
   [Kitzman, Dalane W.; Becton, Thomas] Wake Forest Sch Med, Dept Internal Med Gerontol & Geriatr Med, Winston Salem, NC USA.
C3 Wake Forest University; Wake Forest University; Wake Forest University
RP Yadav, H (corresponding author), Wake Forest Sch Med, Dept Internal Med Mol Med, Winston Salem, NC 27101 USA.; Yadav, H (corresponding author), Wake Forest Sch Med, Dept Microbiol & Immunol, Winston Salem, NC 27101 USA.
EM hyadav@wakehealth.edu
RI Ahmadi, Shokouh/ABA-1007-2020; Yadav, Hariom/I-2455-2018; Wang,
   Shaohua/G-8194-2018; Nagpal, PhD, Ravinder/H-5358-2019
OI Subashchandrabose, Sargurunathan/0000-0003-1217-9813; Yadav,
   Hariom/0000-0003-4504-1597; Wang, Shaohua/0000-0002-8548-1602; Nagpal,
   PhD, Ravinder/0000-0002-4250-1749
FU Center for Diabetes, Obesity and Metabolism, the Kermit Glenn Phillips
   II Chair in Cardiovascular Medicine at Wake Forest School of Medicine;
   National Institutes of Health at Wake Forest School of Medicine
   [P30AG12232]; Wake Forest School of Medicine [R01AG18915, R01DK114224];
   Clinical and Translational Science Center (Clinical Research Unit) at
   Wake Forest School of Medicine [UL1TR001420]; Department of Defense
   [PR170446]
FX We thank Bright Horizon day care center (Winston-Salem, NC) for
   providing unidentified infant diapers. The authors gratefully
   acknowledge funding support for this work from the Center for Diabetes,
   Obesity and Metabolism, the Kermit Glenn Phillips II Chair in
   Cardiovascular Medicine; the National Institutes of Health funded Claude
   D. Pepper Older Americans Center (funded by P30AG12232); R01AG18915;
   R01DK114224 and the Clinical and Translational Science Center (Clinical
   Research Unit, funded by UL1TR001420), all at Wake Forest School of
   Medicine. We also acknowledge support from Department of Defense funding
   (Grant number: PR170446).
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NR 66
TC 245
Z9 268
U1 6
U2 112
PU NATURE PORTFOLIO
PI BERLIN
PA HEIDELBERGER PLATZ 3, BERLIN, 14197, GERMANY
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD AUG 23
PY 2018
VL 8
AR 12649
DI 10.1038/s41598-018-30114-4
PG 15
WC Multidisciplinary Sciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Science & Technology - Other Topics
GA GR3XD
UT WOS:000442530000013
PM 30139941
OA Green Published, gold
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Nakayama, S
   Endo, A
   Hirose, T
   Matsumoto, K
   Kamada, A
   Ito, H
   Hashimoto, H
   Ishiyama, K
   Oba-Yabana, I
   Kimura, T
   Nakamura, H
   Ebina, M
   Mori, T
AF Nakayama, Shingo
   Endo, Akari
   Hirose, Takuo
   Matsumoto, Keiji
   Kamada, Ayaka
   Ito, Hiroki
   Hashimoto, Hideaki
   Ishiyama, Katsuya
   Oba-Yabana, Ikuko
   Kimura, Tomoyoshi
   Nakamura, Hannah
   Ebina, Masahito
   Mori, Takefumi
TI MPO-ANCA-positive conversion and microscopic polyangiitis development in
   idiopathic interstitial pneumonia: a case report
SO CEN CASE REPORTS
LA English
DT Article
DE Idiopathic interstitial pneumonia; MPO-ANCA-positive conversion;
   Microscopic polyangiitis; Malignancy
ID ANTIBODY-ASSOCIATED VASCULITIS; RESECTION
AB Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis is a systemic autoimmune disease characterized by necrotizing inflammation of the small blood vessels. ANCA-associated vasculitis is subclassified into three variants: granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, and microscopic polyangiitis (MPA). Myeloperoxidase (MPO) ANCA is a marker antibody for MPA. Interstitial pneumonia (IP) is occasionally complicated with MPA. However, only a few cases of idiopathic IP develop MPO-ANCA-positive conversion and MPA. Therefore, we present a case of a 70-year-old Japanese man with idiopathic IP who developed MPO-ANCA-positive conversion and MPA. We performed renal biopsy, which revealed pauci-immune crescentic glomerulonephritis. The patient was treated with intravenous methylprednisolone pulse therapy and oral prednisone, and the patient's laboratory data gradually improved with steroid therapy. The association between the production of MPO-ANCA and IP remains unclear, and the present case suggests that IP plays a role in inducing MPO-ANCA production. Patients with idiopathic IP should be followed-up carefully for an examination of increased MPO-ANCA levels and MPA development. In addition, early gastric cancer was detected during upper gastrointestinal endoscopy in our case, and it could also be important not to miss malignancy in patients with ANCA-associated vasculitis.
C1 [Nakayama, Shingo; Endo, Akari; Hirose, Takuo; Matsumoto, Keiji; Kamada, Ayaka; Ito, Hiroki; Hashimoto, Hideaki; Ishiyama, Katsuya; Oba-Yabana, Ikuko; Kimura, Tomoyoshi; Nakamura, Hannah; Mori, Takefumi] Tohoku Med & Pharmaceut Univ, Fac Med, Div Nephrol & Endocrinol, Miyagino Ku, 1-15-1 Fukumuro, Sendai, Miyagi 9838536, Japan.
   [Hirose, Takuo] Tohoku Univ, Dept Endocrinol & Appl Med Sci, Grad Sch Med, Sendai, Miyagi, Japan.
   [Hirose, Takuo; Mori, Takefumi] Tohoku Med & Pharmaceut Univ, Fac Med, Div Integrat Renal Replacement Therapy, Sendai, Miyagi, Japan.
   [Ebina, Masahito] Tohoku Med & Pharmaceut Univ, Dept Resp Med, Sendai, Miyagi, Japan.
C3 Tohoku Medical & Pharmaceutical University; Tohoku University; Tohoku
   Medical & Pharmaceutical University; Tohoku Medical & Pharmaceutical
   University
RP Nakayama, S (corresponding author), Tohoku Med & Pharmaceut Univ, Fac Med, Div Nephrol & Endocrinol, Miyagino Ku, 1-15-1 Fukumuro, Sendai, Miyagi 9838536, Japan.
EM nakayama-s@tohoku-mpu.ac.jp
RI Nakayama, Shingo/MEK-8268-2025; Ishiyama, Katsuya/I-1064-2019; Hirose,
   Takuo/B-3793-2010
OI Nakamura, Hannah/0009-0009-0414-3897; Ito, Hiroki/0000-0003-1239-6551;
   Hirose, Takuo/0000-0002-8761-3779; Nakayama, Shingo/0000-0003-1009-9860
FU Ministry of Education, Culture, Sports, Science, and Technology of Japan
   (MEXT) [19H03677, 19K21596, 20K08612]; Takeda Research Foundation;
   Grants-in-Aid for Scientific Research [19H03677, 19K21596, 20K08612]
   Funding Source: KAKEN
FX This work was supported in part by Grants-in-Aid for Scientific Research
   (19H03677, 19K21596, and 20K08612) from the Ministry of Education,
   Culture, Sports, Science, and Technology of Japan (MEXT), and the Takeda
   Research Foundation.
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NR 13
TC 1
Z9 1
U1 0
U2 0
PU SPRINGER JAPAN KK
PI TOKYO
PA SHIROYAMA TRUST TOWER 5F, 4-3-1 TORANOMON, MINATO-KU, TOKYO, 105-6005,
   JAPAN
SN 2192-4449
J9 CEN CASE REP
JI CEN CASE REP.
PD FEB
PY 2023
VL 12
IS 1
BP 39
EP 44
DI 10.1007/s13730-022-00717-y
EA JUN 2022
PG 6
WC Urology & Nephrology
WE Emerging Sources Citation Index (ESCI)
SC Urology & Nephrology
GA 9Y2CE
UT WOS:000815437100001
PM 35749013
OA Green Published
DA 2025-06-01
ER

PT J
AU Sionov, RV
   Ahdut-HaCohen, R
AF Sionov, Ronit Vogt
   Ahdut-HaCohen, Ronit
TI A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing
   Langerhans Islets with a Specific Emphasis on The Secretome
SO BIOMEDICINES
LA English
DT Review
DE beta-cells; growth factors; insulin; Langerhans' islets; mesenchymal
   stem cells
ID PANCREATIC BETA-CELLS; NF-KAPPA-B; HEPATOCYTE-GROWTH-FACTOR;
   TUMOR-NECROSIS-FACTOR; MARROW STROMAL CELLS; GLUCAGON-LIKE PEPTIDE-1;
   PRO-INFLAMMATORY CYTOKINES; TYPE-1 DIABETES-MELLITUS; GASTRIC-INHIBITORY
   POLYPEPTIDE; NITRIC-OXIDE SYNTHASE
AB Type 1 Diabetes (T1D) is a chronic autoimmune disease characterized by a gradual destruction of insulin-producing beta-cells in the endocrine pancreas due to innate and specific immune responses, leading to impaired glucose homeostasis. T1D patients usually require regular insulin injections after meals to maintain normal serum glucose levels. In severe cases, pancreas or Langerhans islet transplantation can assist in reaching a sufficient beta-mass to normalize glucose homeostasis. The latter procedure is limited because of low donor availability, high islet loss, and immune rejection. There is still a need to develop new technologies to improve islet survival and implantation and to keep the islets functional. Mesenchymal stem cells (MSCs) are multipotent non-hematopoietic progenitor cells with high plasticity that can support human pancreatic islet function both in vitro and in vivo and islet co-transplantation with MSCs is more effective than islet transplantation alone in attenuating diabetes progression. The beneficial effect of MSCs on islet function is due to a combined effect on angiogenesis, suppression of immune responses, and secretion of growth factors essential for islet survival and function. In this review, various aspects of MSCs related to islet function and diabetes are described.
C1 [Sionov, Ronit Vogt] Hebrew Univ Jerusalem, Inst Biomed & Oral Res IBOR, Fac Dent Med, IL-9112102 Jerusalem, Israel.
   [Ahdut-HaCohen, Ronit] Hebrew Univ Jerusalem, Inst Med Res, Hadassah Med Sch, Dept Med Neurobiol, IL-9112102 Jerusalem, Israel.
   [Ahdut-HaCohen, Ronit] David Yellin Acad Coll Educ, Dept Sci, IL-9103501 Jerusalem, Israel.
C3 Hebrew University of Jerusalem; Hebrew University of Jerusalem
RP Sionov, RV (corresponding author), Hebrew Univ Jerusalem, Inst Biomed & Oral Res IBOR, Fac Dent Med, IL-9112102 Jerusalem, Israel.
EM ronit.sionov@mail.huji.ac.il; ronit.ahdut@mail.huji.ac.il
RI Sionov, Ronit/ADQ-2239-2022
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NR 743
TC 1
Z9 1
U1 4
U2 16
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
EI 2227-9059
J9 BIOMEDICINES
JI Biomedicines
PD SEP
PY 2023
VL 11
IS 9
AR 2558
DI 10.3390/biomedicines11092558
PG 66
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental;
   Pharmacology & Pharmacy
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Research & Experimental Medicine;
   Pharmacology & Pharmacy
GA T1RZ7
UT WOS:001075839900001
PM 37761001
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Bian, ZL
   Miao, Q
   Zhong, W
   Zhang, HY
   Wang, QX
   Peng, YS
   Chen, XY
   Guo, CJ
   Shen, L
   Yang, F
   Xu, J
   Qiu, DK
   Fang, JY
   Friedman, S
   Tang, RQ
   Gershwin, ME
   Ma, X
AF Bian, Zhaolian
   Miao, Qi
   Zhong, Wei
   Zhang, Haiyan
   Wang, Qixia
   Peng, Yanshen
   Chen, Xiaoyu
   Guo, Canjie
   Shen, Li
   Yang, Fan
   Xu, Jie
   Qiu, Dekai
   Fang, Jingyuan
   Friedman, Scott
   Tang, Ruqi
   Gershwin, M. Eric
   Ma, Xiong
TI Treatment of cholestatic fibrosis by altering gene expression of Cthrc1:
   Implications for autoimmune and non-autoimmune liver disease
SO JOURNAL OF AUTOIMMUNITY
LA English
DT Article
DE Hepatic fibrosis; Cholestatic liver fibrosis; Hepatic stellate cell;
   Anti-fibrotic treatment; TGF-beta pathway
ID PRIMARY BILIARY-CIRRHOSIS; TRANSFORMING-GROWTH-FACTOR; TRIPLE-HELIX
   REPEAT; GASTRIC-CANCER; HEPATIC FIBROGENESIS; COLLAGEN EXPRESSION;
   CELLS; PROTEIN; ACTIVATION; IDENTIFICATION
AB Collagen triple helix repeat containing-1 (Cthrc1) is a documented specific inhibitor of TGF-beta. signaling. Based on this observation, we developed the hypothesis that knocking in/knocking out the Cthrc1 gene in murine models of cholestasis would alter the natural history of cholestatic fibrosis. To study this thesis, we studied two murine models of fibrosis, first, common bile duct ligation (CBDL) and second, feeding of 3, 5-diethoxy-carbonyl-1, 4-dihydrocollidine (DDC). In both models, we administered well-defined adenoviral vectors that expressed either Cthrc1 or, alternatively, a short hairpin RNA (shRNA)-targeting Cthrc1 either before or after establishment of fibrosis. Importantly, when Cthrc1 gene expression was enhanced, we noted a significant improvement of hepatic fibrosis, both microscopically and by analysis of fibrotic gene expression. In contrast, when Cthrc1 gene expression was deleted, there was a significant exacerbation of fibrosis. To identify the mechanism of action of these significant effects produced by knocking in/knocking out Cthrc gene expression, we thence studied the interaction of Cthrc1 gene expression using hepatic stellate cells (HSCs) and human LX-2 cells. Importantly, we demonstrate that Cthrc1 is induced by TGF-beta 1 via phospho-Smad3 binding to the promoter with subsequent transcription activation. In addition, we demonstrate that Cthrc1 inhibits TGF-beta signaling by accelerating degradation of phospho-Smad3 through a proteosomal pathway. Importantly, the anti-fibrotic effects can be recapitulated with a truncated fragment of Cthrc1. In conclusion, our findings uncover a critical negative feedback regulatory loop in which TGF-beta 1 induces Cthrc1, which can attenuate fibrosis by accelerating degradation of phospho-Smad3. (C) 2015 Elsevier Ltd. All rights reserved.
C1 [Bian, Zhaolian; Miao, Qi; Zhong, Wei; Zhang, Haiyan; Wang, Qixia; Peng, Yanshen; Chen, Xiaoyu; Guo, Canjie; Shen, Li; Yang, Fan; Xu, Jie; Qiu, Dekai; Fang, Jingyuan; Tang, Ruqi; Ma, Xiong] Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Minist Hl, Key Lab Gastroenterol & Hepatol,Ren Ji Hosp,Shang, Div Gastroenterol & Hepatol,Sch Med,Shanghai Inst, Shanghai 200001, Peoples R China.
   [Friedman, Scott] Icahn Sch Med Mt Sinai, Div Liver Dis, New York, NY 10029 USA.
   [Gershwin, M. Eric] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
C3 Shanghai Jiao Tong University; Icahn School of Medicine at Mount Sinai;
   University of California System; University of California Davis
RP Ma, X (corresponding author), Shanghai Jiao Tong Univ, State Key Lab Oncogenes & Related Genes,Minist Hl, Key Lab Gastroenterol & Hepatol,Ren Ji Hosp,Shang, Div Gastroenterol & Hepatol,Sch Med,Shanghai Inst, 145 Middle Shandong Rd, Shanghai 200001, Peoples R China.
EM bianzhaolian1998@163.com; miaoqi0730@126.com; rjzhongwei@163.com;
   heidi0509@163.com; wqx0221155@126.com; pengyanshen@yahoo.com.cn;
   1621508481@qq.com; guocanjie@yahoo.com.cn; shirleypear@126.com;
   flyingfish_yf@163.com; jiexu@yahoo.com; qiudekai2008@126.com;
   fangjingyuan_new@163.com; scott.friedman@mssm.edu; ruqi_tang@126.com;
   megershwin@ucdavis.edu; maxiongmd@hotmail.com
RI Friedman, Scott/AFV-6304-2022; Xu, Jie/K-3712-2019; Zhang,
   Haiyan/KWT-8071-2024; FANG, Jing-Yuan/JOZ-1388-2023; Chen,
   Xiaoyu/JQL-1125-2023; Xu, Jie/C-4283-2016
OI Xu, Jie/0000-0001-9163-3898; Ma, Xiong/0000-0001-9616-4672; Zhang,
   Haiyan/0009-0002-6401-7090
FU National Natural Science Foundation of China [81170380, 81325002,
   81421001, 81400608, 81200309, 81200293, 81100296]; National Institutes
   of Health [DK090019, DK56621]; Doctoral Innovation Fund Projects from
   Shanghai Jiaotong University School of Medicine [BXJ201321]
FX Financial Support: This work was supported by grants from the National
   Natural Science Foundation of China (# 81170380 and # 81325002 to Xiong
   Ma, #81421001 to Jingyuan Fang, #81400608 to Ruqi Tang, #81200309 to Wei
   Zhong, #81200293 to Qi Miao and # 81100296 to Canjie Guo); National
   Institutes of Health grants DK090019 (M. Eric Gershwin) and DK56621
   (Scott Friedman); Doctoral Innovation Fund Projects from Shanghai
   Jiaotong University School of Medicine BXJ201321 (Zhaolian Bian).
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NR 50
TC 33
Z9 33
U1 0
U2 25
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0896-8411
EI 1095-9157
J9 J AUTOIMMUN
JI J. Autoimmun.
PD SEP
PY 2015
VL 63
BP 76
EP 87
DI 10.1016/j.jaut.2015.07.010
PG 12
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA CS2UM
UT WOS:000361927500008
PM 26238209
OA Green Submitted, Green Accepted
DA 2025-06-01
ER

