Cancer Therapy-Associated Thrombosis

Patients with cancer have an increased risk of both arterial and venous thrombotic events compared with the general population. Both the site and stage of cancer are known to contribute to the increased risk of thrombotic events. In addition, several treatment-related factors enhance the risk of thrombosis, including hospitalization, surgery, central venous catheters, radiation, and anticancer agents. Chemotherapy serves as a mainstay treatment for a broad range of malignancies. Chemotherapeutic agents typically exert antineoplastic effects through either direct cytotoxicity or inhibition of cellular processes necessary for the proliferation of malignant cells. Unfortunately, in addition to targeting malignant cells, chemotherapeutic agents are also cytotoxic to nonmalignant cells. Chemotherapeutic agents have been associated with an increased risk of arterial and venous thrombosis. More recently, targeted agents have been developed that offer improved selectivity towards malignant cells. However, some of these agents are also associated with an increased risk of both arterial and venous thrombosis. Here, we review the association between specific anticancer agents and thrombotic events in patients with cancer. Despite an established association in most cases, the mechanism by which these agents increase thrombosis is poorly understood. Anticancer agents may damage the endothelium, decrease anticoagulants or increase procoagulants leading to activation of coagulation, or activate platelets. An improved understanding of the mechanisms that drive the increased risk of thrombotic events associated with anticancer agents will enable treatment strategies that mitigate this risk.

Automated summary

Cancer patients are at a higher risk of arterial and venous thrombotic events compared to the general population, with factors such as cancer site and stage, treatment-related factors, and cytotoxic effects of chemotherapeutic agents contributing to this increased risk. Despite advancements in targeted therapies, some anticancer agents still carry a risk of thrombosis, necessitating a better understanding of the mechanisms involved to develop effective treatment strategies.