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作 者:王兆钺[1] 万海英[1] 陈德春[1] 何扬[1] 阮长耿[1]
机构地区:[1]苏州医学院血栓与止血研究室
出 处:《肿瘤》1989年第5期212-213,共2页Tumor
摘 要:已经发现人和动物的多种肿瘤细胞都能在体外引起血小板聚集,并且这种反应与恶性肿瘤的转移能力有关,但有关肿瘤细胞诱导血小板聚集的机理研究甚少。最近我们观察了Lewis肺癌细胞诱导人血小板聚集的作用,并且利用单克隆抗体与多种抑制剂研究了这种聚集的机理,现报告如下。The rate of platelet aggregation induced by Lewis lung earoinoma was 16.37±8.08%. This aggregation was not inhibited by anti-glycoprotein (GP) Ib monoclonalantibodies AN51 and SZ-2, but was inhibited to 3.23±3.41% by anti-GP Ⅱb/Ⅲa mono-clonal antibody SZ-21. Inhibitors, such as aspirin and CP/CPK did have no effect onthis aggregation. These results suggest that the platelet aggregation induced by Lewislung cancer depends on the fibrinogen receptor site on GPⅡb/Ⅲa, but its mechanismis different from that induced by common, inducers.
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