PT J
AU Wang, X
   Zhang, CZ
   Wu, ZW
   Chen, Y
   Shi, WM
AF Wang, Xin
   Zhang, Chengzhong
   Wu, Zhouwei
   Chen, Yue
   Shi, Weimin
TI CircIBTK inhibits DNA demethylation and activation of AKT signaling
   pathway via miR-29b in peripheral blood mononuclear cells in systemic
   lupus erythematosus
SO ARTHRITIS RESEARCH & THERAPY
LA English
DT Article
DE Systemic lupus erythematosus; Circular RNAs; miR-29b; DNA methylation;
   AKT signaling
ID BRUTONS TYROSINE KINASE; CIRCULAR RNA; T-CELLS; GASTRIC-CANCER;
   GLOMERULONEPHRITIS; HYPOMETHYLATION; METHYLATION; MECHANISMS;
   EXPRESSION; DISEASE
AB Background: Systemic lupus erythematosus (SLE) is a chronic and incurable autoimmune disease involving the dysfunction of lymphocytes. Circular RNAs (circRNAs) are noncoding RNAs (ncRNAs) with a covalently closed loop structure, with abnormal expression in various human diseases may participate in the pathogenesis, while further study is needed in SLE. In this study, we aimed to find the circRNAs abnormally expressed in SLE and explore the function of circRNAs in SLE.
   Methods: CircRNA sequencing was used to find the abnormally expressed circRNA and qRT-PCR was used to detect the expression. Correlation analysis was used to analyze the correlation between circIBTK or miR-29b and clinicopathological variables in patients with SLE. Cell culture, nuclear-cytoplasmic fractionation, qRT-PCR, transfection, luciferase reporter assay, western blot analysis, DNA extraction and global methylation analysis were used to explain the function of circIBTK and miR-29b in the progression of SLE. SPSS 18.0 software was used to perform statistics.
   Results: We found that the expression of circIBTK was downregulated in SLE and correlated with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score, anti-double-stranded (ds)DNA and complement C3 level in patients with SLE. Then miR-29b expression was upregulated in SLE and correlated with SLEDAI score, anti-dsDNA and complement C3 level in patients with SLE. Mechanistic investigations indicated that miR-29b could induce DNA demethylation and activate the AKT signaling pathway and circIBTK might reverse the DNA demethylation and activation of the AKT signaling pathway induced by miR-29b via binding to miR-29b in SLE.
   Conclusions: CircIBTK was downregulated in SLE and might regulate DNA demethylation and the AKT signaling pathway via binding to miR-29b in SLE. CircIBTK and miR-29 could also act as biomarkers and therapeutic targets for SLE.
C1 [Wang, Xin; Zhang, Chengzhong; Wu, Zhouwei; Shi, Weimin] Shanghai Jiao Tong Univ, Sch Med, Shanghai Gen Hosp, Dept Dermatol, Haining Rd 100, Shanghai 200080, Peoples R China.
   [Chen, Yue] Nanjing Med Univ, Shanghai Gen Hosp, Dept Dermatol, Haining Rd 100, Shanghai 200080, Peoples R China.
C3 Shanghai Jiao Tong University; Nanjing Medical University
RP Shi, WM (corresponding author), Shanghai Jiao Tong Univ, Sch Med, Shanghai Gen Hosp, Dept Dermatol, Haining Rd 100, Shanghai 200080, Peoples R China.
EM weiminshisjtu@163.com
FU National Natural Science Foundation of China [81573031]
FX This work was supported by grants from the National Natural Science
   Foundation of China (grant number 81573031).
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NR 32
TC 77
Z9 89
U1 0
U2 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1478-6354
EI 1478-6362
J9 ARTHRITIS RES THER
JI Arthritis Res. Ther.
PD JUN 8
PY 2018
VL 20
AR 118
DI 10.1186/s13075-018-1618-8
PG 10
WC Rheumatology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Rheumatology
GA GI7HH
UT WOS:000434672900002
PM 29884225
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU Surdea-Blaga, T
   Caragut, R
   Caraiani, C
   Sparchez, Z
   al Hajjar, N
   Dumitrascu, DL
AF Surdea-Blaga, Teodora
   Caragut, Roxana L.
   Caraiani, Cosmin
   Sparchez, Zeno
   al Hajjar, Nadim
   Dumitrascu, Dan L.
TI Overlap syndrome of autoimmune hepatitis and primary biliary cholangitis
   complicated with atypical hepatocellular carcinoma: a case report
SO JOURNAL OF MEDICAL CASE REPORTS
LA English
DT Article
DE Hepatocellular carcinoma; Primary biliary cholangitis; Autoimmune
   hepatitis; Liver cirrhosis; Atypical liver resection; Case report
ID PRIMARY SCLEROSING CHOLANGITIS
AB BackgroundHepatocellular carcinoma (HCC) is a primary tumor of the liver. The majority of HCCs are associated most frequently with chronic B or C viral hepatitis, alcohol intake or aflatoxin exposure. Cirrhosis is a strong risk factor associated with HCC. The causes of liver cirrhosis are chronic viral hepatitis, alcohol intake, metabolic diseases (NAFLD), hemocromathosis, alfa 1 antitrypsisn deficiency. All aetiologic forms of cirrhosis are at risk to be complicated by HCC development, but the risk is higher for patients diagnosed with chronic viral hepatitis. Comparing to the above-mentioned causes, PBC and AIH are less associated with the risk of HCC development.Case summaryA 71-year old Caucasian female previously diagnosed with overlap syndrome (AIH type 1 and PBC-ANA, SMA and AMA antibodies positive), liver cirrhosis, a nodule in the VI/VIIth hepatic segment, systemic sclerosis sine scleroderma, Hashimoto's thyroiditis, antiphospholipid syndrome, gastric antral vascular ectasia (GAVE) (with 2 previous sessions of argon plasma coagulation), cholecystectomy, arterial hypertension and nephro-angiosclerosis presented to the 2nd Department of Internal Medicine in Cluj-Napoca for a follow-up. The patient was following treatment with UDCA (Ursodeoxycholic acid), azathioprine, Plaquenil, calcium channel blockers, angiotensin-converting-enzyme inhibitor, calcium and vitamin D supplementation. The abdominal ultrasound showed a subcapsular hypoechoic nodule with a diameter of 29 mm (at the moment of the diagnosis the diameter was 9/10 mm) in the VI/VIIth hepatic segment. The contrast-enhanced ultrasound (CEUS) characterised the nodule as specific for hepatocellular carcinoma (LI-RADS 5). On MRI with gadoxetate disodium the nodule was hypovascular, non-specific, being classified as LI-RADS 3. An atypical resection of the VIIth hepatic segment was performed and the histohistological examination and imunohistochemistry (Hep Par-a positive, Glypican3 positive, CD34 positive) revealed a moderately differentiated hepatocellular carcinoma (G2), pT2 N0 M0 L0 V1 R0.ConclusionAutoimmune hepatitis, PBC and the overlap syndrome are less associated with the development of liver cirrhosis and HCC than other chronic liver diseases, especially if other risk factors are not associated. This case highlights the importance of a proper surveillance of cirrhotic patients every 6 months including abdominal ultrasound and AFP levels is crucial for an early diagnosis of a HCC.
C1 [Surdea-Blaga, Teodora; Caraiani, Cosmin; Sparchez, Zeno; al Hajjar, Nadim; Dumitrascu, Dan L.] Iuliu Hatieganu Univ Med & Pharm, Cluj Napoca, Romania.
   [Surdea-Blaga, Teodora; Dumitrascu, Dan L.] Cty Emergency Hosp, Dept Internal Med 2, Cluj Napoca, Romania.
   [Caragut, Roxana L.; Sparchez, Zeno; al Hajjar, Nadim] Reg Inst Gastroenterol & Hepatol, 19 21 Croitorilor St, Cluj Napoca 400162, Romania.
C3 Iuliu Hatieganu University of Medicine & Pharmacy; Regional Institute of
   Gastroenterology & Hepatology
RP Caragut, R (corresponding author), Reg Inst Gastroenterol & Hepatol, 19 21 Croitorilor St, Cluj Napoca 400162, Romania.
EM roxanacaragut@gmail.com
RI Surdea-Blaga, Teodora/IAM-5919-2023; Caraiani, Cosmin/HZL-7882-2023;
   AlHajjar, Nadim/I-3147-2017; Dumitrascu, Dan/C-4618-2011
OI Caragut, Roxana-Luiza/0000-0003-4174-0390
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NR 19
TC 1
Z9 1
U1 1
U2 3
PU BMC
PI LONDON
PA CAMPUS, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
EI 1752-1947
J9 J MED CASE REP
JI J. Med. Case Rep.
PD JUL 25
PY 2023
VL 17
IS 1
AR 328
DI 10.1186/s13256-023-03932-y
PG 8
WC Medicine, General & Internal
WE Emerging Sources Citation Index (ESCI)
SC General & Internal Medicine
GA M8BY8
UT WOS:001032426200001
PM 37488645
OA gold, Green Published
DA 2025-06-01
ER

PT J
AU DE la Vieja, A
   Dohan, O
   Levy, O
   Carrasco, N
AF DE la Vieja, A
   Dohan, O
   Levy, O
   Carrasco, N
TI Molecular analysis of the sodium/iodide symporter: Impact on thyroid and
   extrathyroid pathophysiology
SO PHYSIOLOGICAL REVIEWS
LA English
DT Review
ID SODIUM-IODIDE SYMPORTER; THYROTROPIN-RECEPTOR GENE; TRANSCRIPTION
   FACTOR-I; NECROSIS-FACTOR-ALPHA; NA+/I SYMPORTER; CONGENITAL
   HYPOTHYROIDISM; MEMBRANE-VESICLES; TRANSPORT DEFECT; CYCLIC-AMP;
   PROMOTER CHARACTERIZATION
AB The Na+/I- symporter (NIS) is an intrinsic membrane protein that mediates the active transport of iodide into the thyroid and other tissues, such as salivary glands, gastric mucosa, and lactating mammary gland. NIS plays key roles in thyroid pathophysiology as the route by which iodide reaches the gland for thyroid hormone biosynthesis and as a means for diagnostic scintigraphic imaging and for radioiodide therapy in hyperthyroidism and thyroid cancer. The molecular characterization of NIS started with the 1996 isolation of a cDNA encoding rat NIS and has since continued at a rapid pace. Anti-NIS antibodies have been prepared and used to study NIS topology and its secondary structure. The biogenesis and posttranslational modifications of NIS have been examined, a thorough electrophysiological analysis of NIS has been conducted, the cDNA encoding human NIS (hNIS) has been isolated, the genomic organization of hNIS has been elucidated, the regulation of NIS by thyrotropin and I- has been analyzed, the regulation of NIS transcript:ion has been studied, spontaneous NIS mutations have been identified as causes of congenital iodide transport defect resulting in hypothyroidism, the roles of NIS in thyroid cancer and thyroid autoimmune disease have been examined, and the expression and regulation of NIS in extrathyroidal tissues have been investigated. In gene therapy experiments, the rat NIS gene has been transduced into various types of human cells, which then exhibited active iodide transport and became susceptible to destruction with radioiodide. The continued molecular analysis of NIS clearly holds the potential of an even greater impact on a wide spectrum of fields, ranging from structure/function of transport proteins to the diagnosis and treatment of cancer, both in the thyroid and beyond.
C1 Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA.
C3 Montefiore Medical Center; Albert Einstein College of Medicine; Yeshiva
   University
RP Carrasco, N (corresponding author), Albert Einstein Coll Med, Dept Mol Pharmacol, 1300 Morris Pk Ave, Bronx, NY 10461 USA.
RI Carrasco, Nancy/AAH-1053-2019; Dohan, Orsolya/B-3750-2012; De la Vieja,
   Antonio/I-4774-2013
OI Dohan, Orsolya/0000-0001-6235-5657; De la Vieja,
   Antonio/0000-0002-1187-1907
FU NIDDK NIH HHS [DK-41544] Funding Source: Medline
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NR 134
TC 272
Z9 295
U1 0
U2 27
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0031-9333
J9 PHYSIOL REV
JI Physiol. Rev.
PD JUL
PY 2000
VL 80
IS 3
BP 1083
EP 1105
DI 10.1152/physrev.2000.80.3.1083
PG 23
WC Physiology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Physiology
GA 332TE
UT WOS:000088088900008
PM 10893432
DA 2025-06-01
ER

