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Life sciences · Journal article
Frontiers in Oncology · October 15, 2026
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Gastric cancer peritoneal metastasis (GCPM), particularly associated with diffuse and poorly cohesive cancers, in which tumour cells grow singly or in small, loosely associated groups, presents an anatomical and immunological treatment challenge. This review examines the peritoneal surface and surrounding fluid as an interacting immune compartment comprising tumour implants, malignant ascites, free tumour cells, stroma and immune populations. Human studies identify cytotoxic-cell depletion or exhaustion, macrophage-rich ascites and suppressive soluble mediators; experimental findings support complement-pathway involvement in immune-checkpoint ligand expression. These observations offer a biological explanation for impaired local immunity but do not establish clinical resistance to checkpoint inhibition. Systemic therapy remains the treatment backbone, yet pivotal trials rarely report the Peritoneal Cancer Index (PCI), cytology, ascites response or peritoneal-specific progression. Early studies combine checkpoint blockade with pressurised intraperitoneal aerosol chemotherapy (PIPAC), repeated intraperitoneal paclitaxel or hyperthermic intraperitoneal chemotherapy (HIPEC); direct intraperitoneal antibodies, cytokines and cellular therapies are also under investigation. Feasibility and local pharmacodynamic changes do not establish synergistic benefit. Future trials should compare an added intraperitoneal treatment against an otherwise identical systemic regimen, collect matched blood, ascites and peritoneal tissue samples over time, and relate immune changes to cytological clearance, PCI, symptoms and survival. Operative consolidation requires a separate randomised assessment in prospectively defined responders. Treatment continuity, quality of life, nutrition and hospital-free survival are essential measures of net benefit.