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Oncogenes, Trousseau Syndrome, and Cancer-Related Changes in the Coagulome of Mice and Humans

¹ Montreal Children's Hospital Research Institute, McGill University, Montreal, Quebec, Canada; ² Henderson Research Centre, McMaster University, Hamilton, Ontario, Canada; and ³ The Scripps Research Institute, La Jolla, California

Requests for reprints: Janusz Rak, Montreal Children's Hospital Research Institute, McGill University, 4060 Saint Catherine West, PT-232, Montreal, Quebec, Canada, H3Z 2Z3. Phone: 514-412-4400; E-mail: janusz.rak{at}mcgill.ca.

Cancer is often associated with venous thrombosis, a phenomenon that was first described by Trousseau in 1865 (Trousseau syndrome). Recent studies have begun to explain how oncogenic events may deregulate the hemostatic system. For instance, activated oncogenes (K-ras, EGFR, PML-RAR, and MET) or inactivated tumor suppressors (e.g., 53 or PTEN) may increase the risk of thrombosis by inducing the expression of tissue factor, a potent procoagulant molecule, and plasminogen activator inhibitor-1, a fibrinolysis inhibitor. In a more complex clinical reality, transforming genes may often act in concert with numerous epigenetic factors, including hypoxia, inflammation, anticancer therapy, contact between blood and metastatic cancer cells, and emission of procoagulant vesicles from tumors and their stroma into the circulation. To add to mechanistic insights gained from mouse models, which may not fully phenocopy human Trousseau syndrome, we suggest that valuable clues to progression and thrombosis risk may be obtained by monitoring multiple hemostatic variables in cancer patients ("coagulomics"). (Cancer Res 2006; 66(22): 10643-6)

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