PT J
AU Urai, S
   Tomofuji, S
   Bando, H
   Kanzawa, M
   Yamamoto, M
   Fukuoka, H
   Tsuda, M
   Iguchi, G
   Ogawa, W
AF Urai, Shin
   Tomofuji, Seiji
   Bando, Hironori
   Kanzawa, Maki
   Yamamoto, Masaaki
   Fukuoka, Hidenori
   Tsuda, Masahiro
   Iguchi, Genzo
   Ogawa, Wataru
TI The early-stage clinical course of anti-pituitary-specific transcription
   factor-1 hypophysitis diagnosed post-immune checkpoint inhibitor
   treatment: A case with review of literature
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Article
DE hormones; hypophysitis; immune-related adverse event; paraneoplastic
   syndrome; pituitary-specific transcription factor-1
ID PIT-1
AB Anti-pituitary-specific transcription factor-1 (PIT-1) hypophysitis, a paraneoplastic syndrome resulting from an autoimmune response against PIT-1, typically manifests with undetectable levels of growth hormone (GH) and prolactin (PRL), and significantly low levels of serum thyroid-stimulating hormone (TSH) at diagnosis. These hormonal levels are highly specific to this disease and serve as key diagnostic indicators. Herein, we present a detailed clinical course of a 69-year-old male with a history of gastric cancer and lymph node metastases who developed anti-PIT-1 hypophysitis after the initiation of immune checkpoint inhibitor (ICI) therapy, specifically nivolumab, oxaliplatin, and capecitabine. The patient was referred to our department owing to decreased TSH, free triiodothyronine (T3), and free thyroxine (T4) levels after two doses of nivolumab. Initially suspected as central hypothyroidism due to ICI-related hypophysitis, further assessment confirmed the diagnosis of anti-PIT-1 hypophysitis. Notably, GH, PRL, and TSH levels markedly declined, leading to complete deficiencies 2 months after the first nivolumab dose-a pattern consistent with that of previous cases of anti-PIT-1 hypophysitis. Therefore, this report not only presents an atypical subset of ICI-related hypophysitis but also delineates the process of hormone impairment leading to complete deficiencies in anti-PIT-1 hypophysitis. This case highlights the importance of vigilant monitoring for endocrine issues in patients undergoing ICI therapy, given the escalating incidence of immune-related adverse events associated with the extensive use of ICI therapy for various cancers.
   Anti-pituitary-specific transcription factor-1 (PIT-1) hypophysitis, characterized by an autoimmune response against PIT-1, typically presents with undetectable GH and PRL levels, along with significantly low serum TSH levels at diagnosis. Given the limited number of previously reported cases of anti-PIT-1 hypophysitis and its manifestation with complete hormone deficiencies at diagnosis, the developmental process of this condition remains entirely unclear. This report not only presents an atypical subset of ICI-related hypophysitis but also delineates the process of hormone impairment leading to complete deficiencies in anti-PIT-1 hypophysitis. image
C1 [Urai, Shin; Yamamoto, Masaaki; Iguchi, Genzo; Ogawa, Wataru] Kobe Univ, Grad Sch Med, Dept Internal Med, Div Diabet & Endocrinol, 7-5-1 Kusunoki Cho,Chuo Ku, Kobe, Hyogo650 6500017, Japan.
   [Urai, Shin] Hyogo Canc Ctr, Dept Diabet & Endocrinol, Akashi, Japan.
   [Tomofuji, Seiji; Bando, Hironori; Fukuoka, Hidenori] Kobe Univ Hosp, Dept Internal Med, Div Diabet & Endocrinol, Kobe, Japan.
   [Kanzawa, Maki] Kobe Univ, Grad Sch Med, Div Diagnost Pathol, Kobe, Japan.
   [Tsuda, Masahiro] Hyogo Canc Ctr, Dept Gastroenterol Oncol, Akashi, Japan.
   [Iguchi, Genzo] Kobe Univ, Med Ctr Student Hlth, Kobe, Japan.
   [Iguchi, Genzo] Kobe Univ, Div Biosignal Pathophysiol, Kobe, Japan.
C3 Kobe University; Hyogo Cancer Center; Kobe University; Kobe University;
   Hyogo Cancer Center; Kobe University; Kobe University
RP Iguchi, G (corresponding author), Kobe Univ, Grad Sch Med, Dept Internal Med, Div Diabet & Endocrinol, 7-5-1 Kusunoki Cho,Chuo Ku, Kobe, Hyogo650 6500017, Japan.
EM giendo@med.kobe-u.ac.jp
RI Bando, Hironori/JWP-5467-2024; Urai, Shin/MSW-6215-2025; OGAWA,
   Wataru/AAQ-9586-2020; Fukuoka, Hidenori/AAK-1045-2020
OI Bando, Hironori/0000-0002-7421-2714; Kanzawa, Maki/0000-0003-2806-2011;
   Urai, Shin/0000-0002-7996-232X
FU Japan Society for the Promotion of Science; Grants-in-Aid for Scientific
   Research [21K10469, 21K08555] Funding Source: KAKEN
FX We thank the patient and his family for their cooperation and the
   laboratory members for their excellent discussions and suggestions. We
   would like to thank Editage () for the English language editing.
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NR 34
TC 2
Z9 3
U1 0
U2 3
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
EI 1365-2826
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD JUN
PY 2024
VL 36
IS 6
DI 10.1111/jne.13395
EA APR 2024
PG 8
WC Endocrinology & Metabolism; Neurosciences
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA SW9B7
UT WOS:001204036800001
PM 38631695
DA 2025-06-01
ER

PT J
AU Jang, J
   Lee, JS
   Jang, YJ
   Choung, ES
   Li, WY
   Lee, SW
   Kim, E
   Kim, JH
   Cho, JY
AF Jang, Jiwon
   Lee, Jong Sub
   Jang, Young-Jin
   Choung, Eui Su
   Li, Wan Yi
   Lee, Sang Woo
   Kim, Eunji
   Kim, Jong-Hoon
   Cho, Jae Youl
TI Sorbaria kirilowii Ethanol Extract Exerts Anti-Inflammatory
   Effects In Vitro and In Vivo by Targeting Src/Nuclear Factor (NF)-κB
SO BIOMOLECULES
LA English
DT Article
DE Sorbaria kirilowii; anti-inflammatory effect; NF-kappa B signaling
   pathway; IKK alpha/beta Src
ID NF-KAPPA-B; NITRIC-OXIDE; INFLAMMATION; RECOGNITION; SUPPRESSION;
   RECEPTORS; COX-2; AKT; SYK
AB Inflammation is a fundamental process for defending against foreign antigens that involves various transcriptional regulatory processes as well as molecular signaling pathways. Despite its protective roles in the human body, the activation of inflammation may also convey various diseases including autoimmune disease and cancer. Sorbaria kirilowii is a plant originating from Asia, with no anti-inflammatory activity reported. In this paper, we discovered an anti-inflammatory effect of S. kirilowii ethanol extract (Sk-EE) both in vivo and in vitro. In vitro effects of Sk-EE were determined with lipopolysaccharide (LPS)-stimulated RAW264.7 cells, while ex vivo analysis was performed using peritoneal macrophages of thioglycollate (TG)-induced mice. Sk-EE significantly reduced the nitric oxide (NO) production of induced macrophages and inhibited the expression of inflammation-related cytokines and the activation of transcription factors. Moreover, treatment with Sk-EE also decreased the activation of proteins involved in nuclear factor (NF)-kappa B signaling cascade; among them, Src was a prime target of Sk-EE. For in vivo assessment of the anti-inflammatory effect of Sk-EE, HCl/EtOH was given by the oral route to mice for gastritis induction. Sk-EE injection dose-dependently reduced the inflammatory lesion area of the stomach in gastritis-induced mice. Taking these results together, Sk-EE exerts its anti-inflammatory activity by regulating intracellular NF-kappa B signaling pathways and also shows an authentic effect on reducing gastric inflammation.
C1 [Jang, Jiwon; Kim, Eunji; Cho, Jae Youl] Sungkyunkwan Univ, Dept Integrat Biotechnol, Suwon 16419, South Korea.
   [Jang, Jiwon; Cho, Jae Youl] Sungkyunkwan Univ, Res Inst Biomol Control, Suwon 16419, South Korea.
   [Jang, Jiwon; Cho, Jae Youl] Sungkyunkwan Univ, Biomed Inst Convergence SKKU BICS, Suwon 16419, South Korea.
   [Lee, Jong Sub; Choung, Eui Su] DanjoungBio Co Ltd, Wonju 26303, South Korea.
   [Jang, Young-Jin; Kim, Jong-Hoon] Chonbuk Natl Univ, Coll Vet Med, Iksan 54596, South Korea.
   [Li, Wan Yi] Yunnan Acad Agr Sci, Inst Med Plants, Kunming 650224, Yunnan, Peoples R China.
   [Lee, Sang Woo] Korea Res Inst Biosci & Biotechnol, Int Biol Mat Res Ctr, Daejeon 34141, South Korea.
C3 Sungkyunkwan University (SKKU); Sungkyunkwan University (SKKU);
   Sungkyunkwan University (SKKU); Jeonbuk National University; Yunnan
   Academy of Agricultural Sciences; Korea Research Institute of Bioscience
   & Biotechnology (KRIBB)
RP Kim, E; Cho, JY (corresponding author), Sungkyunkwan Univ, Dept Integrat Biotechnol, Suwon 16419, South Korea.; Cho, JY (corresponding author), Sungkyunkwan Univ, Res Inst Biomol Control, Suwon 16419, South Korea.; Cho, JY (corresponding author), Sungkyunkwan Univ, Biomed Inst Convergence SKKU BICS, Suwon 16419, South Korea.; Kim, JH (corresponding author), Chonbuk Natl Univ, Coll Vet Med, Iksan 54596, South Korea.
EM rhea980327@gmail.com; js.lee@danjoungbio.com; jyj3010@daum.net;
   esavella@hanmail.net; wyli2012@126.com; ethnolee@kribb.re.kr;
   im144069@gmail.com; jhkim1@jbnu.ac.kr; jaecho@skku.edu
RI lee, sangwoo/KUD-1906-2024; Jang, Young/AAT-1192-2020; Lee,
   Yoon/ABA-8808-2020; Lee, Jong-Sub/G-2752-2012; Wang, Jian/AAE-4412-2020
FU Brain Korea 21 program; Basic Science Research Program through the
   National Research Foundation of Korea (NRF) - Ministry of Education
   [2017R1A6A1A03015642]; B-GCTI project, Republic of Korea
FX This research was supported by Brain Korea 21 program and the Basic
   Science Research Program through the National Research Foundation of
   Korea (NRF) funded by the Ministry of Education (Grant number:
   2017R1A6A1A03015642), as well as B-GCTI project, Republic of Korea.
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NR 66
TC 13
Z9 14
U1 0
U2 3
PU MDPI
PI BASEL
PA ST ALBAN-ANLAGE 66, CH-4052 BASEL, SWITZERLAND
EI 2218-273X
J9 BIOMOLECULES
JI Biomolecules
PD MAY
PY 2020
VL 10
IS 5
AR 741
DI 10.3390/biom10050741
PG 17
WC Biochemistry & Molecular Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology
GA ME9ZV
UT WOS:000545013700078
PM 32397672
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU Spitzweg, C
   Joba, W
   Eisenmenger, W
   Heufelder, AE
AF Spitzweg, C
   Joba, W
   Eisenmenger, W
   Heufelder, AE
TI Analysis of human sodium iodide symporter gene expression in
   extrathyroidal tissues and cloning of its complementary deoxyribonucleic
   acids from salivary gland, mammary gland, and gastric mucosa
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID AUTOIMMUNE THYROID-DISEASE; TRANSCRIPTION FACTOR-I; NA+/I-SYMPORTER;
   RADIOIODINE; TRANSPORTER; MUTATION; CANCER; AUTOANTIBODY; PROMOTER;
   PATIENT
AB The ability to concentrate iodide is a fundamental property of normally functioning thyroid tissue and represents the first step in the production of thyroid hormones. Iodide uptake has been demonstrated in various extrathyroidal tissues, including salivary gland, gastric mucosa, and lactating mammary gland. Recently, cloning and molecular characterization of the human sodium iodide symporter (hNIS) have been reported; however, the patterns of hNIS gene expression in human tissues have remained unidentified. To examine the profiles of human hNIS gene expression in various normal human tissues, we performed high-stringency Northern blot analysis using a P-32-labeled hNIS-specific complementary DNA (cDNA) probe (nucleotides 1184-1667). To detect rare hNIS transcripts in small tissue samples, RT-PCR was performed with a pair of hNIS-specific oligonucleotide primers designed to amplify a portion (nucleotides 1184-1667) of the hNIS gene. hNIS-specific transcripts were confirmed by Southern hybridization using a digoxigenin-labeled internal hNIS-specific oligonucleotide probe (nucleotides 1460-1477). To monitor cDNA integrity and quantity, and to rule out DNA contamination and illegitimate transcription, all samples were coamplified with two pairs of intron-spanning primers designed to amplify fragments of the human beta-actin and thyroglobulin genes, respectively. Using Northern blot analysis, hNIS transcripts of approximately 4 kb were detected in thyroid gland and parotid gland but not in a broad range of endocrine and nonendocrine tissues. RT-PCR and Southern hybridization revealed hNIS gene expression in thyroid gland, salivary gland, parotid gland, submandibular gland, pituitary gland, pancreas, testis, mammary gland, gastric mucosa, prostate and ovary, adrenal gland, heart, thymus, and lung. By contrast, hNIS transcripts were not detected in normal orbital fibroblasts, colon, and nasopharyngeal mucosa. To further analyze hNIS gene sequences in parotid gland, mammary gland, and gastric mucosa, the EXPAND High Fidelity PCR System and three sets of overlapping NIS oligonucleotide primers were used for amplification and cloning. The resulting PCR products were subcloned into pBluescript-SK II(-)vector, and at least two independent cDNA clones derived from each tissue were subjected to automated sequencing. The nucleotide sequences of hNIS cDNA derived from parotid gland, mammary gland, and gastric mucosa revealed full identity with the recently published human thyroid-derived NIS cDNA sequence. In conclusion, our results demonstrate markedly variable levels of hNIS gene expression in several extrathyroidal tissues. Although the physiological role of hNIS in these tissues awaits further study, our results suggest that the capacity to actively transport iodine may be a feature common to several secretory and endocrine tissues. The diminished capacity to transport and concentrate iodide in extrathyroidal tissues (such as parotid gland, mammary gland, and gastric mucosa), compared with thyroid gland, does not seem to be caused by an altered primary structure of the hNIS cDNA. Variability of NIS gene expression levels in normal extrathyroidal tissues may rather be caused by differences in NIS gene transcriptional activity. Further studies will address this hypothesis and examine the mechanisms of tissue-specific regulation of NIS gene expression.
C1 Ludwigs Maximillian Univ, Klinikum Innenstadt, Med Klin, Mol Thyroid Res Unit, D-80336 Munich, Germany.
   Ludwigs Maximillian Univ, Klinikum Innenstadt, Dept Legal Med, D-80336 Munich, Germany.
C3 University of Munich; University of Munich
RP Ludwigs Maximillian Univ, Klinikum Innenstadt, Med Klin, Mol Thyroid Res Unit, Ziemssenstr 1, D-80336 Munich, Germany.
EM u7g11av@mail.lrz-muenchen.de
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NR 28
TC 291
Z9 310
U1 0
U2 7
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD MAY
PY 1998
VL 83
IS 5
BP 1746
EP 1751
DI 10.1210/jc.83.5.1746
PG 6
WC Endocrinology & Metabolism
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Endocrinology & Metabolism
GA ZM396
UT WOS:000073535300059
PM 9589686
DA 2025-06-01
ER

