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Calorie Restriction Induces a p53-independent Delay of Spontaneous Carcinogenesis in p53-deficient and Wild-Type Mice¹

Laboratory of Nutritional and Molecular Regulation, Division of Basic Sciences, National Cancer Institute, NIH, Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201 [S. D. H., S. N. P., J. M. P.]; Pathology/Histotechnology Laboratory, Science Applications International Corporation-Frederick, Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201 [D. C. H.]; and Biometry Branch, Division of Cancer Prevention and Control, National Cancer Institute, NIH, Bethesda, Maryland 20892 [C. C. B.]

We reported previously that calorie restriction (CR) delays spontaneous carcinogenesis in p53-deficient (p53^-/-) mice, suggesting that CR modulates carcinogenesis by p53-independent mechanisms. To further evaluate the role of p53, we monitored tumor development in p53^-/- and wild-type (p53^+/+) mice fed ad libitum (AL) or a CR regimen (60% of AL calorie intake). CR delayed tumor mortality in p53^-/- and p53^+/+ mice (mean time to death, 169 and 648 days, respectively) relative to AL feeding (104 and 470 days). The estimated age-specific cancer death rate AL:CR ratios were 4.3 for p53^-/- mice and 4.4 for p53^+/+ mice. Thus, despite the accelerated onset of carcinogenesis in p53^-/- mice, the tumor-delaying effect of CR was similar in the two genotypes.

¹ Supported by NCI Grant CA16672 (to S. D. H.).

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

³ To whom requests for reprints should be addressed, at LNMR, Building 560, Room 12-91, NCI-FCRDC, Frederick, MD 21702-1201.

Received 4/10/97. Accepted 6/ 2/97.

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