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Calorie Restriction Induces a P53-Independent Delay of Spontaneous Carcinogenesis in P53-Deficient and Wild-Type Mice

  1. Author:
    Hursting, S. D.
    Perkins, S. N.
    Brown, C. C.
    Haines, D. C.
    Phang, J. M.

  2. Author Address

    Phang JM NCI LAB NUTR & MOL REGULAT DIV BASIC SCI FREDERICK CANC RES & DEV CTR BLDG 560 ROOM 12-91 FREDERICK, MD 21702 USA NCI LAB NUTR & MOL REGULAT DIV BASIC SCI FREDERICK CANC RES & DEV CTR FREDERICK, MD 21702 USA SCI APPLICAT INT CORP FREDERICK CANC RES & DEV CTR PATHOL HISTOTECHNOL LAB FREDERICK, MD 21702 USA NCI BIOMETRY BRANCH DIV CANC PREVENT & CONTROL NIH BETHESDA, MD 20892 USA
    1. Year: 1997
  2. Journal: Cancer Research
    1. 57
    2. 14
    3. Pages: 2843-2846
  4. Type of Article: Article
  1. Abstract:

    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. [References: 15]

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