PT J
AU Schwab, C
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   Schmitt-Graeff, A
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   Frede, N
   Bulashevska, A
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   Okada, S
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   Sumnik, Z
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   Lorenz, HM
   Giese, T
   Lougaris, V
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   Moutschen, M
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   van de Veerdonk, FL
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   Albert, MH
   Hauck, F
   Seneviratne, S
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   Kolios, A
   Unglik, G
   Klemann, C
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   Leichtner, A
   Blumberg, R
   Franke, A
   Snapper, S
   Zeissig, S
   Cunningham-Rundles, C
   Giulino-Roth, L
   Elemento, O
   Dückers, G
   Niehues, T
   Fronkova, E
   Kanderová, V
   Platt, CD
   Chou, J
   Chatila, TA
   Geha, R
   McDermott, E
   Bunn, S
   Kurzai, M
   Schulz, A
   Alsina, L
   Casals, F
   Deyà-Martinez, A
   Hambleton, S
   Kanegane, H
   Taskén, K
   Neth, O
   Grimbacher, B
AF Schwab, Charlotte
   Gabrysch, Annemarie
   Olbrich, Peter
   Patino, Virginia
   Warnatz, Klaus
   Wolff, Daniel
   Hoshino, Akihiro
   Kobayashi, Masao
   Imai, Kohsuke
   Takagi, Masatoshi
   Dybedal, Ingunn
   Haddock, Jamanda A.
   Sansom, David M.
   Lucena, Jose M.
   Seidl, Maximilian
   Schmitt-Graeff, Annette
   Reiser, Veronika
   Emmerich, Florian
   Frede, Natalie
   Bulashevska, Alla
   Salzer, Ulrich
   Schubert, Desiree
   Hayakawa, Seiichi
   Okada, Satoshi
   Kanariou, Maria
   Kucuk, Zeynep Yesim
   Chapdelaine, Hugo
   Petruzelkova, Lenka
   Sumnik, Zdenek
   Sediva, Anna
   Slatter, Mary
   Arkwright, Peter D.
   Cant, Andrew
   Lorenz, Hanns-Martin
   Giese, Thomas
   Lougaris, Vassilios
   Plebani, Alessandro
   Price, Christina
   Sullivan, Kathleen E.
   Moutschen, Michel
   Litzman, Jiri
   Freiberger, Tomas
   van de Veerdonk, Frank L.
   Recher, Mike
   Albert, Michael H.
   Hauck, Fabian
   Seneviratne, Suranjith
   Schmid, Jana Pachlopnik
   Kolios, Antonios
   Unglik, Gary
   Klemann, Christian
   Speckmann, Carsten
   Ehl, Stephan
   Leichtner, Alan
   Blumberg, Richard
   Franke, Andre
   Snapper, Scott
   Zeissig, Sebastian
   Cunningham-Rundles, Charlotte
   Giulino-Roth, Lisa
   Elemento, Olivier
   Dueckers, Gregor
   Niehues, Tim
   Fronkova, Eva
   Kanderova, Veronika
   Platt, Craig D.
   Chou, Janet
   Chatila, Talal A.
   Geha, Raif
   McDermott, Elizabeth
   Bunn, Su
   Kurzai, Monika
   Schulz, Ansgar
   Alsina, Laia
   Casals, Ferran
   Deya-Martinez, Angela
   Hambleton, Sophie
   Kanegane, Hirokazu
   Tasken, Kjetil
   Neth, Olaf
   Grimbacher, Bodo
TI Phenotype, penetrance, and treatment of 133 cytotoxic T-lymphocyte
   antigen 4-insufficient subjects
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Cytotoxic T-lymphocyte antigen 4; primary immunodeficiency;
   autoimmunity; hypogammaglobulinemia; hematopoietic stem cell
   transplantation; abatacept; sirolimus; immune dysregulation; common
   variable immunodeficiency
ID STEM-CELL TRANSPLANTATION; IMMUNE DYSREGULATION; LRBA DEFICIENCY; CTLA-4
   HAPLOINSUFFICIENCY; GERMLINE MUTATIONS; PATIENT; DISEASE;
   CLASSIFICATION; AUTOIMMUNITY; FAMILY
AB Background: Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is a negative immune regulator. Heterozygous CTLA4 germline mutations can cause a complex immune dysregulation syndrome in human subjects.
   Objective: We sought to characterize the penetrance, clinical features, and best treatment options in 133 CTLA4 mutation carriers.
   Methods: Genetics, clinical features, laboratory values, and outcomes of treatment options were assessed in a worldwide cohort of CTLA4 mutation carriers.
   Results: We identified 133 subjects from 54 unrelated families carrying 45 different heterozygous CTLA4 mutations, including 28 previously undescribed mutations. Ninety mutation carriers were considered affected, suggesting a clinical penetrance of at least 67%; median age of onset was 11 years, and the mortality rate within affected mutation carriers was 16%(n = 15). Main clinical manifestations included hypogammaglobulinemia (84%), lymphoproliferation (73%), autoimmune cytopenia (62%), and respiratory (68%), gastrointestinal (59%), or neurological features (29%). Eight affectedmutation carriers had lymphoma, and 3 had gastric cancer. An EBV association was found in 6 patients with malignancies. CTLA4 mutations were associated with lymphopenia and decreased T-, B-, and natural killer (NK) cell counts. Successful targeted therapies included application of CTLA-4 fusion proteins, mechanistic target of rapamycin inhibitors, and hematopoietic stem cell transplantation. EBV reactivation occurred in 2 affected mutation carriers after immunosuppression.
   Conclusions: Affected mutation carriers with CTLA-4 insufficiency can present in any medical specialty. Family members should be counseled because disease manifestation can occur as late as 50 years of age. EBV- and cytomegalovirus-associated complications must be closely monitored. Treatment interventions should be coordinated in clinical trials.
C1 [Schwab, Charlotte; Gabrysch, Annemarie; Warnatz, Klaus; Reiser, Veronika; Frede, Natalie; Bulashevska, Alla; Salzer, Ulrich; Schubert, Desiree; Klemann, Christian; Speckmann, Carsten; Ehl, Stephan; Grimbacher, Bodo] Univ Freiburg, Fac Med, Med Ctr, CCI, Freiburg, Germany.
   [Olbrich, Peter; Neth, Olaf] Hosp Virgen del Rocio, Inst Biomed Sevilla IBiS, Unidad Pediat, Secc Infectol & Inmunopatol, Seville, Spain.
   [Patino, Virginia] Amer Insurance, Immunol Team, Montevideo, Uruguay.
   [Wolff, Daniel] Univ Hosp Regensburg, Dept Internal Med 3, Regensburg, Germany.
   [Hoshino, Akihiro; Kanegane, Hirokazu] Tokyo Med & Dent Univ, Grad Sch Med & Dent Sci, Dept Pediat & Dev Biol, Tokyo, Japan.
   [Imai, Kohsuke; Takagi, Masatoshi] Tokyo Med & Dent Univ, Dept Community Pediat Perinatal & Maternal Med, Tokyo, Japan.
   [Kobayashi, Masao; Hayakawa, Seiichi; Okada, Satoshi] Hiroshima Univ, Grad Sch Biomedical& Hlth Sci, Dept Pediat, Hiroshima, Japan.
   [Dybedal, Ingunn] Oslo Univ Hosp, Dept Hematol, Oslo, Norway.
   [Haddock, Jamanda A.] UCL, Royal Free Hosp, Dept Radiol, London, England.
   [Sansom, David M.] Royal Free Hosp, UCL Inst Immun & Transplantat, London, England.
   [Lucena, Jose M.] Hosp Univ Virgen del Rocio, Inst Biomed Sevilla IBiS, Unidad Inmunol, Seville, Spain.
   [Seidl, Maximilian] Univ Freiburg, Dept Pathol, Ctr Chron Immunodeficiency & Mol Pathol, Freiburg, Germany.
   [Schmitt-Graeff, Annette] Univ Freiburg, Dept Pathol, Univ Med Ctr, Freiburg, Germany.
   [Reiser, Veronika] Univ Freiburg, Fac Med, Inst Med Biometry & Stat, Freiburg, Germany.
   [Reiser, Veronika] Univ Freiburg, Med Ctr, Freiburg, Germany.
   [Emmerich, Florian] Univ Med Ctr Freiburg, Inst Transfus Med & Gene Therapy, Freiburg, Germany.
   [Schubert, Desiree] Freiburg Univ, Spemann Grad Sch Biol & Med, Freiburg, Germany.
   [Kanariou, Maria] Aghia Sophia Childrens Hosp, Ctr Primary Immunodeficiencies, Dept Immunol & Histocompatibil, Athens, Greece.
   [Kucuk, Zeynep Yesim] Cincinnati Childrens Hosp Med Ctr, Div Bone Marrow Transplantat & Immune Deficiency, Cincinnati, OH 45229 USA.
   [Chapdelaine, Hugo] Univ Montreal, CHUM, Dept Med, Clin Immunol & Allergy Div, Montreal, PQ, Canada.
   [Petruzelkova, Lenka; Sumnik, Zdenek] Univ Hosp Motol, Dept Pediat, Prague, Czech Republic.
   [Sediva, Anna] Univ Hosp Motol, Dept Immunol, Prague, Czech Republic.
   Charles Univ Prague, Fac Med 2, Prague, Czech Republic.
   [Slatter, Mary; Cant, Andrew; Hambleton, Sophie] Newcastle Upon Tyne Hosp NHS Fdn Trust, Great North Childrens Hosp, Newcastle Upon Tyne, Tyne & Wear, England.
   [Slatter, Mary; Cant, Andrew; Hambleton, Sophie] Newcastle Univ, Inst Cellular Med, Newcastle Upon Tyne, Tyne & Wear, England.
   [Arkwright, Peter D.] Univ Manchester, Royal Manchester Childrens Hosp, Manchester, Lancs, England.
   [Lorenz, Hanns-Martin] Heidelberg Univ, Dept Internal Med 5, Div Rheumatol, Heidelberg, Germany.
   [Giese, Thomas] Univ Hosp Heidelberg, Inst Immunol, Heidelberg, Germany.
   [Lougaris, Vassilios; Plebani, Alessandro] Univ Brescia, ASST Spedali Civili Brescia, Pediat Clin, Brescia, Italy.
   [Lougaris, Vassilios; Plebani, Alessandro] Univ Brescia, ASST Spedali Civili Brescia, Inst Mol Med A Nocivelli, Dept Clin & Expt Sci, Brescia, Italy.
   [Price, Christina] Yale Univ, Sch Med, Sect Allergy & Clin Immunol, New Haven, CT USA.
   [Sullivan, Kathleen E.] Univ Penn, Childrens Hosp Philadelphia, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Moutschen, Michel] Univ Hosp Liege, Dept Infect Dis & Gen Internal Med, Liege, Belgium.
   [Litzman, Jiri] Masaryk Univ, Fac Med, Dept Clin Immunol & Allergol, Brno, Czech Republic.
   [Freiberger, Tomas] Masaryk Univ, Cent European Inst Technol, Med Genom RG, Brno, Czech Republic.
   [Litzman, Jiri] St Annes Univ Hosp, Dept Clin Immunol & Allergol, Brno, Czech Republic.
   [Freiberger, Tomas] Ctr Cardiovasc Surg & Transplantat, Mol Genet Lab, Brno, Czech Republic.
   [van de Veerdonk, Frank L.] Radboudumc Ctr Infect Dis RCI, Dept Internal Med, Nijmegen, Netherlands.
   [Recher, Mike] Univ Hosp, Med Outpatient Unit, Immunodeficiency Clin, Basel, Switzerland.
   [Recher, Mike] Univ Hosp, Dept Biomed, Immunodeficiency Lab, Basel, Switzerland.
   [Albert, Michael H.; Hauck, Fabian] Ludwig Maximilians Univ Munchen, Dr von Hauner Childrens Hosp, Dept Pediat Immunol & Stem Cell Transplantat, Munich, Germany.
   [Seneviratne, Suranjith; Grimbacher, Bodo] UCL, Royal Free Hosp, Inst Immunol & Transplantat, London, England.
   [Schmid, Jana Pachlopnik] Univ Zurich, Univ Childrens Hosp Zurich, Div Immunol, Zurich, Switzerland.
   [Kolios, Antonios] Univ Zurich, Univ Hosp Zurich, Dept Immunol, Zurich, Switzerland.
   [Unglik, Gary] Royal Melbourne Hosp, Dept Clin Immunol & Allergy, Melbourne, Vic, Australia.
   [Speckmann, Carsten] Univ Freiburg, Fac Med, Univ Med Ctr, Ctr Pediat, Freiburg, Germany.
   [Leichtner, Alan] Harvard Med Sch, Div Gastroenterol, Boston, MA USA.
   [Leichtner, Alan] Harvard Med Sch, Dept Pediat, Boston, MA USA.
   [Blumberg, Richard; Zeissig, Sebastian] Harvard Med Sch, Brigham & Womens Hosp, Dept Med, Div Gastroenterol Hepatol & Endoscopy, Boston, MA USA.
   [Franke, Andre] Christian Albrechts Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
   [Snapper, Scott] Childrens Hosp, Dept Med, Div Pediat Gastroenterol Hepatol & Nutr, Boston, MA 02115 USA.
   [Zeissig, Sebastian] Tech Univ Dresden, Univ Med Ctr Dresden, Dept Med 1, Dresden, Germany.
   [Zeissig, Sebastian] Univ Med Ctr Schleswig Holstein, Dept Internal Med 1, Kiel, Germany.
   [Cunningham-Rundles, Charlotte] Mt Sinai Hosp, Mt Sinai St Lukes & Mt Sinai West, Dept Med Allergy & Immunol, New York, NY 10029 USA.
   [Giulino-Roth, Lisa] Weill Cornell Med, Div Pediat Hematol Oncol, Dept Pediat, New York, NY USA.
   [Elemento, Olivier] Weill Cornell Med Coll, Dept Physiol & Biophys, Inst Computat Biomed, New York, NY USA.
   [Dueckers, Gregor; Niehues, Tim] HELIOS Childrens Hosp, Krefeld, Germany.
   [Fronkova, Eva; Kanderova, Veronika] Charles Univ Prague, Fac Med 2, Dept Paediat Haematol Oncol, CLIP, Prague, Czech Republic.
   [Fronkova, Eva; Kanderova, Veronika] Univ Hosp Motol, Prague, Czech Republic.
   [Platt, Craig D.; Chou, Janet; Chatila, Talal A.; Geha, Raif] Boston Childrens Hosp, Div Immunol, Boston, MA USA.
   [Platt, Craig D.; Chou, Janet; Chatila, Talal A.; Geha, Raif] Boston Childrens Hosp, Dept Pediat, Boston, MA USA.
   [McDermott, Elizabeth] Nottingham Univ Hosp, Clin Immunol & Allergy Unit, Nottingham, England.
   [Bunn, Su] Great North Childrens Hosp, Dept Paediat Gastroenterol, Newcastle Upon Tyne, Tyne & Wear, England.
   [Kurzai, Monika] Univ Hosp Jena, Dept Pediat, Jena, Germany.
   [Schulz, Ansgar] Univ Med Ctr Ulm, Dept Pediat, Ulm, Germany.
   [Alsina, Laia; Deya-Martinez, Angela] Hosp St Joan de Deu, Inst Recerca Pediat, Allergy & Clin Immunol Dept, Funct Unit,Immunol SJD Clin, Esplugas de Llobregat, Spain.
   [Casals, Ferran] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Serv Genom, Parc Recerca Biomed Barcelona, Barcelona, Spain.
   [Tasken, Kjetil] Univ Oslo, Nord EMBL Partnership, Ctr Mol Med Norway, Oslo, Norway.
   [Tasken, Kjetil] Univ Hosp Oslo, Inst Canc Res, Oslo, Norway.
   [Klemann, Christian] Hannover Med Sch, Dept Pediat Pneumol Allergy & Neonatol, Hannover, Germany.
   [Klemann, Christian] Hannover Med Sch, Ctr Pediat Surg, Hannover, Germany.
C3 University of Freiburg; Virgen del Rocio University Hospital; Consejo
   Superior de Investigaciones Cientificas (CSIC); University of Sevilla;
   CSIC-JA-USE - Instituto de Biomedicina de Sevilla (IBIS); University of
   Regensburg; Institute of Science Tokyo; Tokyo Medical & Dental
   University (TMDU); Institute of Science Tokyo; Tokyo Medical & Dental
   University (TMDU); Hiroshima University; University of Oslo; University
   of London; University College London; Royal Free London NHS Foundation
   Trust; UCL Medical School; University of London; University College
   London; Royal Free London NHS Foundation Trust; UCL Medical School;
   Virgen del Rocio University Hospital; Consejo Superior de
   Investigaciones Cientificas (CSIC); University of Sevilla; CSIC-JA-USE -
   Instituto de Biomedicina de Sevilla (IBIS); University of Freiburg;
   University of Freiburg; University of Freiburg; University of Freiburg;
   University of Freiburg; University of Freiburg; The Aghia Sophia
   Children's Hospital; Cincinnati Children's Hospital Medical Center;
   Universite de Montreal; Motol University Hospital; Motol University
   Hospital; Charles University Prague; Motol University Hospital;
   Newcastle Upon Tyne Hospitals NHS Foundation Trust; Newcastle University
   - UK; University of Manchester; Manchester University NHS Foundation
   Trust; Royal Manchester Children's Hospital; Ruprecht Karls University
   Heidelberg; Ruprecht Karls University Heidelberg; Hospital Spedali
   Civili Brescia; University of Brescia; Hospital Spedali Civili Brescia;
   University of Brescia; Yale University; University of Pennsylvania;
   Pennsylvania Medicine; Childrens Hospital of Philadelphia; University of
   Liege; Masaryk University Brno; Masaryk University Brno; St. Anne's
   University Hospital Brno (FNUSA); University of Munich; University of
   London; University College London; UCL Medical School; Royal Free London
   NHS Foundation Trust; University Children's Hospital Zurich; University
   of Zurich; University of Zurich; University Zurich Hospital; Melbourne
   Health; Royal Melbourne Hospital; University of Freiburg; Harvard
   University; Harvard Medical School; Harvard University; Harvard Medical
   School; Harvard University; Harvard Medical School; Harvard University
   Medical Affiliates; Brigham & Women's Hospital; University of Kiel;
   Harvard University; Harvard University Medical Affiliates; Boston
   Children's Hospital; Technische Universitat Dresden; University of Kiel;
   Schleswig Holstein University Hospital; Mount Sinai West; Mount Sinai
   St. Luke's; Icahn School of Medicine at Mount Sinai; Cornell University;
   Weill Cornell Medicine; Cornell University; Weill Cornell Medicine;
   Motol University Hospital; Charles University Prague; Motol University
   Hospital; Harvard University; Harvard University Medical Affiliates;
   Boston Children's Hospital; Harvard University; Harvard University
   Medical Affiliates; Boston Children's Hospital; University of
   Nottingham; Nottingham University Hospital NHS Trust; Friedrich Schiller
   University of Jena; Ulm University; Pompeu Fabra University; University
   of Oslo; University of Oslo; Hannover Medical School; Hannover Medical
   School
RP Grimbacher, B (corresponding author), Univ Klinikum Freiburg, CCI, Breisacher Str 115, D-79106 Freiburg, Germany.
EM bodo.grimbacher@uniklinik-freiburg.de
RI Ehl, Stephan/AAM-6006-2020; Arkwright, Peter/C-5149-2012; Warnatz,
   Klaus/AAD-3464-2022; Freiberger, Tomas/D-8421-2011; Seidl,
   Maxmilian/ABF-3322-2021; Pérez-Martínez, Antonio/AAF-5797-2019; Imai,
   Kohsuke/Q-2602-2015; Hauck, Fabian/H-5556-2016; Seneviratne,
   Suranjith/N-2617-2018; Kolios, Antonios/LBH-0714-2024; Bulashevska,
   Alla/C-4910-2019; Kanderova, Veronika/ADX-8309-2022; Zeissig,
   Sebastian/B-6297-2012; Takagi, Masatoshi/F-3713-2011; van de Veerdonk,
   Frank/C-7256-2008; Franke, Andre/B-2151-2010; Klemann,
   Christian/AAQ-9301-2020; Elemento, Olivier/ADL-3192-2022; Litzman,
   Jiri/E-2746-2012; Sediva, Anna/AAE-2774-2019; Alsina,
   Laia/GQI-3516-2022; Casals, Ferran/H-4347-2015; Okada,
   Satoshi/B-8901-2011; Neth, Olaf/F-1167-2015; Olbrich,
   Peter/AAV-3601-2021; Tasken, Kjetil/GQR-0078-2022; Pachlopnik Schmid,
   Jana/N-8018-2018
OI Seidl, Maxmilian/0000-0002-5559-4980; Alsina, Laia/0000-0002-3559-0018;
   Casals, Ferran/0000-0002-8941-0369; Hauck, Fabian/0000-0001-9644-2003;
   Litzman, Jiri/0000-0002-1926-5426; Sansom, David/0000-0001-6506-3115;
   Kanderova, Veronika/0000-0001-8513-1066; Chapdelaine,
   Hugo/0000-0001-6256-0271; Okada, Satoshi/0000-0002-4622-5657; Frede,
   Natalie/0000-0002-6415-6376; Ehl, Stephan/0000-0002-9265-2721; Neth,
   Olaf/0000-0001-5018-0466; Speckmann, Carsten/0000-0002-6217-1556;
   Deya-Martinez, Angela/0000-0002-8026-7674; Olbrich,
   Peter/0000-0001-9853-7903; Sediva, Anna/0000-0001-7730-2304; Sumnik,
   Zdenek/0000-0002-6462-6462; Tasken, Kjetil/0000-0003-2841-4697; Recher,
   Mike/0000-0002-9121-6936; Zeissig, Sebastian/0000-0001-5124-0897;
   Pachlopnik Schmid, Jana/0000-0002-6653-9047; Kolios,
   Antonios/0000-0002-3897-4578; Klemann, Christian/0000-0002-5639-8690;
   Hambleton, Sophie/0000-0001-7954-3267; Salzer,
   Ulrich/0000-0002-1769-1157; Duckers, Gregor/0000-0003-2220-6010;
   Chatila, Talal/0000-0001-7439-2762
FU German Ministry of Education and Research (BMBF) [01E01303, 01ZX1306 F];
   German Center for Infection Research [DZIF 8039807801]; Deutsche
   Forschungsgemeinschaft (DFG) [SFB1160]; Bristol-Myers Squibb
   [BMS_OT125-252]; National Institute of Health;  [NV15-30626A]; BBSRC
   [BB/H013598/2, BB/H013598/1] Funding Source: UKRI
FX Supported by the German Ministry of Education and Research (BMBF, grant
   no. 01E01303 and sysINFLAME (grant no 01ZX1306 F) by the German Center
   for Infection Research (DZIF 8039807801), the Deutsche
   Forschungsgemeinschaft (DFG; grant SFB1160, IMPATH, P07), and
   Bristol-Myers Squibb (BMS_OT125-252). E.F. and V.K. were supported by
   NV15-30626A. T.C. was funded by the National Institute of Health. The
   funding organizations had no role in the study design; collection,
   analysis and interpretation of data; writing of the report; or decision
   to submit the paper for publication. The authors are responsible for the
   content of this research.
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NR 42
TC 320
Z9 332
U1 1
U2 43
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2018
VL 142
IS 6
BP 1932
EP 1946
DI 10.1016/j.jaci.2018.02.055
PG 15
WC Allergy; Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Allergy; Immunology
GA HD2BJ
UT WOS:000452315800026
PM 29729943
OA Green Submitted, Green Accepted, Bronze
HC Y
HP N
DA 2025-06-01
ER

