Abstract

Cancer-associated thrombosis (CAT) is a leading cause of mortality in cancer patients and its incidence varies in different parts of the world. Venous thromboembolism (VTE) is a prominent manifestation of CAT, and significantly impacts morbidity and survival compared to arterial thrombosis in cancer patients. Several risk factors for developing VTE such as chemotherapy and immobilization have also been found co-existing with cancer patients and contributing to the increased risk of VTE in cancer patients than in non-cancer patients. This review highlights recent mechanisms in the pathogenesis of hypercoagulable syndromes associated with cancer, multiple mechanisms implicated in promoting cancer-associated thrombosis and their diagnostic approaches. Cancer cells interact with every part of the hemostatic system; generating their own procoagulant factors, through stimulation of the prothrombotic properties of other blood cell components or the initiation of clotting by cancer therapies which can all directly activate the coagulation cascade and contribute to the VTE experienced in CAT. It is our hope that the multiple interconnections between the hemostatic system and cancer biology and the improved biomarkers reported in this study can be relevant in establishing a predictive model for VTE, optimize early detection of asymptomatic microthrombosis for more personalized prophylactic strategies and incorporate effective therapeutic options and patient management to reduce mortality and morbidity, and improve the quality of life of affected cancer patients.

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