Pathogenesis of thrombosis in patients with malignancy

Cancer cells can contribute to activation of the clotting system by their c apacity to produce and release procoagulant/fibrinolytic substances and inf lammatory cytokines, and by their interaction with host cells (endothelial, monocytes, platelets, and neutrophils). Moreover, anticancer drugs (chemot herapy/hormone therapy) may greatly affect the risk of thromboembolic compl ications in cancer patients by similar mechanisms, eg, through the release of procoagulants by tumor cells, through endothelial damage, or stimulation of tissue factor production by host cells. The interactions between cancer /metastatic processes and thrombosis have been reviewed here from the patho genetic viewpoint. We hope that better knowledge of these pathogenetic path ways will lead to the development of more targeted strategies to prevent th romboembolism in cancer patients. (C) 2001 The Japanese Society of Hematolo gy.