PT J
AU Victor, AR
   Nalin, AP
   Dong, WJ
   McClory, S
   Wei, M
   Mao, C
   Kladney, RD
   Youssef, Y
   Chan, WK
   Briercheck, EL
   Hughes, T
   Scoville, SD
   Pitarresi, JR
   Chen, C
   Manz, S
   Wu, LC
   Zhang, JY
   Ostrowski, MC
   Freud, AG
   Leone, GW
   Caligiuri, MA
   Yu, JH
AF Victor, Aaron R.
   Nalin, Ansel P.
   Dong, Wenjuan
   McClory, Susan
   Wei, Min
   Mao, Charlene
   Kladney, Raleigh D.
   Youssef, Youssef
   Chan, Wing Keung
   Briercheck, Edward L.
   Hughes, Tiffany
   Scoville, Steven D.
   Pitarresi, Jason R.
   Chen, Charlie
   Manz, Sarah
   Wu, Lai-Chu
   Zhang, Jianying
   Ostrowski, Michael C.
   Freud, Aharon G.
   Leone, Gustavo W.
   Caligiuri, Michael A.
   Yu, Jianhua
TI IL-18 Drives ILC3 Proliferation and Promotes IL-22 Production via NF-κB
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID INNATE LYMPHOID-CELLS; NATURAL-KILLER-CELLS; TISSUE-INDUCER CELLS;
   INTERFERON-GAMMA PRODUCTION; DIFFERENTIATION IN-VIVO; HUMAN
   GASTRIC-CANCER; TNF-ALPHA PRODUCTION; EPITHELIAL-CELLS;
   AUTOIMMUNE-DISEASE; INDUCED COLITIS
AB Group 3 innate lymphoid cells (ILC3s) are important regulators of the immune system, maintaining homeostasis in the presence of commensal bacteria, but activating immune defenses in response to microbial pathogens. ILC3s are a robust source of IL-22, a cytokine critical for stimulating the antimicrobial response. We sought to identify cytokines that can promote proliferation and induce or maintain IL-22 production by ILC3s and determine a molecular mechanism for this process. We identified IL-18 as a cytokine that cooperates with an ILC3 survival factor, IL-15, to induce proliferation of human ILC3s, as well as induce and maintain IL-22 production. To determine a mechanism of action, we examined the NF-kappa B pathway, which is activated by IL-18 signaling. We found that the NF-kB complex signaling component, p65, binds to the proximal region of the IL22 promoter and promotes transcriptional activity. Finally, we observed that CD11c(+) dendritic cells expressing IL-18 are found in close proximity to ILC3s in human tonsils in situ. Therefore, we identify a new mechanism by which human ILC3s proliferate and produce IL-22, and identify NF-kappa B as a potential therapeutic target to be considered in pathologic states characterized by overproduction of IL-18 and/or IL-22.
C1 [Victor, Aaron R.; Nalin, Ansel P.; McClory, Susan; Briercheck, Edward L.; Scoville, Steven D.] Ohio State Univ, Med Scientist Training Program, Columbus, OH 43210 USA.
   [Dong, Wenjuan; McClory, Susan; Wei, Min; Mao, Charlene; Kladney, Raleigh D.; Chan, Wing Keung; Briercheck, Edward L.; Hughes, Tiffany; Scoville, Steven D.; Pitarresi, Jason R.; Chen, Charlie; Manz, Sarah; Wu, Lai-Chu; Ostrowski, Michael C.; Freud, Aharon G.; Leone, Gustavo W.; Caligiuri, Michael A.; Yu, Jianhua] Ohio State Univ, Ctr Comprehens Canc, James Canc Hosp, Columbus, OH 43210 USA.
   [Dong, Wenjuan; McClory, Susan; Wei, Min; Mao, Charlene; Kladney, Raleigh D.; Chan, Wing Keung; Briercheck, Edward L.; Hughes, Tiffany; Scoville, Steven D.; Pitarresi, Jason R.; Chen, Charlie; Manz, Sarah; Wu, Lai-Chu; Ostrowski, Michael C.; Freud, Aharon G.; Leone, Gustavo W.; Caligiuri, Michael A.; Yu, Jianhua] Ohio State Univ, Ctr Comprehens Canc, Solove Res Inst, Columbus, OH 43210 USA.
   [Kladney, Raleigh D.; Pitarresi, Jason R.; Ostrowski, Michael C.; Leone, Gustavo W.] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
   [Kladney, Raleigh D.; Leone, Gustavo W.] Ohio State Univ, Coll Biol Sci, Dept Mol Genet, Columbus, OH 43210 USA.
   [Youssef, Youssef; Freud, Aharon G.] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA.
   [Zhang, Jianying] Ohio State Univ, Dept Bioinformat, Ctr Biostat, Columbus, OH 43210 USA.
   [Caligiuri, Michael A.; Yu, Jianhua] Ohio State Univ, Dept Internal Med, Div Hematol, Columbus, OH 43210 USA.
C3 University System of Ohio; Ohio State University; James Cancer Hospital
   & Solove Research Institute; University System of Ohio; Ohio State
   University; University System of Ohio; Ohio State University; James
   Cancer Hospital & Solove Research Institute; University System of Ohio;
   Ohio State University; University System of Ohio; Ohio State University;
   University System of Ohio; Ohio State University; University System of
   Ohio; Ohio State University; University System of Ohio; Ohio State
   University
RP Caligiuri, MA; Yu, JH (corresponding author), Ohio State Univ, Dept Internal Med, Div Hematol, Coll Med, 320 West 10th Ave, Columbus, OH 43210 USA.
EM michael.caligiuri@osumc.edu; jianhua.yu@osumc.edu
RI Wu, Lai-Chu/E-4328-2011; Caligiuri, Michael/KFR-7485-2024; Ostrowski,
   Michael/H-3108-2011
OI Victor, Aaron/0000-0003-4118-3088; Pitarresi, Jason/0000-0001-9549-4768;
   Ostrowski, Michael/0000-0003-2948-6297; McClory,
   Susan/0000-0002-4607-5230; Manz, Sarah N./0000-0002-0489-9645
FU National Institutes of Health [AI129582, CA095426, CA185301, CA097189];
   American Cancer Society [RSG-14-243-01-LIB]; Gabrielle's Angel
   Foundation for Cancer Research; Leukemia and Lymphoma Society
FX This work was supported by National Institutes of Health Grants
   AI129582, CA095426, CA185301, and CA097189, American Cancer Society
   Research Scholar Grant RSG-14-243-01-LIB, a grant from Gabrielle's Angel
   Foundation for Cancer Research, and by a grant from the Leukemia and
   Lymphoma Society.
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NR 76
TC 74
Z9 81
U1 1
U2 17
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
EI 1550-6606
J9 J IMMUNOL
JI J. Immunol.
PD OCT 1
PY 2017
VL 199
IS 7
BP 2333
EP 2342
DI 10.4049/jimmunol.1601554
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA FH2JR
UT WOS:000410965700016
PM 28842466
OA Green Accepted
DA 2025-06-01
ER

