[Pathogenic mechanisms of thrombosis in neoplasia: therapeutic implications]

Malignancy is associated with a hypercoagulable state and a high risk for thrombohemorragic complications. Activation of blood coagulation in cancer is a complex phenomenon, involving many different pathways of the hemostatic system and numerous interactions of the tumour cell with other blood cells, including platelet, monocyte and endothelial cells. In addition, the involvement of fibrin formation in the processes of tumour spread and metastasis is important in this area. Experimental evidence suggest that TF expression in tumour cells is associated with enhanced procoagulant activity as well as increased tumour cell invasion, primary tumour growth and increased tumoral metastatic potential. Moreover, a close correlation exists between TF and the synthesis of the angiogenic cytokine VEGF in tumour cells and with angiogenesis in vivo. A number of agents designed specifically for targeting TF, VEGF and/or receptors are being evaluated in various clinical trials in cancer patients. This review discuss the current status in pharmacological interventions to block thrombogenicity and angiogenesis in the treatment of cancer.