title: 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.
authors.affiliation: Division of Hematology and Oncology, Department of Medicine, Northwestern University Medical School and Robert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, Illinois 60611, USA. h-kwaan@nothwestern.edu
authors.forename: Hau C
authors.initials: HC
authors.lastname: Kwaan
authors.forename: Simrit
authors.initials: S
authors.lastname: Parmar
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
mesh_terms: D017209:Apoptosis; D001779:Blood Coagulation Factors / Q000096:biosynthesis; D006801:Humans; D009369:Neoplasms / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D013925:Thromboplastin / Q000096:biosynthesis; D013927:Thrombosis / Q000209:etiology*
chemical_list: D001779:Blood Coagulation Factors; D013925:Thromboplastin