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Thromboembolism (TE) has been well-recognized complication of cancer since the days of Trousseau who first described the clinical association between thrombosis and malignant disease.Cancer and its treatment may affect all three arms ofVirchows triad, which include damage to vessel endothelium, alteration in blood flow, and increased production of procoagulants.The pathogenesis of haemostatic disorders in cancer reflects the interaction of different mechanisms, including the increased procoagulant activity of tumor cells, co morbid conditions associated with cancer and effects of therapy, especially chemotherapy or hormone therapy.In addition to these factors, the last few years indicate a role of novel genetic risk factors, mainly related to the haemostatic system.These include mutations in the genes that encode antithrombin, protein C and protein S and the factor V Leiden (FVL) and factor Ⅱ (PT) 20210G-A polymorphism.We have routinely determined FVL and PT G20210A polymorphism by the method ofpolymerase chain reaction-based genomic DNA isolation in cancer patients with TE.In addition to these, possible risk factor for TE, including 23-bp endothelial protein C receptor gene insertion mutation, vascular endothelial growth factor gene 936 C/T, plasminogen activator inhibitorol gene 4G/5G and intron F 79GA of protein Z gene polymorphisms have been investigated in cancer cases with and without TE.