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Transl. Med."],"published-print":{"date-parts":[[2026,5,27]]},"abstract":"<jats:p>\n                    Cancer-associated fibroblasts (CAFs) are central architects of immunosuppression and therapy resistance across malignancies, yet how tumor-intrinsic genomic instability instructs stromal reprogramming remains unresolved. Integrated single-cell transcriptomics and epigenomics of samples from patients with high-grade serous ovarian carcinoma revealed POSTN\n                    <jats:sup>+<\/jats:sup>\n                    myofibroblast-like cancer-associated fibroblasts (myCAFs) and effector regulatory T cells (eT\n                    <jats:sub>reg<\/jats:sub>\n                    cells) as critical mediators of immunosuppression in tumors with high genomic instability. Mechanistically, unstable genomes activated tumor-intrinsic STING signaling, triggering WNT3a\/7a secretion. WNT\/\u03b2-catenin signaling in fibroblasts established a POSTN-dependent positive feedback loop that epigenetically locked cells into a POSTN\n                    <jats:sup>+<\/jats:sup>\n                    myCAF lineage. These myCAFs reciprocally expanded eT\n                    <jats:sub>reg<\/jats:sub>\n                    cells and exhausted CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells, thereby converting genomic instability\u2013driven immune activation into suppression and limiting poly(ADP-ribose) polymerase inhibitor (PARPi) efficacy. Therapeutic POSTN blockade reinvigorated T cell cytotoxicity, depleted eT\n                    <jats:sub>reg<\/jats:sub>\n                    cells, and potentiated PARP inhibition in ovarian and breast cancer models, overcoming resistance. Our work resolves the dual roles of genomic instability and identifies POSTN as a stromal-specific checkpoint to mediate immunosuppression in genomically unstable tumors.\n                  <\/jats:p>","DOI":"10.1126\/scitranslmed.ady2719","type":"journal-article","created":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T17:58:36Z","timestamp":1779904716000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":6,"title":["Genomic instability drives POSTN\n                    <sup>+<\/sup>\n                    myofibroblasts via STING-WNT axis to promote immunosuppression and PARPi resistance in ovarian cancer"],"prefix":"10.1126","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9971-2264","authenticated-orcid":true,"given":"Dan","family":"Liu","sequence":"first","affiliation":[{"name":"National Clinical Research Center for Obstetrics and Gynecology, Department of Gynecological Oncology, Tongji Hospital, Tongji 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