Semin Thromb Hemost 2004; 30(1): 5-20
DOI: 10.1055/s-2004-822967
Copyright © 2004 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Contribution of the Hemostatic System to Angiogenesis in Cancer

Marek Z. Wojtukiewicz1 , 2 , Ewa Sierko2 , Janusz Rak3
  • 1Professor of Medicine and Oncology
  • 2Department of Oncology, Medical University, Bialystok, Poland
  • 3Henderson Research Centre, Experimental Thrombosis Research, McMaster University, Hamilton, Ontario, Canada
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Publication History

Publication Date:
22 March 2004 (online)

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It is now recognized that the hemostatic system plays an important role in cancer growth and dissemination, processes known to be vitally dependent on new tumor blood vessel formation (angiogenesis). There is also an increasing body of evidence supporting the link between the various components of the coagulation/fibrinolysis systems and angiogenic activity in cancer patients. Tissue factor (TF), thrombin, fibrinogen, fibrin, and plasminogen activation system, as well as platelets, all are able to promote angiogenesis. On the other hand, coagulation inhibitors, as well as cryptic (proteolytically released) domains of hemostatic proteins, are also known to act as angiogenesis inhibitors. Indeed, modulation (stimulation or inhibition) of angiogenesis may result from either classical functions of various molecular components of the hemostatic cascade, their less studied “alternative” activities, or both. Although much remains to be understood about this complex circuitry these considerations support the judicious use of anticoagulants in patients with malignancy as well as encourage the search for novel antiangiogenic activities that may reside within molecular and cellular components of the hemostatic system.

REFERENCES

Marek Z WojtukiewiczM.D. 

Department of Oncology, Medical University

12 Ogrodowa St, 15-027 Bialystok, Poland

Email: mwojtuk@polbox.com