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Blood, 15 July 2004, Vol. 104, No. 2, pp. 397-401. Prepublished online as a Blood First Edition Paper on March 18, 2004; DOI 10.1182/blood-2004-02-0434. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-02-0434v1 104/2/397    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Camerer, E. Articles by Coughlin, S. R. Search for Related Content PubMed PubMed Citation Articles by Camerer, E. Articles by Coughlin, S. R. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Signal Transduction Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Platelets, protease-activated receptors, and fibrinogen in hematogenous metastasis Eric Camerer, Aisha A. Qazi, Daniel N. Duong, Ivo Cornelissen, Rommel Advincula, and Shaun R. Coughlin From the Cardiovascular Research Institute, University of California, San Francisco, CA. Procoagulant activity on tumor cells can enhance their ability to spread via the circulation to colonize distant organs. Toward defining the relative importance of the main host responses to coagulation for hematogenous metastasis, we examined lung metastases after intravenous injection of melanoma cells in Nf-E2-/- mice, which have virtually no circulating platelets; Par4-/- mice, which have platelets that fail to respond to thrombin; Par1 and Par2-/- mice, which have markedly attenuated endothelial responses to coagulation proteases; and Fib-/- mice, which lack fibrinogen. In a severe combined immunodeficiency (SCID) background, median lung tumor count in Nf-E2-/-, Par4-/-, and Fib-/- mice was 6%, 14%, and 24% of wild type, respectively; total tumor burden was only 4%, 9%, and 3% of wild type, respectively. Similar results were seen in a syngeneic C57BL6 background. By contrast, deficiencies of protease-activated receptor 1 (PAR1) or PAR2 did not provide protection. These results provide strong genetic evidence that platelets play a key role in hematogenous metastasis and contribute to this process by both thrombin-dependent and -independent mechanisms. Importantly, PAR4 heterozygosity conferred some protection against metastasis in this model. Thus even partial attenuation of platelet function may be sufficient to provide benefit. (Blood. 2004;104:397-401) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Clotting and cancer progression: platelets count Michael E. Bromberg Blood 2004 104: 300. [Full Text] [PDF] This article has been cited by other articles: L. Hu, S. Ibrahim, C. Liu, J. Skaar, M. Pagano, and S. Karpatkin Thrombin Induces Tumor Cell Cycle Activation and Spontaneous Growth by Down-regulation of p27Kip1, in Association with the Up-regulation of Skp2 and MiR-222 Cancer Res., April 15, 2009; 69(8): 3374 - 3381. [Abstract] [Full Text] [PDF] T. Sousou and A. A. 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