Molecular basis for the relationship between thrombosis and cancer
Molecular basis for the relationship between thrombosis and cancer
复制标题
DOI：
10.1016/s0049-3848(01)00285-7
复制
发表时间：
2001-06-15
影响因子：
7.5
通讯作者：
Falanga, A
中科院分区：
文献类型：
--
作者：
Rickles, FR;Falanga, A
癌症患者极易出现血栓栓塞并发症，一些人估计血栓栓塞并发症占该疾病发病率和死亡率的很大比例。并非所有的机制的生产高凝状态的特点是癌症完全理解。已知的那些似乎将癌症的生物学与介导血液凝固、血小板-血管壁相互作用、纤维蛋白溶解和炎性细胞因子产生的主要调节途径相互交错。换句话说，导致癌症中血栓形成的事件似乎是试图限制肿瘤生长的过度旺盛的宿主反应的结果。因此，在这篇简短的综述中，我们试图将静脉血栓栓塞症（VTE）发病机制的当前信息纳入肿瘤生长、血管生成和转移的背景中。(C)2001爱思唯尔科技有限公司版权所有。
Cancer patients are highly susceptible to thromboembolic complications, which some have estimated accounts for a significant percentage of the morbidity and mortality of the disease. Not all of the mechanisms for the production of the hypercoagulable state characteristic of cancer are entirely understood. Those that are known seem to interdigitate the biology of cancer with the major regulatory pathways that mediate blood coagulation, platelet-vessel wall interaction, fibrinolysis and inflammatory cytokine production. In other words, the events responsible for thrombosis in cancer appears to be a result of an over exuberant host response in an attempt to delimit tumor growth. In this brief review, therefore, we attempt to put into the context of tumor growth, angiogenesis and metastasis the current information about the pathogenesis of venous thromboembolism (VTE). (C) 2001 Elsevier Science Ltd. All rights reserved.