This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rak, J. Articles by Mackman, N. Search for Related Content PubMed PubMed Citation Articles by Rak, J. Articles by Mackman, N. Related Collections Tumor Biology Tumor Biology: Invasion and Metastasis

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)

This article has been cited by other articles:

				A. P. B. Batschauer, C. P. Figueiredo, E. C. Bueno, M. A. Ribeiro, L. M. S. Dusse, A. P. Fernandes, K. B. Gomes, and M. G. Carvalho D-dimer as a possible prognostic marker of operable hormone receptor-negative breast cancer Ann. Onc., October 30, 2009; (2009) mdp474v1. [Abstract] [Full Text] [PDF]

				M. Zangari, L. M. Fink, F. Elice, F. Zhan, D. M. Adcock, and G. J. Tricot Thrombotic Events in Patients With Cancer Receiving Antiangiogenesis Agents J. Clin. Oncol., October 10, 2009; 27(29): 4865 - 4873. [Abstract] [Full Text] [PDF]

				C. Boccaccio and P. M. Comoglio Genetic Link Between Cancer and Thrombosis J. Clin. Oncol., October 10, 2009; 27(29): 4827 - 4833. [Abstract] [Full Text] [PDF]

				H. H. Versteeg, F. Schaffner, M. Kerver, H. H. Petersen, J. Ahamed, B. Felding-Habermann, Y. Takada, B. M. Mueller, and W. Ruf Inhibition of tissue factor signaling suppresses tumor growth Blood, January 1, 2008; 111(1): 190 - 199. [Abstract] [Full Text] [PDF]

				A. Varki Trousseau's syndrome: multiple definitions and multiple mechanisms Blood, September 15, 2007; 110(6): 1723 - 1729. [Abstract] [Full Text] [PDF]

				G. Lippi, M. Franchini, C. Biasiutti, G. Dellagiacoma, G.L. Salvagno, and G.C. Guidi Increased D-dimer value and occult cancer in the absence of detectable thrombosis Haematologica, April 1, 2007; 92(4): e53 - e55. [Abstract] [Full Text] [PDF]