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.
| Original language | English |
|---|---|
| Pages (from-to) | 228-233 |
| Number of pages | 6 |
| Journal | British Journal of Cancer |
| Volume | 40 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 1979 |
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ASJC Scopus subject areas
- Cancer Research
- Oncology
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Evidence that cells from experimental tumours can activate coagulation factor X. / Curatolo, L.; Colucci, M.; Cambini, A. L.; Poggi, A.; Morasca, L.; Donati, M. B.; Semeraro, N.
In: British Journal of Cancer, Vol. 40, No. 2, 1979, p. 228-233.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Evidence that cells from experimental tumours can activate coagulation factor X
AU - Curatolo, L.
AU - Colucci, M.
AU - Cambini, A. L.
AU - Poggi, A.
AU - Morasca, L.
AU - Donati, M. B.
AU - Semeraro, N.
PY - 1979
Y1 - 1979
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0018581695&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018581695&partnerID=8YFLogxK
U2 - 10.1038/bjc.1979.170
DO - 10.1038/bjc.1979.170
M3 - Article
C2 - 573131
AN - SCOPUS:0018581695
VL - 40
SP - 228
EP - 233
JO - British Journal of Cancer
JF - British Journal of Cancer
SN - 0007-0920
IS - 2
ER -