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.
KEYWORDS
Hemostatic system - angiogenesis - neoplasia
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Marek Z WojtukiewiczM.D.
Department of Oncology, Medical University
12 Ogrodowa St, 15-027 Bialystok, Poland
Email: mwojtuk@polbox.com