**3. Cancer-associated thrombosis mechanisms**

Patients with malignancy often have several predisposing factors for thrombus formation. Traditionally, Virchow's triad including stasis, thrombophilia, and endothelial damage have a critical role in pathophysiology of thromboembolism in these patients. Tumor compression and bed rest condition can lead to blood stasis. Homeostasis disturbance, hypercoagulable state, and inflammation have a key role in pathogenesis of thrombosis. Endothelial dysfunction can be the result of abnormal tumor vascularity as a mechanism for thrombosis formation [4, 12–14]. Cancer can conduce to the presence of antiphospholipid antibody, decrease in hepatic anticoagulant synthesis, and reduced hepatic clearance of coagulation factors, too [14]. Finally, imbalance between procoagulative factors and fibrinolytic system lead to cancerassociated thrombosis [12].
