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实验性肿瘤细胞可激活凝血因子X的证据。

Evidence that cells from experimental tumours can activate coagulation factor X.

作者信息

Curatolo L, Colucci M, Cambini A L, Poggi A, Morasca L, Donati M B, Semeraro N

出版信息

Br J Cancer. 1979 Aug;40(2):228-33. doi: 10.1038/bjc.1979.170.

Abstract

The procoagulant activity of cells from some experimental tumours isolated in culture or in single-cell suspensions from ascitic fluid was investigated. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, Factor VIII- and Factor VII-deficient but not of Factor X-deficient human plasma. The same cells generated thrombin when mixed with a source of prothrombin and Factor X, absorbed bovine serum (as a source of Factor V), phospholipid and calcium chloride. Thrombin formation was not influenced by the presence of Factor VII. Cells from Sarcoma 180 ascites were completely inactive in both test systems. It is concluded that cells from some experimental tumours have the capacity to activate Coagulation Factor X directly. These findings suggest the existence of an alternative "cellular" pathway in the initiation of blood clotting distinct from both the intrinsic and extrinsic mechanisms.

摘要

对从培养物中分离的一些实验性肿瘤细胞或从腹水的单细胞悬液中的促凝活性进行了研究。来自Lewis肺癌(原发灶和转移灶)、艾氏腹水癌和JW肉瘤腹水的细胞能够显著缩短正常、缺乏因子VIII和因子VII但不缺乏因子X的人血浆的再钙化时间。当与凝血酶原和因子X来源、吸附牛血清(作为因子V来源)、磷脂和氯化钙混合时,相同的细胞会产生凝血酶。凝血酶的形成不受因子VII存在的影响。肉瘤180腹水的细胞在两个测试系统中完全无活性。结论是一些实验性肿瘤的细胞具有直接激活凝血因子X的能力。这些发现表明在血液凝固起始过程中存在一种不同于内源性和外源性机制的替代性“细胞”途径。

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