ArticleCellular and molecular life sciences : CMLS2025
Proteomic characterization of MET-amplified esophageal adenocarcinomas reveals enrichment of alternative splicing- and androgen signaling-related proteins.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MET Expression in Upper Gastrointestinal Adenocarcinoma: Prevalence, Prognostic Impact, and Implications for Anti-MET Antibody-Drug Conjugate Therapy.International journal of cancer · 2026Article
- Proteomic characterization of SMARCA-deficient esophageal adenocarcinoma reveals complement evasion and DNA repair-associated prognostic subgroups.British journal of cancer · 2026Article
- SMARCA2 and SMARCA4-deficiency is associated with a distinct molecular and microenvironmental subtype of esophageal adenocarcinoma.Scientific reports · 2026Article
- MDM2-amplified esophageal adenocarcinomas exhibit an activated metabolic and immunosuppressive phenotype with multiple potential therapeutic targets.BMC cancer · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
backgroundEsophageal adenocarcinomas (EACs) represent an evolving tumor entity with high mortality rates. MET amplification is a recurrent driver in EACs and is associated with decreased patient survival. However, the response to MET inhibitors is limited. Recent studies have identified several mechanisms that lead to resistance against MET inhibitors in different tumor entities. Nonetheless, a characterization of additional vulnerable targets beyond MET has not been conducted in MET-amplified EACs.
methodsIn this study, we determined the MET amplification status in a cohort of more than 900 EACs using fluorescence in situ hybridization (FISH) and compared the proteomes of MET-amplified (n = 20) versus non-amplified tumors (n = 39) by mass spectrometry.
resultsWe identified a phenotype, present in almost all MET-amplified tumors, which shows an enrichment of alternative RNA splicing, and androgen receptor signaling proteins, as well as decreased patient survival. Additionally, our analyses revealed a negative correlation between MET expression and patient survival in MET-amplified EACs, indicating biological heterogeneity with clinical relevance despite the presence of MET amplification as the predominant oncogenic driver. Furthermore, quantitative immunohistochemical analysis of the inflammatory tumor microenvironment showed that an increased percentage of M2 macrophages is associated with lower overall survival in MET-amplified EACs.
conclusionsOur results provide valuable insights into possible new therapeutic approaches for MET-amplified EACs for further research.
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