Key result
Gynecologic and breast cancers display distinct thrombotic phenotypes driven by tumor biology, hormones, and therapies.
Why the study?
Venous thromboembolism is a leading cause of morbidity and mortality in cancer, driven by complex interactions among tumor biology, endocrine signaling, and therapies in hormone-sensitive malignancies.
Answers are grounded in this paper and cite their sources.
This review emphasizes the distinct mechanisms of cancer-associated thrombosis in hormone-sensitive malignancies and supports individualized thromboprophylaxis based on current guidelines.
Cancer-associated thrombosis (CAT) is defined as venous or arterial thrombotic events occurring in patients with active malignancy or during anticancer treatment, most commonly presenting as venous thromboembolism and representing a leading cause of morbidity and mortality in oncology. Hormone-sensitive malignancies, including breast, ovarian, and endometrial cancers, are characterized by a complex interaction among tumor biology, endocrine signaling, inflammation, endothelial dysfunction, and coagulation activation. In these malignancies, venous thromboembolism (VTE) risk is influenced not only by intrinsic tumor-related mechanisms but also by patient-specific factors and anticancer therapies, particularly endocrine treatments, chemotherapy, targeted agents, and extensive surgical procedures. Breast cancer is generally associated with an intermediate thrombotic risk, although endocrine therapy—especially tamoxifen—significantly increases VTE incidence. Ovarian cancer represents one of the most thrombogenic solid tumors because of elevated tissue factor expression, inflammatory activation, advanced-stage presentation, and aggressive multimodal treatment strategies. Endometrial cancer exhibits a strong association with obesity, metabolic syndrome, prolonged estrogen exposure, and perioperative thrombotic complications. Emerging evidence highlights the role of immune-thrombosis, extracellular vesicles, inflammatory cytokines, and sex-specific coagulation pathways in cancer-associated hypercoagulability. Current guidelines increasingly support individualized thromboprophylaxis based on tumor biology, patient-specific risk factors, and bleeding risk assessment. This review summarizes the biological mechanisms linking hormones and thrombosis in breast and gynecologic cancers, discusses current evidence regarding VTE risk factors and treatment-related thrombotic complications, and explores modern approaches to biomarkers, risk stratification, and personalized thromboprophylaxis.
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Sorrentino et al. (2026) conducted a review in Cancer-associated thrombosis in breast, ovarian, and endometrial cancer. Hormone-sensitive malignancies and anticancer therapies was evaluated. Breast, ovarian, and endometrial cancers exhibit distinct thrombotic phenotypes shaped by endocrine signaling, tumor biology, systemic inflammation, obesity, and anticancer therapies.
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