QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Patel, A. C. Articles by Hursting, S. D. Search for Related Content PubMed PubMed Citation Articles by Patel, A. C. Articles by Hursting, S. D.

---

Supplement: International Research Conference on Food, Nutrition, and Cancer

Effects of Energy Balance on Cancer in Genetically Altered Mice¹

Arti C. Patel^*,, Nomeli P. Nunez^*,, Susan N. Perkins^*,, J. Carl Barrett^* and Stephen D. Hursting^*,,2

^* Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892 and Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD 20892

²To whom correspondence should be addressed. E-mail: sh63v{at}nih.gov.

Evidence has accumulated from laboratory-based animal experiments and population-based human epidemiological studies that lifestyle factors that affect energy balance, such as caloric intake, nutritional status, and exercise, act in concert with genetic susceptibility to influence cancer development and progression. The use of animal models with specific genetic alterations, in combination with lifestyle modifications that alter overall energy balance, has contributed to a greater understanding of the mechanistic changes occurring during carcinogenesis and to the identification of points of intervention. Studies in our laboratory focusing on the role of energy balance and genetic susceptibility in mice deficient in one (+/–) or both (–/–) alleles of the p53 tumor suppressor gene and mice with a mutant APC allele (APC^Min) showed that calorie restriction decreases tumor burden, increases tumor latency, and decreases serum insulin-like growth factor (IGF)-1 and leptin levels. Data from our studies, combined with results from other animal and human studies, have established a role for IGF-1 in carcinogenesis. Studies using genetic models of cancer that have been interbred with mice with abnormal levels of IGF-1 will enable the examination of combined effects of energy balance and genetic alterations on the cancer process. Models that integrate lifestyle and genetic effects in a single system provide a physiologically intact system in which combination interventions and therapies for cancer prevention can be tested and validated, thus building a strong preclinical foundation that will inform the development of clinical trials and add perspective to epidemiological studies.

KEY WORDS: • energy balance • diet • nutrition • chemoprevention • transgenic • calorie restriction • insulin-like growth factor-1 • leptin

This article has been cited by other articles:

				P. A. Davis, M. Jenab, J. P. Vanden Heuvel, T. Furlong, and S. Taylor Tree Nut and Peanut Consumption in Relation to Chronic and Metabolic Diseases Including Allergy J. Nutr., September 1, 2008; 138(9): 1757S - 1762S. [Abstract] [Full Text] [PDF]

				K. A. Varady, D. J. Roohk, B. K. McEvoy-Hein, B. D. Gaylinn, M. O. Thorner, and M. K. Hellerstein Modified alternate-day fasting regimens reduce cell proliferation rates to a similar extent as daily calorie restriction in mice FASEB J, June 1, 2008; 22(6): 2090 - 2096. [Abstract] [Full Text] [PDF]

				T. Moore, L. Beltran, S. Carbajal, S. Strom, J. Traag, S. D. Hursting, and J. DiGiovanni Dietary Energy Balance Modulates Signaling through the Akt/Mammalian Target of Rapamycin Pathways in Multiple Epithelial Tissues Cancer Prevention Research, June 1, 2008; 1(1): 65 - 76. [Abstract] [Full Text] [PDF]

				J. Y. Jeon, R. L. Bradley, E. G. Kokkotou, F. E. Marino, X. Wang, P. Pissios, and E. Maratos-Flier MCH-/- Mice Are Resistant to Aging-Associated Increases in Body Weight and Insulin Resistance Diabetes, February 1, 2006; 55(2): 428 - 434. [Abstract] [Full Text] [PDF]

				L. Erker, R. Schubert, H. Yakushiji, C. Barlow, D. Larson, J. B. Mitchell, and A. Wynshaw-Boris Cancer chemoprevention by the antioxidant tempol acts partially via the p53 tumor suppressor Hum. Mol. Genet., June 15, 2005; 14(12): 1699 - 1708. [Abstract] [Full Text] [PDF]