Abstract
Patients with malignant tumors are prone to present hypercoagulability of blood and form thrombosis, and its pathogenesis is complex involving various factors from clinical and histopathological to genetic influences. Current studies on the potential mechanism of blood hypercoagulability in patients with malignant tumors focus on the following aspects but are not limited: (1) tumor cells release coagulant-promoting substances, (2) tumor cells interact with the fibrinolytic system, (3) tumor cell-mediated platelet activation, (4) tumor-associated complement activation, and (5) genetic factors and clinical factors. Especially, the pathogenesis of blood hypercoagulability is in-depth analyzed covering tumor cells' release of procoagulant substances, the interplay of cancer cells and fibrinolytic system, platelet activation mediated by cancer cells, cancer-associated complement activation, and the action of genetic and clinical factors. We review the pathogenesis of blood hypercoagulability in patients with malignant tumors, which will assist in the research and development of new drugs and providing theoretical support for the formulation of the best treatment plan for patients, to prolong the survival of patients.