Platelets are recognized as mediators of cancer progression, extending beyond hemostasis to influence tumor growth, metastatic dissemination, immune evasion, and thrombotic complications. Tumors remodel platelets through thrombocytosis and tumor cell-induced platelet aggregation, and locally through tumor-microenvironment cues that reprogram platelet function. These changes enable platelets to shield tumor cells, support epithelial-mesenchymal transition, promote angiogenesis and vascular remodeling, and establish immunosuppressive niches promoting metastasis. Platelets also drive both venous and arterial cancer-associated thrombosis via procoagulant platelet states, platelet-derived extracellular vesicles, and crosstalk with endothelium and innate immune pathways. Platelet RNA signatures and emerging proteomic/multi-omic profiling show promise for cancer detection, classification, and treatment monitoring. Preclinical and translational studies suggest that antiplatelet strategies (e.g., aspirin, P2Y12 inhibition) can modulate metastatic and thromboinflammatory pathways, motivating platelet-targeted interventions that mitigate bleeding risk. This review synthesizes platelet-tumor crosstalk linking tumor progression with cancer-associated thrombosis and vascular events and highlights emerging platelet-based biomarker and therapeutic opportunities.
Santos et al. (Wed,) studied this question.