Cancer-Associated Thrombosis: Epidemiology, Pathophysiological Mechanisms, Treatment, and Risk Assessment

Abstract

Cancer patients represent a growing population with drastically difficult care and a lowered quality of life, especially due to the heightened risk of vast complications. Thus, it is well established so far that one of the most prominent complications in individuals with cancer is venous thromboembolism. Since there are various improved methods for screening and diagnosing cancer and its complications, the incidence of cancer-associated thrombosis has been on the rise in recent years. Therefore, the high mortality and morbidity rates among these patients are not a surprise. Consequently, there is an excruciating need for understanding the mechanisms behind this complex process, as well as the imperative for adequate analysis and application of the most suitable steps for cancer-associated thrombosis prevention. There are various and numerous mechanisms offering potential answers to cancer-associated thrombosis, some of which have already been elucidated in various preclinical and clinical scenarios, yet further and more elaborate studies are crucial to understanding and preventing this complex and harsh clinical entity. This article elaborates on the growing incidence, mortality, morbidity, and risk factors of cancer-associated thrombosis while emphasizing the pathophysiological mechanisms in the light of various types of cancer in patients and summarizes the most novel therapy and prevention guidelines recommendations.

Keywords: Cancer-associated thrombosis; incidence; morbidity; mortality; pathophysiological mechanisms; risk factors.

Figure 1.

Mechanisms of CAT. CAT involves the activation of coagulation, dysregulation of fibrinolytic systems, inflammation, and cytokine production as its underlying mechanisms. FVII indicates factor VII; FXa, factor Xa; NETs, neutrophil extracellular traps; PAI-1, plasminogen activator inhibitor 1; TF, tissue factor; CAT, cancer-associated thrombosis.