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Dietary Fenretinide, a Synthetic Retinoid, Decreases the Tumor Incidence and the Tumor Mass of ras+myc-induced Carcinomas in the Mouse Prostate Reconstitution Model System¹

Scott Department of Urology, Baylor College of Medicine, Houston, Texas [K. S., D. K., S. H. P., P. T. S., T. C. T.]; The Urology Research Laboratory, Veterans Affairs Medical Center, Houston, Texas [K. S., D. K., S. H. P., T. C. T.]; Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030 [T. C. T.]; and Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892 [M. A., M. B. S.]

² To whom requests for reprints should be addressed, at 6535 Fannin, F427A. Houston, TX 77030.

Several epidemiological studies have implicated low dietary and serum levels of retinol with an increased risk for the development of human prostate cancer. In a recent report, dietary fenretinide [N-[(4-hydroxyphenyl)] retinamide], a synthetic retinoid with low toxicity, decreased the incidence of experimentally induced prostate cancer. Fenretinide is currently being evaluated in phase I and phase II clinical trials as an agent for both the treatment and chemoprevention of human prostate cancer. Because of these findings, we investigated whether dietary fenretinide could alter the incidence or phenotype of oncogene-induced prostate cancer in the mouse prostate reconstitution model system. When compared to control-fed animals, dietary fenretinide reduced the tumor incidence by 49% and the tumor mass by 52% of ras+myc-induced cancers in the mouse prostate reconstitution model system, which was modified to prolong the latency period before cancer development. Retinoids have a wide ranging effect on cellular differentiation, growth factor synthesis, and immune function. While its mechanism of action in this system remains unclear, fenretinide is an effective agent for the chemoprevention and growth modulation of oncogene-induced prostate cancer in the mouse prostate reconstitution model system and may be effective for the chemoprevention of human prostate cancer.

¹ This work was primarily supported by Grants CA50588 and SPORE P50-CA58204 from the National Cancer Institute and in part by the Veterans Administration. Additional support was provided by the American Foundation for Urologic Disease Research Scholar Program and the New York Academy of Medicine Ferdinand C. Valentine Fellowship Program.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Received 7/12/93. Accepted 8/18/93.

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