“…Mechanisms potentially involved in chemotherapy-associated hypercoagulability can be classified into (a) alterations of tumor cells and tumor cell interactions with host cells, (b) influences on blood cells including the release of cytokines, (c) damage to the vascular endothelium, and (d) interference with components of the plasmatic system. Examples are an upregulation of TF expression in etoposide-, methotrexate-, and vincristine-treated tumor cell lines, 11 an increased human platelet reactivity and TF-associated procoagulant activity of monocytes after cisplatin treatment, [12][13][14] a downregulation of the protein C anticoagulant pathway and an increased adhesion molecule expression on chemotherapy-treated endothelial cells, 15,16 and decreased plasma levels of free activated protein C, protein C, protein S, or antithrombin in patients treated with different chemotherapeutic agents. [17][18][19][20][21] In recent years, fundamental changes in the understanding of hemostasis have taken place due to the observation that thrombus formation might be augmented by high levels of circulating TF and procoagulant MPs.…”