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This review explores mechanisms behind cancer-associated thrombosis, highlighting implications for treatment strategies.
Cancer-associated thrombosis is a major contributor to morbidity and mortality among patients with cancer, significantly impacting both treatment strategies and the overall quality of life for these patients. The pathogenesis of thrombosis in cancer is multifactorial, involving intricate interactions between both host immune responses and tumor-derived factors. This review highlights several key immune-thrombotic pathways implicated in the development of cancer-associated thrombosis, including neutrophil activation and NETosis, monocyte/macrophage-mediated coagulation, and tumor-induced endothelial activation via inflammatory cytokines. A more profound understanding of these mechanisms is essential for refining risk stratification, developing targeted prophylactic strategies, and improving therapeutic management of cancer-associated thrombosis.
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Zibara et al. (2026) studied this question.
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