PT J
AU Monteiro, MA
   St Michael, F
   Rasko, DA
   Taylor, DE
   Conlan, JW
   Chan, KH
   Logan, SM
   Appelmelk, BJ
   Perry, MB
AF Monteiro, MA
   St Michael, F
   Rasko, DA
   Taylor, DE
   Conlan, JW
   Chan, KH
   Logan, SM
   Appelmelk, BJ
   Perry, MB
TI Helicobacter pylori from asymptomatic hosts expressing
   heptoglycan but lacking Lewis O-chains:: Lewis blood-group O-chains may
   play a role in Helicobacter pylori induced pathology
SO BIOCHEMISTRY AND CELL BIOLOGY
LA English
DT Article
DE lipopolysaccharide; carbohydrates; glycobiology; Helicobacter pylori;
   histo-blood groups
ID GROUP ANTIGENS; MOUSE MODEL; MONOCLONAL-ANTIBODIES; PHASE VARIATION;
   LIPOPOLYSACCHARIDES; STRAINS; SURFACE; TYPE-1; INFECTION; ULCER
AB Helicobacter pylori is a widespread Gram-negative bacterium responsible for the onset of various gastric pathologies and cancers in humans. A familiar trait of H. pylori is the production of cell-surface lipopolysaccharides (LPSs; O-chain right arrow core right arrow lipid A) with O-chain structures analogous to some mammalian histo-blood-group antigens, those being the Lewis determinants (Le(a), Le(b), Le(x), sialyl Le(x), Le(y)) and blood groups A and linear B. Some of these LPS antigens have been implicated as autoimmune, adhesion, and colonization components of H. pylori pathogenic mechanisms. This article describes the chemical structures of LPSs from H. pylori isolated from subjects with no overt signs of disease. Experimental data from chemical- and spectroscopic-based studies unanimously showed that these H. pylori manufactured extended heptoglycans composed of 2- and 3-linked D-glycero-alpha-D-manno-heptopyranose units and did not express any blood-group O-antigen chains. The fact that another H. pylori isolate with a similar LPS structure was shown to be capable of colonizing mice indicates that H. pylori histo-blood-group structures are not an absolute prerequisite for colonization in the murine model also. The absence of O-chains with histo-blood groups may cause H. pylori to become inept in exciting an immune response. Additionally, the presence of elongated heptoglycans may impede exposure of disease-causing outer-membrane antigens. These factors may render such H. pylori incapable of creating exogenous contacts essential for pathogenesis of severe gastroduodenal diseases and suggest that histo-blood groups in the LPS may indeed play a role in inducing a more severe H. pylori pathology.
C1 Natl Res Council Canada, Inst Biol Sci, Ottawa, ON K1A 0R6, Canada.
   Univ Alberta, Dept Med Microbiol & Immunol, Edmonton, AB, Canada.
   Vrije Univ Amsterdam, Dept Med Microbiol, Amsterdam, Netherlands.
C3 National Research Council Canada; University of Alberta; Vrije
   Universiteit Amsterdam
RP Natl Res Council Canada, Inst Biol Sci, 100 Sussex Dr, Ottawa, ON K1A 0R6, Canada.
EM Mario.Monteiro@nrc.ca
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NR 38
TC 28
Z9 33
U1 0
U2 8
PU CANADIAN SCIENCE PUBLISHING
PI OTTAWA
PA 65 AURIGA DR, SUITE 203, OTTAWA, ON K2E 7W6, CANADA
SN 0829-8211
EI 1208-6002
J9 BIOCHEM CELL BIOL
JI Biochem. Cell Biol.
PD AUG
PY 2001
VL 79
IS 4
BP 449
EP 459
DI 10.1139/bcb-79-4-449
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Cell Biology
GA 456EL
UT WOS:000170070100007
PM 11527214
DA 2025-06-01
ER

PT J
AU Huang, JM
   Fan, W
   Chen, XY
   Wu, SF
   Dong, ZG
   Zhang, Y
   Lin, YW
   Xiao, PP
AF Huang, Jinmei
   Fan, Wei
   Chen, Xuyan
   Wu, Shufan
   Dong, Zhigao
   Zhang, Yi
   Lin, Yiwan
   Xiao, Pingping
TI Case report: Rituximab combined with plasma exchange treatment for
   systemic lupus erythematosus complicated with thrombotic microangiopathy
   and non-cirrhotic portal hypertension
SO FRONTIERS IN IMMUNOLOGY
LA English
DT Article
DE systemic lupus erythematosus; thrombotic microangiopathy; non-cirrhotic
   portal hypertension; rituximab; case report
ID NODULAR REGENERATIVE HYPERPLASIA; THROMBOCYTOPENIC PURPURA; ASSOCIATION;
   PATIENT; COHORT; LIVER
AB Introduction Systemic lupus erythematosus (SLE) complicated by thrombotic microangiopathy (TMA) and non-cirrhotic portal hypertension (NCPH) is rare. We present a case of a female patient with SLE who developed TMA and NCPH and responded positively to rituximab and plasma exchange treatment.Case description A 53-year-old woman was admitted with 6 h of confusion. Upon admission, she was diagnosed with SLE complicated by lupus encephalopathy, blood system impairment, cardiomyopathy, and nephritis. Initial treatment with high-dose methylprednisolone, immunoglobulin shock therapy, and tacrolimus (1 mg, twice daily) improved her symptoms and laboratory indicators. However, after a pulmonary infection and infection with the 2019 novel coronavirus, the patient's condition deteriorated further. She experienced confusion and a delayed response. Hemoglobin levels and platelet counts decreased, lactate dehydrogenase and creatinine levels increased, and the percentage of peripheral schistocytes was approximately 6.5%. Abdominal ultrasonography revealed a substantial amount of ascites, diffuse liver lesions, splenomegaly, and splenic varices. Enhanced computed tomography revealed diffuse liver disease along the portal veins, intrahepatic lymphatic dilatation, esophageal and gastric varices, a splenorenal vein shunt, and splenomegaly. The patient was negative for hepatitis virus, autoimmune liver disease antibodies, ceruloplasmin, and tumor markers. Therefore, SLE complicated by TMA and NCPH was considered. She was treated with high-dose methylprednisolone (500 mg) for 3 days and immunoglobulin (0.4 g/kg/day) for 5 days, followed by rituximab (500 mg) for suppressive immunotherapy combined with plasma exchange (seven times), low-molecular-weight heparin (5,000 U every 12 h) for anticoagulation, and a diuretic. The patient's symptoms and laboratory indicators improved.Conclusion This case suggests that a combination of rituximab, plasma exchange, anticoagulation, and diuretics may be an effective treatment for patients with SLE complicated by TMA and NCPH.
C1 [Huang, Jinmei; Fan, Wei; Chen, Xuyan; Wu, Shufan; Dong, Zhigao; Zhang, Yi; Lin, Yiwan; Xiao, Pingping] Xiamen Med Coll, Affiliated Hosp 2, Dept Rheumatol & Immunol, Xiamen, Peoples R China.
C3 Xiamen Medical College
RP Huang, JM; Xiao, PP (corresponding author), Xiamen Med Coll, Affiliated Hosp 2, Dept Rheumatol & Immunol, Xiamen, Peoples R China.
EM jinmei201696@163.com; xiaopp0026@163.com
FU Xiamen Medical and Health Guidance Project [3502Z20224ZD1251]; Xiamen
   Medical College university-level project [K2023-41]
FX The author(s) declare financial support was received for the research,
   authorship, and/or publication of this article. This work was supported
   by the Xiamen Medical and Health Guidance Project (No. 3502Z20224ZD1251)
   and Xiamen Medical College university-level project (No. K2023-41).
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NR 28
TC 0
Z9 0
U1 1
U2 1
PU FRONTIERS MEDIA SA
PI LAUSANNE
PA AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND
SN 1664-3224
J9 FRONT IMMUNOL
JI Front. Immunol.
PD JAN 3
PY 2025
VL 15
AR 1475303
DI 10.3389/fimmu.2024.1475303
PG 10
WC Immunology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Immunology
GA S5O2A
UT WOS:001398703600001
PM 39830503
OA gold
DA 2025-06-01
ER

PT J
AU Patricio, CDE
   Eleanor, THG
   José, CZF
   Gabriela, ACM
   Hyland, AO
   Fernando, GL
   María, TA
   Beatriz, N
   Marcos, SD
   Alfredo, GPW
AF Edgar Patricio, Correa-Diaz
   Germaine Eleanor, Torres Herran
   Francisco Jose, Caiza-Zambrano
   Maria Gabriela, Acuna Chong
   Hyland, Arroyo-Ortega
   Lopez Fernando, Guillen
   Ana Maria, Toral
   Beatriz, Narvaez
   Marcos, Serrano-Duenas
   Wilson Alfredo, Gualotuna Pachacama
TI Clinical and radiological profile of neuromyelitis optica spectrum
   disorders in an Ecuadorian cohort
SO MULTIPLE SCLEROSIS AND RELATED DISORDERS
LA English
DT Article
DE Neuromyelitis optica spectrum disorder; Epidemiology; AQP4-IgG; Ecuador
ID DIAGNOSTIC-CRITERIA; MULTIPLE-SCLEROSIS; SYSTEM; EPIDEMIOLOGY;
   MULTICENTER; PREVALENCE; FEATURES; MS
AB Background: Neuromyelitis optica spectrum disorder (NMOSD) is a complex disease characterized by a severe inflammation of the central nervous system (CNS). This disease typically manifests with recurrent optic neuritis (ON) and acute transverse myelitis (ATM). The clinical and radiological spectrum of NMOSD is little known in Latin America (LATAM) and few reports have been published in the literature so far. In Ecuador, no reports on NMOSD have been published. For this reason we aimed to assess the demographic, clinical and imaging characteristics of patients with NMOSD from third level hospitals from Ecuador.
   Methods: This is a descriptive study in which we assessed medical reports of patients with inflammatory demyelinating diseases who were attended in third level hospitals from Ecuador in 2017. Then we applied the 2015 diagnostic criteria, those patients who met the new NMOSD diagnostic criteria were selected and analyzed. Additionally, exploratory sub-analyses were subsequently carried out.
   Results: We identified 59 patients with NMOSD, the relative frequency of NMOSD was 15.9%. The multiple sclerosis (MS) /NMOSD ratio was 5.2:1. Twenty four percent of patients were newly defined as having NMOSD when 2015 criteria was applied. The median time to diagnoses was shorter by the 2015 criteria than 2006 criteria (p<0.001). NMOSD was more prevalent in women (female/male ratio 4.4:1). The disease onset was more frequent at the fourth decade of life. The most common symptoms at the disease onset were ON and the association of ON with ATM. The mean of expanded disability status scale (EDSS) was 4.8 (SD +/- 1.8). Concomitant autoimmune diseases were infrequent in this population (11.9%). The brain magnetic resonance imaging (MRI) abnormalities were present in 25.7% of patients at disease onset. Spinal cord MRI showed longitudinally extensive transverse myelitis (LETM) in 91.5% of cases. Recurrent NMOSD was frequent in this cohort (88%). Positivity for antibodies against aquaporin-4 (AQP4-IgG) which was measured through indirect immunofluorescence assay (IIF) was identified in 81% of the patients tested. Patients with seronegative AQP4-IgG had higher grade of disability than seropositive patients (p<0.05). Ninety eight percent of patients received treatment with immunosuppressive drugs. Three patients died due to gastric cancer (1 patient) and infectious diseases (2 patients).
   Conclusions: This is the first descriptive study in an Ecuadorian cohort of patients with NMOSD. We show a wide epidemiological, clinical and radiological spectrum of NMOSD.
C1 [Edgar Patricio, Correa-Diaz; Germaine Eleanor, Torres Herran; Francisco Jose, Caiza-Zambrano; Marcos, Serrano-Duenas; Wilson Alfredo, Gualotuna Pachacama] Hosp Carlos Andrade Marin, Dept Neurol, Ave 18 Septiembre & Ayacucho, Quito, Ecuador.
   [Maria Gabriela, Acuna Chong] Hosp Teodoro Maldonado Carbo, Dept Neurol, Ave 25 Julio, Guaayaquil, Ecuador.
   [Hyland, Arroyo-Ortega] Hosp Especialidades Eugenio Espejo, Dept Neurol, Ave Gran Colombia, Quito, Ecuador.
   [Lopez Fernando, Guillen; Ana Maria, Toral] Hosp Jose Carrasco Arteaga Cuenca, Dept Neurol, Cuenca, Ecuador.
   [Beatriz, Narvaez] Hosp Mil, Dept Neurol, Ave Gran Colombia, Quito, Ecuador.
   [Edgar Patricio, Correa-Diaz; Marcos, Serrano-Duenas] Pontificia Univ Catolica Ecuador PUCE, Ave 12 Octubre, Quito, Ecuador.
C3 Pontificia Universidad Catolica del Ecuador
RP Patricio, CDE (corresponding author), Hosp Carlos Andrade Marin, Dept Neurol, Ave 18 Septiembre & Ayacucho, Quito, Ecuador.; Patricio, CDE (corresponding author), Pontificia Univ Catolica Ecuador PUCE, Ave 12 Octubre, Quito, Ecuador.
EM patocorrea2010@yahoo.com; gerth137@gmail.com; pancho_jcz@hotmail.com;
   mgac_md@yahoo.com; hylandneuro@outlook.com;
   fernandoguillenl@hotmail.com; anitoralg@yahoo.com; beatrizanc@yahoo.es;
   mserranod@puce.edu.ec; wislongp13@outlook.es
RI ; Serrano-Duenas, Marcos/E-8845-2015
OI Acuna Chong, Maria Gabriela/0000-0002-7630-1737; CORREA,
   PATRICIO/0000-0001-6363-8886; GUALOTUNA-PACHACAMA,
   WILSON/0000-0001-7256-8795; Serrano-Duenas, Marcos/0000-0002-4496-6654;
   Caiza Zambrano, Francisco/0000-0001-6902-1545
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NR 43
TC 13
Z9 13
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2211-0348
EI 2211-0356
J9 MULT SCLER RELAT DIS
JI Mult. Scler. Relat. Disord.
PD SEP
PY 2020
VL 44
AR 102208
DI 10.1016/j.msard.2020.102208
PG 6
WC Clinical Neurology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Neurosciences & Neurology
GA PG6VA
UT WOS:000599869900033
PM 32562910
DA 2025-06-01
ER

