Pathogenesis of increased risk of thrombosis in cancer

Abstract

Since the observations of Trousseau, not only has the association of cancer and thrombosis been widely recognized but its pathogenesis is now better understood. Attention to the tumor cell as an important source of procoagulants has also contributed to our knowledge of this problem. Tumor cells express tissue factor (TF) and a cancer procoagulant (CP). TF is dormant in the living cell. However, it is activated during apoptosis of the cell, initiating the coagulation cascade and leading to thrombin generation. Because increased apoptosis occurs during treatment with chemotherapeutic agents, hormones, radiation, and hematopoietic growth factors, as well as when there is rapid tumor proliferation, the thrombosis risk is heightened accordingly. These developments have obvious basic and clinical implications.

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original_citation: Kwaan, H. C., Parmar, S., & Wang, J. (2003). Pathogenesis of increased risk of thrombosis in cancer. Semin Thromb Hemost, 29(3), 283-290. doi:10.1055/s-2003-40966

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