ArticleBritish journal of cancer2025
Smad4 loss identifies aggressive subtype with immunotherapy and anti-HER-2 treatment resistance in gastric cancer.
Article in British journal of cancer, 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.
- TGF‑β1 in cancer: From tumour suppressor to promoter, molecular mechanisms, and precision therapeutic strategies (Review).International journal of oncology · 2026Review
- Genetic Medicine Approaches for Tumor Suppressor Loss: Therapeutic Replacement with Self-Amplifying RNA.Pharmaceutical research · 2026Review
- CD8Cancer science · 2026Article
- Putative identification of CASTOR1 as one of the targets of ganoderic acid a via thermal proteome profiling and molecular docking.Frontiers in pharmacology · 2026Article
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Authors and funding
11 authors.
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Abstract
backgroundSMAD4 mutation and homozygous deletion represent the most prevalent genomic events driving aggressive biological behavior in gastric cancer (GC). However, clinical outcome and therapeutic response in GC patients with Smad4-loss remains obscure.
methodsThis study included 990 GC patients from four independent clinical centers including the Zhongshan Hospital (ZSHS) cohort, the Cancer Genomic Atlas (TCGA) cohort, the Samsung Medical Center (SMC) cohort and the Memorial Sloan Kettering Cancer Center (MSKCC) cohort.
resultsIn ZSHS cohort, 60/454 GC patients harbored Smad4-loss are characterized by lower pN stage, well histology differentiation, lower EBV infection, null p53 staining and lower tumor proliferation. Smad4-loss GC patients exhibit miserable overall survival across ZSHS cohort and TCGA cohort. Moreover, Smad4-loss GC patients yield no impact on adjuvant chemotherapy, poor outcome upon anti-PD-1 immunotherapy or anti-HER-2 therapy. Interestingly, Smad4-loss GC show more well and intermediate differentiation and lower Ki67 staining. Furthermore, Smad4-loss GC exhibit tumor immunosuppressive contexture characterized with enriched CXCL13
conclusionsSmad4 loss yields poor clinical outcome, immunotherapy and anti-HER-2 treatment resistance and tumor immunosuppressive contexture in GC patients. Our findings provide clues for further detailed biological investigation and aggressive clinical management in Smad4-loss GC patients.
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