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Inhibition of Mouse Bladder Tumor Proliferation by Murine Interferon- and Its Synergism with Interferon-ß¹

Department of Surgery, Division of Urology, Washington University School of Medicine at The Jewish Hospital of St. Louis [T. L. R., D. K., A. S.]; Urologic Oncology Research Laboratory, Department of Surgery, Division of Urology [W. D. W. H.], and Department of Obstetrics and Gynecology [A. J. J.], Washington University School of Medicine, St. Louis, Missouri 63110

We studied the effect of interferon- (IFN-) and mouse L-cell interferon (IFN-ß) on the proliferation of a mouse bladder tumor, MBT-2. A liquid culture clonogenic assay was used, and a linear relationship was obtained between the number of cells plated and the number of colonies formed. When the cells were assayed in the presence of various doses of murine IFN- or IFN-ß, colony formation was inhibited in a dose-dependent manner. Partially purified IFN- was more effective than IFN-ß in inhibiting MBT-2 colony formation in that IFN-ß exhibited a 50% inhibition dose of approximately 1000 units/ml, while the 50% inhibition dose for the partially purified IFN- was approximately 70 units/ml. The 50% inhibition dose for recombinant IFN- was 700 units/ml, suggesting that multiple lymphokines were active in the partially purified preparation. Further studies with partially purified IFN- showed that the inhibitory effect was time dependent with the maximal effect observed after 48 hr of exposure in a 5-day assay. Treatment of partially purified IFN- for 24 hr at pH 2.0 resulted in the abrogation of the antiproliferative effect. Studies in which partially purified IFN- preparations were treated with a monoclonal antibody against IFN- also resulted in abrogation of antiproliferative activity, confirming the nature of the antiproliferative agent to be IFN-. Further studies showed that murine recombinant IFN- also inhibited MBT-2 proliferation in a dose-dependent manner, confirming that IFN- alone mediates anti-proliferative activity. Combinations of IFN-ß and recombinant IFN- acted synergistically in the inhibition of MBT-2 proliferation.

¹ This work was supported by USPHS Grant CA 28860 from the National Cancer Institute through the National Bladder Cancer Project.

² To whom requests for reprints should be addressed.

³ Present address: Department of Urology, Hadassah University Hospital, Jerusalem, Israel.

Received 3/19/84. Accepted 7/ 3/84.

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