There is strong evidence linking venous thromboembolic events and malignancy. Laboratory markers of coagulation activation such as thrombin–antithrombin complex or prothrombin fragments 1+2 support the premise that malignancy is a hypercoagulable state. Inflammatory cytokines (e.g. tumor necrosis factor and interferon-γ), coagulation proteins (e.g. tissue factor and factor VIII), and procoagulant microparticles may be elevated in patients with malignancy. However, the molecular basis for cancer associated thrombosis remains unknown and the relative contribution of chemotherapeutics, tumor cells, endothelium, and circulating procoagulants in promoting thrombus formation continues to be investigated.