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1 Immune Disease Institute and 2 Department of Pathology, Harvard Medical School, Boston, Massachusetts; and 3 Inserm Unit 698, Bichat Hospital, Paris, France, and 4 University of Münster, Department of Dermatology, Münster, Germany
Requests for reprints: Denisa D. Wagner, Immune Disease Institute, 3 Blackfan Circle, Boston, MA 02115. Phone: 617-713-8300; Fax: 617-713-8333; E-mail: wagner{at}idi.harvard.edu.
Solid tumors generate a prothrombotic environment capable of platelet activation. Recent findings indicate that the activated platelets are crucial regulators of tumor vascular homeostasis in that they prevent tumor hemorrhage. Surprisingly, this effect is independent of platelets' capacity to form thrombi and instead relies on the secretion of their granule content. Thus, targeting platelet secretory activities may represent a new approach to specifically destabilize tumor vasculature. [Cancer Res 2009;69(14):5623–6]
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G. C. Prendergast Platelets in Maintaining Tumor Vasculature and Applying Evolution Theory in Cancer Cancer Reviews Online Content, August 1, 2009; 2009(8): 15 - 15. [Full Text] [PDF] |
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