Evidence that cells from experimental tumours can activate coagulation factor X.
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.
D000818:Animals; D001777:Blood Coagulation; D002286:Carcinoma, Ehrlich Tumor / Q000097:blood; D005170:Factor X / Q000378:metabolism*; D006801:Humans; D008175:Lung Neoplasms / Q000097:blood; D051379:Mice; D008815:Mice, Inbred Strains; D009374:Neoplasms, Experimental / Q000097:blood*; D012510:Sarcoma 180 / Q000097:blood; D013917:Thrombin / Q000096:biosynthesis
D005170:Factor X; D013917:Thrombin