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恶性肿瘤中血栓形成的发病机制。

Pathogenetic mechanisms of thrombosis in malignancy.

作者信息

Donati M B, Falanga A

机构信息

Department of Vascular Medicine and Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Via Nazionale, I-66030 Santa Maria Imbaro, Italy.

出版信息

Acta Haematol. 2001;106(1-2):18-24. doi: 10.1159/000046585.

DOI:10.1159/000046585
PMID:11549773
Abstract

The interactions between components of the hemostatic system and cancer cells are multifaceted. Strong clinical evidence is accumulating on the prothrombotic tendency of cancer patients, which is enhanced by anticancer therapy, such as surgery and chemotherapy. The mechanisms of thrombus promotion in malignancy include some general responses of the host to the tumor (acute phase, inflammation, angiogenesis) and specific interactions of tumor cells with the clotting/fibrinolysis systems and with blood (leukocytes, platelets) or vascular cells. It is at present difficult to rank the relative weight of these multiple interactions on the basis of the well-recognized clinical evidence of enhanced thrombotic episodes in tumor patients. In any case, the mechanisms explored so far offer a sound experimental basis for prevention/treatment of thrombosis in tumor patients and leave open the possibility that some antithrombotic strategies may also affect the processes of tumor growth and dissemination.

摘要

止血系统各成分与癌细胞之间的相互作用是多方面的。越来越多有力的临床证据表明癌症患者存在促血栓形成倾向,而手术和化疗等抗癌治疗会加剧这种倾向。恶性肿瘤中血栓形成的机制包括宿主对肿瘤的一些一般反应(急性期、炎症、血管生成)以及肿瘤细胞与凝血/纤溶系统、血液(白细胞、血小板)或血管细胞的特异性相互作用。目前,根据肿瘤患者血栓形成事件增加这一公认的临床证据,很难对这些多重相互作用的相对权重进行排序。无论如何,迄今为止所探索的机制为预防/治疗肿瘤患者的血栓形成提供了坚实的实验基础,并且也为一些抗血栓策略可能会影响肿瘤生长和扩散过程留下了可能性。

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