Molecular basis for the relationship between thrombosis and cancer

Cancer patients are highly susceptible to thromboembolic complications, which some have estimated accounts for a significant percentage of the morbidity and mortality of the disease. Not all of the mechanisms for the production of the hypercoagulable state characteristic of cancer are entirely understood. Those that are known seem to interdigitate the biology of cancer with the major regulatory pathways that mediate blood coagulation, platelet-vessel wall interaction, fibrinolysis and inflammatory cytokine production. In other words, the events responsible for thrombosis in cancer appears to be a result of an over exuberant host response in an attempt to delimit tumor growth. In this brief review, therefore, we attempt to put into the context of tumor growth, angiogenesis and metastasis the current information about the pathogenesis of venous thromboembolism (VTE).