ArticleJournal of advanced research2026
Genomic landscape of paired primary and peritoneal metastatic lesions in gastric cancer highlights evolutionary dynamics and mutational drivers.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Multi-site sequencing supports dual-track evolution and identifies candidate metastasis-associated factors in gastric cancer ovarian metastasis.Clinical and translational medicine · 2026Article
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- Review
- Divergent clonal evolution and tumor microenvironment remodeling shape gastric cancer peritoneal metastasis.Communications biology · 2026Article
- Decoding clone evolution in HER2 amplified breast cancer through single-cell and spatial transcriptomics analysis of copy number variations.Scientific reports · 2026Article
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- Pan-cancer clinicopathological and genomic characteristics of peritoneal metastasis.NPJ precision oncology · 2025Article
Corrections and comments
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Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPeritoneal metastasis is a prevalent form of gastric cancer spread, often resulting in poor outcomes. Due to the lack of clinical recommendation for surgery, current omics studies are limited to analyzing suspending malignant cells in ascites using external controls, rather than examining peritoneal metastatic nodules alongside their paired primary tumors.
objectivesThis study aims to elucidate the genomic landscape of gastric cancer peritoneal metastasis and identify key genetic drivers by comparing peritoneal dissemination lesions and their corresponding primary samples.
methodsWhole-exome sequencing of 30 samples from 15 gastric cancer patients with peritoneal metastasis was conducted. We compared mutational and copy number variations, explored actionable targets and biomarkers, and contextualized our findings with the TCGA cohort.
resultsWe identified distinct mutation patterns in gastric cancer with peritoneal metastasis, including increased mutation frequency in the cadherin superfamily and Fanconi anemia pathway. Peritoneal metastasis and primary lesions frequently harbored both parental clones and specific subclones. Well-known driver mutations (e.g., TP53, FAT1, CDH1, ARID1A) occurred early in gastric cancer tumorigenesis, while peritoneal metastasis-specific mutations (e.g., FADS6, NDUFS7, DUSP4) and mutational signatures were linked to adverse outcomes. DEK amplification was significantly higher in peritoneal metastasis lesions (46.7 %) versus primary tumors (13.3 %), with DEK expression levels closely associated with gastric cancer stemness signatures, validated through in vitro and in vivo studies.
conclusionOur study elucidates clonal evolution in gastric cancer peritoneal metastasis, identifies mutational drivers, and highlights potential therapeutic targets. These findings provide valuable insights for developing precise treatment strategies for gastric cancer patients with peritoneal metastasis.
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