From Primary Tumor to Peritoneal Niche: Microenvironmental Divergence in Gastric Cancer Peritoneal Metastasis

Gastric cancer peritoneal metastasis is not simply an extension of the primary tumor into the abdominal cavity. It represents a biologically distinct disease context shaped by interactions between disseminated tumor cells, peritoneal fluid, mesothelial surfaces, submesothelial stroma, extracellular matrix, immune populations, and malignant ascites. In this narrative review, we examine peritoneal metastasis as a transition between three related but physiologically different states: the primary gastric tumor, free-floating tumor cells or spheroids in the peritoneal fluid, and established mesothelial or submesothelial metastatic implants. We discuss how tumor cells acquire dissemination competence in the primary tumor, survive detachment and fluid-phase stress, adhere to remodeled mesothelium, recruit stromal and immune support, and adapt to ascites-mediated signaling. We also review how the peritoneal niche may contribute to biomarker discordance, immune exclusion, therapeutic resistance, and limitations of conventional response assessment. Where relevant, we distinguish evidence derived directly from gastric cancer peritoneal metastasis from preclinical data, extrapolation from other peritoneal malignancies, and hypothesis-generating interpretation. Finally, we summarize practical implications for tissue sampling, ascites and lavage analysis, biomarker interpretation, translational modeling, and peritoneal-directed therapeutic strategies. A clearer understanding of the biological divergence between the primary tumor, the fluid-phase compartment, and peritoneal implants may improve the study and clinical management of gastric cancer peritoneal metastasis.