Elsevier

Neoplasia

Volume 3, Issue 5, 2001, Pages 371-384
Neoplasia

The Hemostatic System and Angiogenesis in Malignancy1

https://doi.org/10.1038/sj.neo.7900184Get rights and content
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open access

Abstract

Coagulopathy and angiogenesis are among the most consistent host responses associated with cancer. These two respective processes, hitherto viewed as distinct, may in fact be functionally inseparable as blood coagulation and fibrinolysis, in their own right, influence tumor angiogenesis and thereby contribute to malignant growth. In addition, tumor angiogenesis appears to be controlled through both standard and non-standard functions of such elements of the hemostatic system as tissue factor, thrombin, fibrin, plasminogen activators, plasminogen, and platelets. “Cryptic” domains can be released from hemostatic proteins through proteolytic cleavage, and act systemically as angiogenesis inhibitors (e.g., angiostatin, antiangiogenic antithrombin III aaATIII). Various components of the hemostatic system either promote or inhibit angiogenesis and likely act by changing the net angiogenic balance. However, their complex influences are far from being fully understood. Targeted pharmacological and/ or genetic inhibition of pro-angiogenic activities of the hemostatic system and exploitation of endogenous angiogenesis inhibitors of the angiostatin and aaATIII variety are under study as prospective anti-cancer treatments.

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1

This work was supported by the Terry Fox grant from the National Cancer Institute of Canada and the HCHRC grant to J.R., and by the grant 6 P05A 096 21 from the Polish Committee of Scientific Research (KBN) to M.W.