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Chemoprevention of Spontaneous Tumorigenesis in p53-Knockout Mice¹

Laboratory of Nutritional and Molecular Regulation [S. D. H., S. N. P., J. M. P.], Pathology/Histotechnology Laboratory, Science Applications International Corporation [D. C. H.], and Veterinary and Tumor Pathology, Office of Laboratory Animal Science [J. M. W.], National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201

Spontaneous tumorigenesis was evaluated in male p53-knockout (p53^-/-) mice treated with dehydroepiandrosterone (DHEA), quercetin, d-limonene, or all-trans retinoic acid to determine whether tumor development in these mice can be modulated by cancer-chemopreventive agents. DHEA-treated mice experienced a delay in tumorigenesis (particularly lymphomas) and subsequent mortality (P < 0.01) relative to untreated control mice. Quercetin, d-limonene, and all-trans retinoic acid each had no effect on spontaneous tumor development in p53^-/- mice. These data demonstrate that tumor development in p53^-/- mice can be delayed by DHEA and suggest that p53^-/- mice provide a useful model for evaluating strategies to offset the increased risk of tumorigenesis resulting from loss of p53 tumor suppressor function.

¹ This work was supported in part by a United States Public Health Service contract to Science Applications International Corporation.

² Present address: Departments of Epidemiology and Carcinogenesis, Box 189, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030-4095.

³ To whom correspondence should be addressed, at LNMR, Building 560, Room 12-48, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702-1201.

Received 5/23/95. Accepted 8/ 2/95.

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