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Streptokinase inhibits pulmonary tumor seeding in an animal experimental model
Author(s) -
McCulloch Peter,
Choy Alfred,
Purushotham Anand D.,
Brown Douglas C.,
George William D.
Publication year - 1994
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930570103
Subject(s) - streptokinase , fibrinolysis , fibrin , medicine , metastasis , pathology , pharmacology , cancer research , immunology , cancer , myocardial infarction
One aspect of the metastatic process involves entrapment of tumor cells within the microcirculation of organs in a “fibrin‐platelet mesh.” We postulate that destruction of this mesh by fibrinolysis might discourage tumor seeding, thereby inhibiting metastasis. To study this hypothesis, the effect of intravenous streptokinase on pulmonary tumor seeding was examined in a rodent model. In vitro experiments demonstrated that streptokinase had no cytotoxic or cytostatic effect on the Mtln3 cell line. Pharmacokinetic studies showed that at 30,000 U/kg, streptokinase caused systemic fibrinolysis in the Fischer rat, as demonstrated by the thrombin time and fibrin plate lysis assay. Streptokinase administered at this dose, 30 min after tumor cell injection, caused a significant decrease in pulmonary tumor seeding (median 23.0 in the streptokinase‐treated group vs, 67.5 in untreated controls, P < 0.0001, Mann‐Whitney U‐test). Analysis of fibrin degradation products in the streptokinase‐treated group suggested that this effect might be secondary to fibrinolysis. The implications of these findings are discussed. © 1994 Wiley‐Liss, inc.