PT J
AU Grulich, AE
   Vajdic, CM
AF Grulich, AE
   Vajdic, CM
TI The epidemiology of non-Hodgkin lymphoma
SO PATHOLOGY
LA English
DT Review
DE non-Hodgkin lymphoma; epidemiology
ID FRANCISCO BAY AREA; SOLAR ULTRAVIOLET-RADIATION; POPULATION-BASED
   COHORT; VITAMIN SUPPLEMENT USE; HISTORY RISK-FACTORS; PRIOR MEDICATION
   USE; C VIRUS-INFECTION; RHEUMATOID-ARTHRITIS; MALIGNANT-LYMPHOMAS;
   CANCER INCIDENCE
AB Non-Hodgkin lymphoma (NHL) includes a group of more than 20 different malignant lymphoproliferative diseases that originate from lymphocytes. Rates of NHL have increased dramatically over the past few decades, although the rate of increase has recently slowed. It is now the sixth most common cancer in Australia. Globally, it is somewhat more common in men than in women, and rates are highest in North America and Australia.
   The causes of the increase in NHL rates are largely unknown. The best described risk factor for NHL is immune deficiency; rates of NHL are greatly increased, with relative risks of 10-100 or more, in people with immune deficiency associated with immune suppressive therapy after transplantation, HIV/AIDS, and congenital conditions. In addition, some NHL subtypes are associated with specific infections. These include immune-deficiency-associated central nervous system NHL (Epstein-Barr virus); gastric mucosa-associated lymphoid tissue NHL (Helicobacter pylori); adult T-cell leukemia/lymphoma (human T-lymphotrophic virus type 1) and body cavity-based lymphoma (human herpesvirus 8). However, these specific infections account for a very small proportion of total NHL incidence.
   In addition to immune deficiency and infection, other immune-related conditions are increasingly being recognised as related to NHL risk. Specific autoimmune conditions, including rheumatoid arthritis, systemic lupus erythema, Sjogren's syndrome, psoriasis and coeliac disease are associated with moderately increased risk of NHL. On the other hand, allergic and atopic conditions and their correlates such as early birth order, appear to be associated with a decreased risk of NHL.
   A variety of other exposures are less strongly related to NHL risk. These include occupational exposures, including some pesticides, herbicides, and solvents. Recently, two studies have reported that sun exposure is associated with a decreased risk of NHL. Smoking appears to be weakly positively associated with risk of follicular NHL, and alcohol intake is associated with a decreased risk of NHL.
   The pooled analysis of several case-control studies of NHL risk that are currently in the field promises to help clarify which of these risk factors are real, and will contribute to the elucidation of the mechanisms of how disorders of the immune system, and other factors, are related to NHL risk.
C1 Univ New S Wales, Natl Ctr HIV Epidemiol & Clin Res, HIV Epidemiol & Prevent Program, Darlinghurst, NSW 2010, Australia.
C3 University of New South Wales Sydney; Kirby Institute
RP Univ New S Wales, Natl Ctr HIV Epidemiol & Clin Res, HIV Epidemiol & Prevent Program, Level 2,376 Victoria St, Darlinghurst, NSW 2010, Australia.
EM agrulich@nchecr.unsw.edu.au
RI Vajdic, Claire/AAP-5940-2020
OI Vajdic, Claire/0000-0002-3612-8298
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NR 147
TC 103
Z9 115
U1 0
U2 13
PU ELSEVIER
PI AMSTERDAM
PA RADARWEG 29, 1043 NX AMSTERDAM, NETHERLANDS
SN 0031-3025
EI 1465-3931
J9 PATHOLOGY
JI Pathology
PD DEC
PY 2005
VL 37
IS 6
BP 409
EP 419
DI 10.1080/00313020500370192
PG 11
WC Pathology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Pathology
GA 995TE
UT WOS:000234126100002
PM 16373224
DA 2025-06-01
ER

PT J
AU Kiya, S
   Morino, S
   Iwasaki, K
   Nakamura, A
AF Kiya, Soichiro
   Morino, Shigeyuki
   Iwasaki, Keisuke
   Nakamura, Akihiro
TI Surgical resection of pulmonary crystal-storing histiocytosis with
   Sjogren's syndrome: A case report
SO INTERNATIONAL JOURNAL OF SURGERY CASE REPORTS
LA English
DT Article
DE Pulmonary crystal-storing histiocytosis (CSH); Sjogren's syndrome;
   Surgical resection; Case report
ID MARGINAL ZONE LYMPHOMA; IMMUNOGLOBULIN; PATIENT
AB Introduction and importance: Crystal-storing histiocytosis (CSH) is a rare clinical entity characterized by an abnormal increase in the number of histiocytes with massive accumulation of crystallized immunoglobulins. Yano et al. reported only one case of gastric CSH associated with Sjogren's syndrome. In this report, we present a case of pulmonary CSH with Sjogren's syndrome, and discuss the relevant literature.
   Case presentation: A 64-year-old woman who had never smoked presented with cough 2 years earlier. Chest CT showed that the nodule in the right lower lobe had slowly enlarged to 12 x 10 mm. We suspected primary lung cancer and performed video-assisted thoracoscopic right S6 segmentectomy. Histopathological evaluation of the resected specimen revealed crystal-storing histiocytosis. As of 6 months postoperatively, no recurrence has been identified.
   Clinical discussion: Eighteen cases of pulmonary CSH have been described in the English language peer-reviewed literature, including our case. In this case, the patient had a history of Sjogren's syndrome, but no lymphoproliferative or plasma cell disorder (LP-PCD). Therapy for all patients without LP-PCD was excisional resection of the lung. Treatment and prognosis of patients with CSH varied according to the defined pathology. Jones et al. reported the case of 54-year-old woman without LP-PCD who presented with a solitary asymptomatic focus of CSH in the lung and initially underwent lesion resection, but showed recurrence 10 years later.
   Conclusion: Pulmonary CSH is one differential diagnosis for pulmonary nodule enlargement in patients with autoimmune disease. Surgical resection appears to represent an effective therapeutic option for localized CSH, but long-term follow-up remains necessary.
C1 [Kiya, Soichiro; Morino, Shigeyuki; Nakamura, Akihiro] Sasebo City Gen Hosp, Dept Chest Surg, 9-3 Hirase Cho, Nagasaki 8578511, Japan.
   [Iwasaki, Keisuke] Sasebo City Gen Hosp, Dept Pathol, 9-3 Hirase Cho, Nagasaki 8578511, Japan.
RP Nakamura, A (corresponding author), Sasebo City Gen Hosp, Dept Chest Surg, 9-3 Hirase Cho, Nagasaki 8578511, Japan.
EM k-iwasaki@hospital.sasebo.nagasaki.jp; dzx00673@nifty.com
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NR 17
TC 3
Z9 4
U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 2210-2612
J9 INT J SURG CASE REP
JI Int. J. Surg. Case Rep.
PD AUG
PY 2021
VL 85
AR 106196
DI 10.1016/j.ijscr.2021.106196
EA JUL 2021
PG 5
WC Surgery
WE Emerging Sources Citation Index (ESCI)
SC Surgery
GA UA7LF
UT WOS:000685338900021
PM 34314972
OA Green Published, gold
DA 2025-06-01
ER

PT J
AU D'Angeli, F
   Granata, G
   Romano, IR
   Distefano, A
   Lo Furno, D
   Spila, A
   Leo, M
   Miele, C
   Ramadan, D
   Ferroni, P
   Li Volti, G
   Accardo, P
   Geraci, C
   Guadagni, F
   Genovese, C
AF D'Angeli, Floriana
   Granata, Giuseppe
   Romano, Ivana Roberta
   Distefano, Alfio
   Lo Furno, Debora
   Spila, Antonella
   Leo, Mariantonietta
   Miele, Chiara
   Ramadan, Dania
   Ferroni, Patrizia
   Li Volti, Giovanni
   Accardo, Paolo
   Geraci, Corrada
   Guadagni, Fiorella
   Genovese, Carlo
TI Biocompatible Poly(ε-Caprolactone) Nanocapsules Enhance the
   Bioavailability, Antibacterial, and Immunomodulatory Activities of
   Curcumin
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Article
DE poly(epsilon-caprolactone) nanocapsules; curcumin; bioaccessibility;
   antibacterial activity; probiotics; inflammation; ADSCs; LPS; cytokines;
   immunomodulatory activity
ID ESCHERICHIA-COLI; GUT MICROBIOTA; INFLAMMATION; CELLS; ANTIOXIDANT;
   STABILITY; COMPONENT; DISEASES; POLYMER; DESIGN
AB Curcumin (Cur), the primary curcuminoid found in Curcuma longa L., has garnered significant attention for its potential anti-inflammatory and antibacterial properties. However, its hydrophobic nature significantly limits its bioavailability. Additionally, adipose-derived stem cells (ADSCs) possess immunomodulatory properties, making them useful for treating inflammatory and autoimmune conditions. This study aims to verify the efficacy of poly(epsilon-caprolactone) nanocapsules (NCs) in improving Cur's bioavailability, antibacterial, and immunomodulatory activities. The Cur-loaded nanocapsules (Cur-NCs) were characterized for their physicochemical properties (particle size, polydispersity index, Zeta potential, and encapsulation efficiency) and stability over time. A digestion test simulated the behavior of Cur-NCs in the gastrointestinal tract. Micellar phase analyses evaluated the Cur-NCs' bioaccessibility. The antibacterial activity of free Cur, NCs, and Cur-NCs against various Gram-positive and Gram-negative strains was determined using the microdilution method. ADSC viability, treated with Cur-NCs and Cur-NCs in the presence or absence of lipopolysaccharide, was analyzed using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide assay. Additionally, ADSC survival was assessed through the Muse apoptotic assay. The expression of both pro-inflammatory (interleukin-1 beta and tumor necrosis factor-alpha) and anti-inflammatory (IL-10 and transforming growth factor-beta) cytokines on ADSCs was evaluated by real-time polymerase chain reaction. The results demonstrated high stability post-gastric digestion of Cur-NCs and elevated bioaccessibility of Cur post-intestinal digestion. Moreover, Cur-NCs exhibited antibacterial activity against Escherichia coli without affecting Lactobacillus growth. No significant changes in the viability and survival of ADSCs were observed under the experimental conditions. Finally, Cur-NCs modulated the expression of both pro- and anti-inflammatory cytokines in ADSCs exposed to inflammatory stimuli. Collectively, these findings highlight the potential of Cur-NCs to enhance Cur's bioavailability and therapeutic efficacy, particularly in cell-based treatments for inflammatory diseases and intestinal dysbiosis.
C1 [D'Angeli, Floriana; Spila, Antonella; Leo, Mariantonietta; Miele, Chiara; Ramadan, Dania; Ferroni, Patrizia; Guadagni, Fiorella] San Raffaele Roma Open Univ, Dept Promot Human Sci & Qual Life, I-00166 Rome, Italy.
   [Granata, Giuseppe; Accardo, Paolo; Geraci, Corrada] CNR Inst Biomol Chem, Via Paolo Gaifami 18, I-95126 Catania, Italy.
   [Romano, Ivana Roberta; Lo Furno, Debora] Univ Catania, Dept Biomed & Biotechnol Sci, Sect Physiol, I-95123 Catania, Italy.
   [Distefano, Alfio; Li Volti, Giovanni] Univ Catania, Dept Biomed & Biotechnol Sci, Sect Biochem, I-95123 Catania, Italy.
   [Ferroni, Patrizia; Guadagni, Fiorella] IRCCS San Raffaele, Interinst Multidisciplinary Biobank BioBIM, I-00166 Rome, Italy.
   [Genovese, Carlo] Kore Univ Enna, Dept Med & Surg, I-94100 Enna, Italy.
   [Genovese, Carlo] Spin Off Univ Catania, Nacture Srl, Via Santa Sofia 97, I-95123 Catania, Italy.
C3 University of Catania; University of Catania; IRCCS San Raffaele Pisana;
   Vita-Salute San Raffaele University; IRCCS Ospedale San Raffaele;
   Universita Kore di ENNA
RP D'Angeli, F (corresponding author), San Raffaele Roma Open Univ, Dept Promot Human Sci & Qual Life, I-00166 Rome, Italy.
EM floriana.dangeli@unikore.it; giuseppe.granata@icb.cnr.it;
   ivanarobertaromano@yahoo.it; distalfio@gmail.com; lofurno@unict.it;
   antonella.spila@sanraffaele.it; mariantonietta.leo@uniroma5.it;
   chiara.miele@sanraffaele.it; dania.ramadan@uniroma5.it;
   patrizia.ferroni@uniroma5.it; livolti@unict.it; paolo.accardo@yahoo.it;
   corrada.geraci@icb.cnr.it; fiorella.guadagni@uniroma5.it;
   carlo.genovese@unikore.it
RI GENOVESE, Carlo/D-7837-2012; leo, mariantonietta/AAL-3165-2021; Volti,
   Giovanni/A-2435-2008; Granata, Giuseppe/C-6093-2015; Furno,
   Debora/P-1667-2019; D'Angeli, Floriana/AAU-5570-2020
FU Italian Ministry of Health (Ricerca Corrente); European Social Fund PO
   FESR Sicily; Curcumin for the development of nutraceuticals, vaccine
   adjuvants, cosmeceuticals [CUP G88I18000710007]
FX This research was funded by the Italian Ministry of Health (Ricerca
   Corrente) and by the European Social Fund PO FESR Sicily 2014-2020
   Action 1.1.5 "NUVACAL-BC-Baicalin and Curcumin for the development of
   nutraceuticals, vaccine adjuvants, cosmeceuticals and functional foods"
   (CUP G88I18000710007).
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NR 153
TC 0
Z9 0
U1 1
U2 1
PU MDPI
PI BASEL
PA MDPI AG, Grosspeteranlage 5, CH-4052 BASEL, SWITZERLAND
SN 1661-6596
EI 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2024
VL 25
IS 19
AR 10692
DI 10.3390/ijms251910692
PG 31
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Biochemistry & Molecular Biology; Chemistry
GA I7Z2K
UT WOS:001332394500001
PM 39409022
OA gold
DA 2025-06-01
ER

