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In samples from patients with high-grade serous ovarian carcinoma, tumors with high genomic instability activated tumor-intrinsic STING signaling and secreted WNT3a/7a, which induced WNT/β-catenin signaling in fibroblasts to epigenetically lock them into a POSTN-expressing myofibroblast-like CAF lineage. These POSTN myCAFs expanded effector regulatory T cells and exhausted CD8 T cells, converting genome-instability–driven immune activation into immunosuppression and limiting PARP inhibitor efficacy, while therapeutic POSTN blockade restored T cell cytotoxicity, depleted effector Tregs, and potentiated PARP inhibition in ovarian and breast cancer models.

Using a Japanese claims database of 1,459 adolescent and young adult (AYA, 15–39 years) cancer patients initiating anthracycline therapy, 60.4% received baseline echocardiography, with much lower proportions undergoing monitoring during treatment and 41.0% having echocardiography within one year after therapy. Baseline echocardiography was more likely in younger AYAs, males, patients with lymphoma/leukemia/bone sarcoma or prior heart failure, and at designated cancer hospitals, and less likely for breast cancer, clinic settings versus university hospitals, and with certain anthracycline agents, indicating suboptimal and unequal cardiac monitoring.

Using METABRIC and a real-world C-CAT cohort of ER-positive/HER2-negative breast cancer, researchers assessed the impact of TP53 mutation on treatment duration with CDK4/6 inhibitors (CDK4/6i) and immune checkpoint inhibitors (ICI). TP53 mutation was linked to worse prognosis in METABRIC and, in the C-CAT cohort, to shorter CDK4/6i treatment duration for both abemaciclib and palbociclib but was not associated with ICI treatment duration; age-stratified analyses showed shorter CDK4/6i duration with TP53 mutation in most age groups except adolescents/young adults, though formal interaction testing was not significant.