Francis J L, Biggerstaff J, Amirkhosravi A
Division of Cell Biology, Hemostasis and Thrombosis Research, Walt Disney Memorial Cancer Institute at Florida Hospital, Altamonte Springs 32701, USA.
Semin Thromb Hemost. 1998;24(2):93-109. doi: 10.1055/s-2007-995829.
There is considerable evidence that the hemostatic system is involved in the growth and spread of malignant disease. There is an increased incidence of thromboembolic disease in patients with cancers and hemostatic abnormalities are extremely common in such patients. Antihemostatic agents have been successfully used to treat a variety of experimental tumors, and several clinical trials in humans have been initiated. Although metastasis is undoubtedly multifactorial, intravascular coagulation activation and peritumor fibrin deposition seem to be important. The mechanisms by which hemostatic activation facilitates the malignant process remain to be completely elucidated. Of central importance may be the presence on malignant cells of tissue factor and urokinase receptor. Recent studies have suggested that these proteins, and others, may be involved at several stages of metastasis, including the key event of neovascularization. Tissue factor, the principal initiator of coagulation, may have additional roles, outside of fibrin formation, that are central to the biology of some solid tumors.
有大量证据表明止血系统参与恶性疾病的生长和扩散。癌症患者血栓栓塞性疾病的发病率增加,并且止血异常在这类患者中极为常见。抗止血剂已成功用于治疗多种实验性肿瘤,并且已经启动了几项针对人类的临床试验。虽然转移无疑是多因素的,但血管内凝血激活和肿瘤周围纤维蛋白沉积似乎很重要。止血激活促进恶性过程的机制仍有待完全阐明。至关重要的可能是恶性细胞上存在组织因子和尿激酶受体。最近的研究表明,这些蛋白质以及其他蛋白质可能参与转移的几个阶段,包括新血管形成这一关键事件。组织因子是凝血的主要启动因子,在纤维蛋白形成之外可能还有其他作用,这些作用对某些实体瘤的生物学特性至关重要。
Semin Thromb Hemost. 1998
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