Cancer cell-derived microparticles are responsible for the thrombotic phenotype observed in mice developing a cancer via interactions between P-selectin expressed by aggregating platelets and activated endothelium and PSGL-1 present at the surface of cancer cell-derived microparticles. Before injury but after their infusion in bloodstream, exogenous labeled cancer cell-derived microparticles were detected in the cremaster microcirculation of non-treated or Clopidogrel treated mice. However, following an injury, cancer cell-derived microparticles were accumulating at the site of thrombus formation only in non-treated mice bearing a PancO2-LowTF or High TF tumor. Tissue Factor (TF) is both a main effector of the coagulation cascade and a protein involved in the development of solid tumors. In vivo, following a laser-induced injury, the activation of the endothelial wall, as well as the presence of activated platelets, are the main source of P-selectin. The quantity of P-selectin present at the site of injury was 4 fold less important in mice bearing a PancO2 tumor and treated by Clopidogrel in comparison with non-treated mice. Interestingly, PanCO2 cancer cell-derived microparticles express both TF and TFPI (Tissue Factor Inhibitor), a biological inhibitor of the coagulation cascade in an active form. To confirm that cancer-cell derived microparticles may participate in the inhibition of the blood coagulation observed when the pathological TF is shut down, the investigators compared fibrin generation at the site of injury in PancO2-High TF and Low-TF cancer mice in presence of absence of Clopidogrel.