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Chemotherapy-induced Cardiotoxicity and Mitigation · Journal article
Cancers · August 18, 2026
A consensus or society position rather than new primary data.
This is a narrative review of cancer-associated thrombosis in hormone-sensitive malignancies (breast, ovarian, endometrial cancer), summarizing biological mechanisms, VTE risk factors, and emerging approaches to risk stratification and personalized thromboprophylaxis. The source synthesizes existing knowledge and recommendations but does not report new empirical findings or comparative efficacy data.
Narrative review. Patients with breast cancer, ovarian cancer, or endometrial cancer; focus on those receiving anticancer treatments (endocrine therapy, chemotherapy, targeted agents, surgery)..
Breast cancer is generally associated with intermediate thrombotic risk; tamoxifen significantly increases VTE incidence. Ovarian cancer represents one of the most thrombogenic solid tumors due to elevated tissue factor expression, inflammatory activation, and advanced-stage presentation. Endometrial cancer shows strong association with obesity, metabolic syndrome, prolonged estrogen exposure, and perioperative thrombotic complications.
No direct evidence on efficacy or safety of specific thromboprophylaxis regimens compared in this source. Current guidelines increasingly support individualized thromboprophylaxis based on tumor biology, patient-specific risk factors, and bleeding risk assessment.
Clinicians managing these hormone-sensitive malignancies should consider individualized VTE risk assessment incorporating tumor biology, patient factors (obesity, estrogen exposure), and treatment type (particularly tamoxifen in breast cancer). This review supports the shift toward personalized thromboprophylaxis strategies rather than uniform approaches.
A narrative review summarizing biological mechanisms, risk factors, and clinical approaches to VTE in hormone-sensitive cancers; provides expert synthesis rather than new empirical evidence.
As stated by the source record.
Clinicians managing these hormone-sensitive malignancies should consider individualized VTE risk assessment incorporating tumor biology, patient factors (obesity, estrogen exposure), and treatment type (particularly tamoxifen in breast cancer). This review supports the shift toward personalized thromboprophylaxis strategies rather than uniform approaches.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
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.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.