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Life sciences · Journal article
Frontiers in Immunology · November 5, 2026
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Ovarian cancer is diagnosed predominantly after menopause, but chronological age, reproductive aging, cellular senescence, immunosenescence, and treatment-related immune dysfunction are frequently conflated. This overlap obscures whether immune phenotypes arise from aging, tumor histotype, therapy, or tumor-derived signals and limits the interpretation of age-associated biomarkers and treatment studies. This narrative review critically evaluates how menopause-associated endocrine remodeling, stromal and cellular senescence, senescence-associated secretory phenotype factors, and IL-6, CXCL8, TNF-α, and IL-1β signaling may interact with the ovarian-cancer immune microenvironment. Histotype-defining genomic pathways, including TP53 alteration, homologous-recombination deficiency, and KRAS–MAPK signaling, are separated from mechanisms plausibly modified by aging. Evidence is interpreted according to four contexts: human ovarian cancer, non-malignant human ovary or pelvic tissue, ovarian cell and animal models, and indirect studies from other cancers or organs; age-resolved findings are considered separately. Human evidence supports marked heterogeneity in immune infiltration, T-cell dysfunction, suppressive myeloid programs, and cytokine signaling, but direct age-resolved clinical evidence remains limited. Tumor-driven immune escape, therapy-induced senescence, and systemic immunosenescence can generate overlapping phenotypes and require explicit separation in study design and interpretation. This review highlights an evidence framework based on histotype, tissue compartment, treatment exposure, functional age, and longitudinal sampling. Progress requires prospective cohorts that include older and frail adults and jointly assess tumor biology, immune state, treatment toxicity, and clinical outcome.