| Abstract | Many studies have indicated that the plasminogen activation system may have a prominent role in cancer. Activation of the zymogen plasminogen into the serine protease plasmin by plasminogen activator is mediated by carboxyterminal basic amino acids in fibrin, including lysines and arginines. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a circulating carboxypeptidase B-type proenzyme that, after activation, removes carboxyterminal lysine or arginine residues in fibrin, resulting in decreased plasminogen activation and attenuated fibrinolysis. To determine directly whether TAFI is involved in primary tumor growth and metastasis formation, we examined the effects of TAFI deficiency on subcutaneous growth and experimentally or spontaneously induced pulmonary metastasis formation of different tumor cell types in mice. In all tumor models TAFI deficiency did not affect the formation and growth of primary and metastasized tumors. |
| Authors | A Reijerkerk, J C M Meijers, S R Havik, B N Bouma, E E Voest, M F B G Gebbink
(Affiliation: Department of Medical Oncology, University Medical Center Utrecht, Utrecht, The Netherlands.)
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| Journal | Journal of thrombosis and haemostasis : JTH
(J Thromb Haemost)
Vol. 2
Issue 5
Pg. 769-79
(May 2004)
ISSN: 1538-7933 England |
| PMID | 15099284
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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| Chemical References |
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| Topics |
- Animals
- Carboxypeptidase U
(deficiency, physiology)
- Carcinoma, Lewis Lung
(pathology, secondary)
- Cell Proliferation
- Kinetics
- Lung Neoplasms
(secondary)
- Melanoma
(pathology)
- Mice
- Mice, Knockout
- Neoplasm Metastasis
- Neoplasm Seeding
- Neoplasms, Experimental
(pathology, secondary)
- Staining and Labeling
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