Calorie restriction induces a p53-independent delay of spontaneous carcinogenesis in p53-deficient and wild-type mice.
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.
Hursting
S D
SD
Division of Basic Sciences, National Cancer Institute, NIH, Frederick Cancer Research and Development Center, Maryland 21702-1201, USA.
Perkins
S N
SN
Brown
C C
CC
Haines
D C
DC
Phang
J M
JM
D000818:Animals; D004038:Diet, Reducing; D002149:Energy Intake; D051379:Mice; D009374:Neoplasms, Experimental / Q000517:prevention & control*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
D016159:Tumor Suppressor Protein p53