Immune Evasion in Ovarian Cancer Peritoneal Metastasis: Mechanisms and Biomarker-Guided Therapeutic Matching.

Ovarian cancer peritoneal metastasis remains a major cause of recurrence and death despite advances in cytoreductive surgery, platinum-based chemotherapy, PARP inhibition, and immune checkpoint blockade. The limited activity of immunotherapy in this setting reflects layered immune resistance shaped by impaired antigen visibility, redundant inhibitory receptor networks, suppressive myeloid and regulatory circuits, and metabolic-epigenetic constraints within ascites and multicellular spheroids. These compartment-specific features distinguish peritoneal disease from anatomically confined tumors and help explain why systemic immune reinvigoration alone rarely produces durable benefit. Here, we synthesize current evidence on the mechanisms that govern immune escape in ovarian cancer peritoneal dissemination, with emphasis on antigen presentation defects, checkpoint-driven T-cell exhaustion, anti-phagocytic signaling, soluble suppressive mediators, and metabolic remodeling of the ascites microenvironment. We further examine how DNA damage response states intersect with innate immune sensing and discuss the translational implications of homologous recombination deficiency for combination treatment design. Finally, we propose a biomarker-guided framework that links antigen-presentation competence, immune engagement, dominant suppressive axes, and ascites-specific biology to rational therapeutic matching. This mechanism-centered view supports more precise trial design and provides a roadmap for combination immunotherapy in advanced ovarian cancer.