凝血功能与非小细胞肺癌相关机制研究进展  

Advances on Mechanisms of Coagulation with Non-small Cell Lung Cancer

作　　者：李艳华[1] 魏素菊[1] 

机构地区：[1]河北医科大学第四医院肿瘤内科,石家庄050000

出　　处：《中国肺癌杂志》2013年第12期676-680,共5页Chinese Journal of Lung Cancer

摘　　要：近来研究越来越多地发现凝血功能紊乱通常是恶性肿瘤的首发迹象。现在已经证实,肿瘤导致血栓形成的风险增加,而凝血功能的过度激活也极大地影响肿瘤的进展。在肺癌患者中,存在着持续的凝血刺激。癌细胞通过组织因子(tissuefactor,TF)的表达激活凝血功能;通过凝血酶的表达和促凝血微粒的释放等影响凝血功能。凝血功能也通过介导血小板释放其颗粒内容物、抑制自然杀伤细胞和募集巨噬细胞而促进肿瘤的进展。非小细胞肺癌(non-small cell lung cancer,NSCLC)占肺癌的80%-85%,本文就凝血系统各个组分在NSCLC发生发展中的病理生理学机制的最新研究进展进行综述。Recently, researchers have been increasingly finding coagulation disorders are commonly the first sign of malignancy. It has now been established that cancer development leads to an increased risk of thrombosis, and conversely, excessive activation of blood coagulation profoundly influences cancer progression. In patients with lung cancer, a sustained stimulation of blood coagulation takes place. Cancer cells trigger coagulation through expression of tissue factor, and affect coagulation through expression of thrombin, release of microparticles that augment coagulation and so on. Coagulation also facilitates tumour progression through release of platelet granule contents, inhibition of natural killer cells and recruitment of macrophages. Non-small cell lung cancer （NSCLC） accounts for about 80%-85% of all lung malignancies. In the present re- view, we summarized the newly updated data about the physiopathological mechanisms of various components of the dotting system in different stages of carcinogenesis in NSCLC.

关 键 词：凝血功能 肺肿瘤 病理生理学 

分 类 号：R734.2[医药卫生—肿瘤]