Journal Article

Diet, cancer and aging in DNA mismatch repair deficient mice

Jen-Lan Tsao, Sandra Dudley, Brian Kwok, Andrea E. Nickel, Peter W. Laird, Kimberly D. Siegmund, R. Michael Liskay and Darryl Shibata

in Carcinogenesis

Volume 23, issue 11, pages 1807-1810
Published in print November 2002 | ISSN: 0143-3334
Published online November 2002 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/23.11.1807
Diet, cancer and aging in DNA mismatch repair deficient mice

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Diet is an important risk factor for many cancers. High fat/low calcium (HFLC) diets are associated with increased tumorigenesis, whereas caloric restriction (CR) reproducibly increases lifespan and decreases tumors. Mutations are involved in aging and cancer, and different diets may alter mutagenesis. However, a number of repair pathways normally counteract mutations by correcting errors before they can be fixed in the genome. To further understand interactions between diet, aging and cancer, mice deficient in a major repair pathway called DNA mismatch repair (MMR) were fed HFLC, CR or control diets. Mlh1 deficient mice are prone to lymphomas and intestinal adenomas and carcinomas. No significant changes in adenocarcinoma or lymphoma incidence were observed with HFLC or CR diets. Significantly more (2.2-fold) adenomas occurred with HFLC diets although adenoma numbers were unchanged with CR. Only a small increase in lifespan (116% of control) was achieved with CR. In addition, levels of microsatellite mutations in the small and large intestines were unchanged with the different diets. Our studies indicate that MMR deficiency may be epistatic to certain otherwise strong environmental influences on carcinogenesis or aging.

Keywords: CR, caloric restriction; HFLC, high fat/low calcium; HNPCC, hereditary non-polyposis colorectal cancer; MMR, mismatch repair; MS, microsatellite; NL, normal diet

Journal Article.  3152 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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