PT J
AU Behl, T
   Mehta, K
   Sehgal, A
   Singh, S
   Sharma, N
   Ahmadi, A
   Arora, S
   Bungau, S
AF Behl, Tapan
   Mehta, Keshav
   Sehgal, Aayush
   Singh, Sukhbir
   Sharma, Neelam
   Ahmadi, Amirhossein
   Arora, Sandeep
   Bungau, Simona
TI Exploring the role of polyphenols in rheumatoid arthritis
SO CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION
LA English
DT Review
DE Polyphenol; rheumatoid arthritis; antioxidant; anti-inflammatory;
   apoptosis
ID NF-KAPPA-B; ADJUVANT-INDUCED ARTHRITIS; COLLAGEN-INDUCED ARTHRITIS;
   MODIFYING ANTIRHEUMATIC DRUGS; FIBROBLAST-LIKE SYNOVIOCYTES;
   ALPHA-INDUCED INFLAMMATION; OLIVE-OIL POLYPHENOL; P-COUMARIC ACID;
   TNF-ALPHA; SYNOVIAL FIBROBLASTS
AB Rheumatoid arthritis (RA) is a chronic, inflammatory and autoimmune disorder which is mainly characterized by inflammation in joints, bone erosions and cartilaginous destruction that leads to joint dysfunction, deformation, and/or permanent functional impairment. The prevalence of RA is increasing, incurring a considerable burden on healthcare systems globally. The exact etiology of RA is unknown, with various pathways implicated in its pathophysiology. Non-steroidal anti-inflammatory drugs (NSAIDs) including celecoxib, diclofenac and ibuprofen, disease-modifying anti-rheumatic drugs (DMARD) including azathioprine, methotrexate and cyclosporine, biological agents including anakinra, infliximab, and rituximab and immunosuppressants are used for symptomatic relief in patients with RA, but these medications have severe adverse effects such as gastric ulcers, hypertension, hepatotoxicity and renal abnormalities which restrict their use in the treatment of RA; new RA treatments with minimal side-effects are urgently required. There is accumulating evidence that dietary polyphenols may show therapeutic efficacy in RA through their antioxidant, anti-inflammatory, apoptotic, and immunosuppressant activities and modulation of the tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, mitogen-activated protein kinase (MAPK), IL-1 beta, c-Jun N-terminal kinase (JNK), and nuclear factor kappa light-chain-enhancer of activated B cell (NF-kappa B) pathways. While resveratrol, genistein, carnosol, epigallocatechin gallate, curcumin, kaempferol, and hydroxytyrosol have also been studied for the treatment of RA, the majority of data are derived from animal models. Here, we review the various pathways involved in the development of RA and the preclinical and clinical data supporting polyphenols as potential therapeutic agents in RA patients. Our review highlights that high-quality clinical studies are required to decisively establish the anti-rheumatic efficacy of polyphenolic compounds.
C1 [Behl, Tapan; Mehta, Keshav; Sehgal, Aayush; Singh, Sukhbir; Sharma, Neelam; Arora, Sandeep] Chitkara Univ, Chitkara Coll Pharm, Rajpura 140401, Punjab, India.
   [Ahmadi, Amirhossein] Mazandaran Univ Medial Sci, Fac Pharm, Sari, Iran.
   [Bungau, Simona] Univ Oradea, Fac Med & Pharm, Dept Pharm, Oradea, Romania.
C3 Chitkara University, Punjab; University of Oradea
RP Behl, T (corresponding author), Chitkara Univ, Chitkara Coll Pharm, Rajpura 140401, Punjab, India.
EM tapanbehl31@gmail.com
RI Bungau, Simona Gabriela/C-1831-2015; Singh, Dr. Sukhbir/AAZ-7468-2020;
   Behl, Tapan/W-3523-2019; Sharma, Dr. Neelam/AAZ-7463-2020; Ahmadi,
   Amirhossein/H-2136-2011
OI Singh, Sukhbir/0000-0003-0692-7002; Sharma, Neelam/0000-0002-5200-7330;
   Ahmadi, Amirhossein/0000-0002-9737-3633
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NR 166
TC 62
Z9 66
U1 2
U2 41
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1040-8398
EI 1549-7852
J9 CRIT REV FOOD SCI
JI Crit. Rev. Food Sci. Nutr.
PD OCT 28
PY 2022
VL 62
IS 19
BP 5372
EP 5393
DI 10.1080/10408398.2021.1924613
EA APR 2021
PG 22
WC Food Science & Technology; Nutrition & Dietetics
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Food Science & Technology; Nutrition & Dietetics
GA 2Q7CU
UT WOS:000651489400001
PM 33998910
DA 2025-06-01
ER

PT J
AU Raderer, M
   Vorbeck, F
   Formanek, M
   Osterreichers, C
   Valencak, J
   Penz, M
   Kornek, G
   Hamilton, G
   Dragosics, B
   Chott, A
AF Raderer, M.
   Vorbeck, F.
   Formanek, M.
   Osterreichers, C.
   Valencak, J.
   Penz, M.
   Kornek, G.
   Hamilton, G.
   Dragosics, B.
   Chott, A.
TI Importance of extensive staging in patients with mucosa-associated
   lymphoid tissue (MALT)-type lymphoma
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE MALT-type lymphoma; multifocal involvement; staging
AB Lymphoma of the mucosa-associated lymphoid tissue (MALT) type usually arises in MALT acquired through chronic antigenic stimulation triggered by persistent infection and/or autoimmune processes. Due to specific ligand receptor interactions between lymphoid cells and high endothelial venules of MALT, both normal and neoplastic lymphoid cells display a pronounced homing tendency to MALT throughout the body. In the case of neoplastic disease these homing properties may be responsible for lymphoma dissemination among various MALT-sites. According to this concept, we have standardized staging procedures in all patients diagnosed with MALT-type lymphoma. All patients with MALT-type lymphoma underwent standardized staging procedures before treatment. Staging included ophthalmologic examination, otolaryngologic investigation, gastroscopy with multiple biopsies, endosonography of the upper gastrointestinal tract, enteroclysis, colonoscopy, computed tomography of thorax and abdomen and bone marrow biopsy. Biopsy was performed in all lesions suggestive for lymphomatous involvement, and evaluation of all biopsy specimens was performed by a reference pathologist. 35 consecutive patients with histologically verified MALT-type lymphoma were admitted to our department. Twenty-four patients (68%) had primary involvement of the stomach, five (15%) had lymphoma of the ocular adnexa, three (8.5%) had lymphoma of the parotid, and three (8,5%) of the lung. Lymph node involvement corresponding to stage Ell disease was found in 13 patients (37%), only one patient with primary gastric lymphoma had local and supradiaphragmatic lymph-node involvement (stage Elll). Bone marrow biopsies were negative in all patients. Overall, eight of 35 patients (23%) had simultaneous biopsy-proven involvement of two MALT-sites: one patient each had lymphoma of parotid and lacrimal gland, conjunctiva and hypopharynx, conjunctiva and skin, lacrimal gland and lung, stomach and colon, and stomach and lung. The remaining two patients had bilateral parotideal lymphoma. Staging work-up was negative for lymph-node involvement in all of these eight patients. The importance of extensive staging in MALT-type lymphoma is emphasized by the demonstration of multiorgan involvement in almost a quarter of patients. In addition, our data suggest that extra-gastrointestinal MALT-type lymphoma more frequently occurs simultaneously at different anatomic sites than MALT-type lymphoma involving the GI-tract. 2000 Cancer Research Campaign
C1 [Raderer, M.; Penz, M.; Kornek, G.] Univ Vienna, Dept Internal Med 1, Div Oncol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
   [Vorbeck, F.] Univ Vienna, Dept Internal Med 1, Div Radiol, A-1090 Vienna, Austria.
   [Formanek, M.] Univ Vienna, Dept Internal Med 1, Div Otolaryngol, A-1090 Vienna, Austria.
   [Osterreichers, C.; Dragosics, B.] Univ Vienna, Dept Internal Med 1, Div Internal Med 4, A-1090 Vienna, Austria.
   [Valencak, J.; Chott, A.] Univ Vienna, Dept Internal Med 1, Div Clin Pathol, A-1090 Vienna, Austria.
   [Hamilton, G.] KH Lainz, Ludwig Boltzmann Inst Clin Oncol, Vienna, Austria.
C3 University of Vienna; University of Vienna; University of Vienna;
   University of Vienna; University of Vienna; Ludwig Boltzmann Institute;
   Ludwig Boltzmann Cluster Oncology (LBC ONC)
RP Raderer, M (corresponding author), Univ Vienna, Dept Internal Med 1, Div Oncol, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
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NR 23
TC 125
Z9 130
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD AUG
PY 2000
VL 83
IS 4
BP 454
EP 457
DI 10.1054/bjoc.2000.1308
PG 4
WC Oncology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Oncology
GA V42ZR
UT WOS:000209652200007
PM 10945490
OA hybrid, Green Published
DA 2025-06-01
ER

PT J
AU Salinas, M
   Flores, E
   López-Garrigós, M
   Leiva-Salinas, C
AF Salinas, Maria
   Flores, Emilio
   Lopez-Garrigos, Maite
   Leiva-Salinas, Carlos
TI High frequency of anti-parietal cell antibody (APCA) and intrinsic
   factor blocking antibody (IFBA) in individuals with severe vitamin B12
   deficiency - an observational study in primary care patients
SO CLINICAL CHEMISTRY AND LABORATORY MEDICINE
LA English
DT Article
DE clinical laboratory services; computer assisted diagnosis; primary
   health care; vitamin B12 deficiency
ID FOLATE-DEFICIENCY; DIAGNOSIS; CANCER; RISK
AB Background: Vitamin B12 deficiency is common worldwide and is also linked to several diseases including autoimmune atrophic gastritis (AAG). The presence of anti-parietal cell antibodies (APCA) and/or intrinsic factor blocking antibodies (IFBA) is indicative of AAG that may develop into pernicious anemia. Both conditions are known to be associated with an increased risk of gastric carcinoma. The aim of this study was to estimate the frequency of individuals positive for APCA and IFBA antibodies in primary care patients with severe vitamin B12 deficiency.
   Methods: An observational study was designed and 5468 consecutive patients from primary care with a request for vitamin B12 status were included and add-on testing for APCA and IF BA that were automatically registered if severe vitamin B12 deficiency was identified (<73.8 pmol/L). For patients included in the intervention, study demographic data, mean corpuscular volume (MCV) and hemoglobin values were collected.
   Results: Seventy-seven patients with severe vitamin B12 deficiency were identified and out of these 44 (57%) presented with antibodies to APCA and 11 (14%) to IFBA, 25 (32.5%) had anemia, and 25 (32.5%) had macrocytosis. The majority of APCA and/or IFBA positive patients were found in the age group >70 years. Both anemia and macrocytosis were more common among APCA positive patients but the association was not statistically significant, neither was the correlation between IFBA status and anemia and/or macrocytosis. Among the patients with anemia, 10 (39%) had macrocytosis, although the rate of macrocytosis among patients with or without anemia did not differ significantly.
   Conclusions: The automated analysis strategy of measuring antibodies to APCA and IFBA in patients with severe vitamin B12 deficiency, efficiently detected positivity in more than 60% the patients. The result point to the presence of a high rate of otherwise undetected AAG and the potential clinical utility of APCA and IFBA as markers in primary care.
C1 [Salinas, Maria; Flores, Emilio; Lopez-Garrigos, Maite] Hosp Univ San Juan, Clin Lab, Carretera Alicante Valencia S-N, Alicante 03550, Spain.
   [Salinas, Maria] Univ Miguel Hernandez, Dept Biochem & Mol Pathol, Elche, Spain.
   [Flores, Emilio] Univ Miguel Hernandez, Dept Clin Med, Elche, Spain.
   [Leiva-Salinas, Carlos] Univ Missouri, Dept Radiol, Columbia, MO USA.
C3 Universidad Miguel Hernandez de Elche; Universidad Miguel Hernandez de
   Elche; University of Missouri System; University of Missouri Columbia
RP Salinas, M (corresponding author), Hosp Univ San Juan, Clin Lab, Carretera Alicante Valencia S-N, Alicante 03550, Spain.; Salinas, M (corresponding author), Univ Miguel Hernandez, Dept Biochem & Mol Pathol, Elche, Spain.
EM salinas_mar@gva.es
RI Lopez-Garrigos, Maite/IVV-4783-2023; FLORES, EMILIO/ACV-7488-2022;
   Salinas, Maria/JMR-2052-2023; Flores, Emilio/F-5536-2017;
   Lopez-Garrigos, Maite/M-7981-2013
OI Flores, Emilio/0000-0001-7524-0808; Lopez-Garrigos,
   Maite/0000-0001-8440-6558
FU Phadia GmbH, Freiburg, Germany
FX The study was financially supported by Phadia GmbH, Freiburg, Germany.
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NR 23
TC 7
Z9 8
U1 0
U2 7
PU WALTER DE GRUYTER GMBH
PI BERLIN
PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY
SN 1434-6621
EI 1437-4331
J9 CLIN CHEM LAB MED
JI Clin. Chem. Lab. Med.
PD MAR
PY 2020
VL 58
IS 3
BP 424
EP 429
DI 10.1515/cclm-2019-0749
PG 6
WC Medical Laboratory Technology
WE Science Citation Index Expanded (SCI-EXPANDED)
SC Medical Laboratory Technology
GA KK8NZ
UT WOS:000512994400026
PM 31714882
DA 2025-06-01
ER

EF