Platelet activation in breast cancer: mechanisms and therapeutic opportunities – a narrative review

Platelet activation is increasingly recognized as a key factor in breast cancer progression, contributing to tumor growth, metastasis, and immune modulation. Platelets interact with tumor cells to promote their survival, facilitate metastasis, and enhance the formation of a pro-inflammatory microenvironment. These interactions are mediated by adhesion molecules such as P-selectin and glycoprotein receptors on both platelets and tumor cells. Additionally, activated platelets release growth factors like vascular endothelial growth factor and platelet-derived growth factor, which promote angiogenesis and tumor vascularization, crucial steps in cancer progression. The coagulation cascade, triggered by platelet activation, further enhances tumor cell dissemination and metastasis. Elevated levels of procoagulant activity in platelets, particularly through the expression of tissue factor, lead to increased thrombin generation, facilitating the formation of fibrin-rich clots that protect circulating tumor cells from immune surveillance. Platelet-derived factors also exert immunomodulatory effects, helping cancer cells evade detection by the immune system, thereby supporting tumor growth and spread.