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Volume 21, Issue 2, Pages 77-88 (February 2010)


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Mouse models for unraveling the importance of diet in colon cancer prevention

Alexandra E. Tammarielloa, John A. MilnerbCorresponding Author Informationemail address

Received 2 February 2009; received in revised form 30 July 2009; accepted 21 September 2009.

Abstract 

Diet and genetics are both considered important risk determinants for colorectal cancer, a leading cause of death worldwide. Several genetically engineered mouse models have been created, including the ApcMin mouse, to aid in the identification of key cancer related processes and to assist with the characterization of environmental factors, including the diet, which influence risk. Current research using these models provides evidence that several bioactive food components can inhibit genetically predisposed colorectal cancer, while others increase risk. Specifically, calorie restriction or increased exposure to n-3 fatty acids, sulforaphane, chafuroside, curcumin and dibenzoylmethane were reported protective. Total fat, calories and all-trans retinoic acid are associated with an increased risk. Unraveling the importance of specific dietary components in these models is complicated by the basal diet used, the quantity of test components provided and interactions among food components. Newer models are increasingly available to evaluate fundamental cellular processes, including DNA mismatch repair, immune function and inflammation as markers for colon cancer risk. Unfortunately, these models have been used infrequently to examine the influence of specific dietary components. The enhanced use of these models can shed mechanistic insights about the involvement of specific bioactive food and components and energy as determinants of colon cancer risk. However, the use of available mouse models to exactly represent processes important to human gastrointestinal cancers will remain a continued scientific challenge.

a Department of Human Nutrition, Foods and Exercise, Virginia Tech, Blacksburg, VA, USA

b Nutritional Science Research Group, Division of Cancer Prevention, National, Cancer Institute, National Institutes of Health, Health and Human Services, Rockville, MD 20892, USA

Corresponding Author InformationCorresponding author. Tel.: +1 301 496 0118; fax: +1 301 480 3925.

PII: S0955-2863(09)00217-4

doi:10.1016/j.jnutbio.2009.09.014


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