Wojtukiewicz Marek Z, Sierko Ewa, Rak Janusz
Department of Oncology, Medical University, Bialystok, Poland.
Semin Thromb Hemost. 2004 Feb;30(1):5-20. doi: 10.1055/s-2004-822967.
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.
目前已认识到，止血系统在癌症生长和扩散过程中发挥着重要作用，而这些过程至关重要地依赖于新的肿瘤血管形成（血管生成）。越来越多的证据支持凝血/纤维蛋白溶解系统的各个组分与癌症患者血管生成活性之间的联系。组织因子（TF）、凝血酶、纤维蛋白原、纤维蛋白以及纤溶酶原激活系统，还有血小板，均能够促进血管生成。另一方面，凝血抑制剂以及止血蛋白的隐蔽（经蛋白水解释放）结构域，也被认为可作为血管生成抑制剂。实际上，血管生成的调节（刺激或抑制）可能源于止血级联反应各种分子组分的经典功能、其研究较少的“替代”活性，或者两者皆有。尽管对于这个复杂的机制仍有许多有待了解之处，但这些考虑支持在恶性肿瘤患者中合理使用抗凝剂，并鼓励寻找可能存在于止血系统分子和细胞组分中的新型抗血管生成活性。
