This procoagulant state could be due to the expression of active TF and transmembrane proteins (PSGL-1, Muc1, …) by the cancer cell itself or cancer cell-derived microparticles leading to platelets activation and aggregation. While studying the key role of TF bearing cancer cell-derived microparticles in cancer associated thrombosis, the investigators have previously shown (Dubois C, INSERM UMR 1076 Marseille) that both endogenously generated and exogenously injected pancreatic cancer cell-derived microparticles expressing TF (PancO2), but not their parental tumor cells, accumulated at the site of injury in a P-selectin dependent manner. Their presence directly correlates with the size of the thrombus. Based on these data, the investigators first hypothesized that treatment with anticoagulant and / or antiplatelet drugs may prevent tumor progression and formation of metastasis, as well as thrombosis associated cancer, in addition to prevention of coagulopathy.