Cancer Therapy–Associated Thrombosis

Abstract

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. 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 incompletely 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.

In situ Pulmonary Artery Thrombosis: A Previously Overlooked Disease

“…indirectly activate platelets (Grover et al, 2021). All of these mechanisms may promote thrombosis under malignancies.…”

“…Alternatively, these drugs may decrease anticoagulants and increase procoagulants, hence tipping the balance towards coagulation. Finally, the anticancer drugs may directly or indirectly activate platelets ( Grover et al, 2021 ). All of these mechanisms may promote thrombosis under malignancies.…”

Novel Mechanisms of Anthracycline-Induced Cardiovascular Toxicity: A Focus on Thrombosis, Cardiac Atrophy, and Programmed Cell Death

“…Observational data suggest that some anti-cancer therapies are associated with increased risk for thrombotic events in the venous and arterial vasculature including deep vein thrombosis (DVT), pulmonary embolism (PE), and arterial thrombosis (AT) as recently summarized by Grover et al ( 3 ). Indeed, Weiss et al reported that 5% of stage II breast cancer patients (22/443) with 2 years of post-mastectomy chemotherapy developed venous thrombosis without signs of metastasis ( 4 ).…”

Molecular Landscape of the Coagulome of Oral Squamous Cell Carcinoma

“…Oral squamous cell carcinoma (OSCC) represents the most frequent histological form of tumor of the oral cavity and arises in the context of chronic exposure to tobacco and alcohol [ 3 ]. Patients with OSCC receive surgical procedures and medical treatments that put them at risk of thrombosis and hemorrhage [ 4 , 5 , 6 ], but they are usually considered to be at low risk of systemic thrombosis [ 7 , 8 ]. Understanding the biological basis for patient susceptibility to this large spectrum of complications requires fundamental studies on tumor physiology.…”