This dataset contains an integrated reanalysis of proteomic and phosphoproteomic results derived from previously published studies. We applied a standardized statistical framework and Kinase-Substrate Enrichment Analysis (KSEA) to identify cross-disease regulatory patterns. The original raw data are available from the respective studies cited in this work.

Source datasets:
Proteomics:
- Lung cancer: LinkedOmics (https://doi.org/10.1093/nar/gkx1090)
- Glioblastoma: https://doi.org/10.1016/j.ccell.2021.01.006
- Alzheimer’s disease: https://neuropro.biomedical.hosting

Phosphoproteomics:
- Lung cancer: LinkedOmics https://www.linkedomics.org/data_download/CPTAC-LUAD/
- Glioblastoma: LinkedOmics https://www.linkedomics.org/data_download/CPTAC-GBM/
- Alzheimer’s disease: https://doi.org/10.1038/s43587-021-00071-1

Processing:
- Analyses performed in R
- Differential analysis using t-tests
- FDR correction applied for cancer datasets
- Kinase activity inferred from phosphosites data using KSEA web tool (https://casecpb.shinyapps.io/ksea/) using only PhosphoSitePlus database integrated within the tool.  

Descriptions:
- Table S1: 16_kinase_substrate_consistent_directions.xlsx: 16 kinase–phosphosite pairs where the regulatory direction of kinase and its substrate is consistent but with opposing patterns between cancer and Alzheimer’s disease, 5 high-confidence pairs are high-lighted.  
- DAP_*: Differentially abundant proteins
- Phosphosites_*: Differentially phosphorylated sites 
- KSEA_Kinase_Scores_*: Kinase activity scores
- 37_DAP_AD_opposite_cancer: 37 proteins with opposing abundance patterns between cancer and Alzheimer’s disease.
- 69_DPS_AD_opposite_cancer: 69 differentially phosphorylated sites with opposing patterns between cancer and Alzheimer’s disease. 
- Combined_Kinase_KSEA_scores: combined KSEA scores from  with directions, sorted by pattern.  24 consistent pairs are color-coded.  
- Combined_Phosphosites_sorted: combined phosphosite with p-values and directions, sorted by pattern

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Opposite patterns refer to proteins/sites that are upregulated in cancer (LU/GBM) but downregulated in AD, or vice-versa.