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...

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Published inCancer research (Chicago, Ill.) Vol. 57; no. 14; pp. 2843 - 2846
Main Authors HURSTING, S. D, PERKINS, S. N, BROWN, C. C, HAINES, D. C, PHANG, J. M
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 15.07.1997
Subjects
Animals
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Diet, Reducing
Energy Intake
Foods and miscellaneous
Medical sciences
Mice
Neoplasms, Experimental - prevention & control
Tumor Suppressor Protein p53 - physiology
Tumors
Calorie
Spontaneous
Rodentia
Malignant tumor
Carcinogenesis
Vertebrata
Mammalia
TP53 Gene
Mouse
Animal
Mechanism of action
Tumor suppressor gene
Low calorie diet
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Summary: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.
ISSN:0008-5472
1538-7445