Diet, Lifestyle, and Genomic Instability in the North Carolina Colon Cancer Study
- Jessie A. Satia1,2,4,
- Temitope Keku3,4,
- Joseph A. Galanko4,
- Christopher Martin4,
- Ryan T. Doctolero5,
- Akihiro Tajima6,
- Robert S. Sandler3,4 and
- John M. Carethers5,6,7
- 1Department of Global Epidemiology, Amgen, Inc., Thousand Oaks, California; 2Department of Nutrition, Schools of Public Health and Medicine; 3Division of Gastroenterology and Hematology, Department of Medicine, and 4Center for Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; 5Veterans Affairs San Diego Healthcare System; 6Department of Medicine and Moore's Comprehensive Cancer Center, University of California at San Diego; and 7Veteran's Medical Research Foundation, San Diego, California
- Requests for reprints:
Jessie A. Satia, Department of Global Epidemiology, Amgen, Inc., One Amgen Center Drive, 24-1-C, Thousand Oaks, CA 91320. Phone: 805-313-4097; Fax: 805-498-5593. E-mail: jessie.satia{at}amgen.com
Abstract
Objective: Microsatellite instability (MSI) is one form of genomic instability that occurs in 10% to 20% of sporadic colon tumors and almost all hereditary nonpolyposis colon cancers. However, little is known about how environmental factors (e.g., diet) may influence MSI in sporadic colon cancer.
Methods: We used data from a population-based case-control study in North Carolina (486 colon cancer cases and 1,048 controls) to examine associations of diet (total energy, macronutrients, micronutrients, and food groups) with MSI. In-person interviews elicited information on potential colon cancer risk factors, and a previously validated food frequency questionnaire adapted to include regional foods was used to assess diet over the year before diagnosis or interview date. MSI was classified as MSI-high (MSI-H) and MSI-low or microsatellite stable (MSI-L/MSS). Multivariate logistic regression models estimated energy-adjusted and non-energy-adjusted odds ratios (OR).
Results: Ten percent of the cases (n = 49) had MSI-H tumors (29% African American). The strongest associations between diet and MSI were observed in case-control comparisons: there was a robust inverse association between MSI-H status and β-carotene [OR, 0.4; 95% confidence interval (95% CI), 0.2-0.9] and positive associations with energy-adjusted refined carbohydrates (OR, 2.2; 95% CI, 0.9-5.4) and non-energy-adjusted read meat intake (OR, 2.0; 95% CI, 0.9-4.2). Compared with controls, MSI-L/MSS tumors were statistically significantly associated with energy-adjusted vitamin C, vitamin E, calcium, dietary fiber, and dark green vegetables and positively associated with total energy intake (all Ps for trend < 0.05). In case-case comparisons, no dietary factors were significantly differently related to MSI-H compared with MSI-L/MSS tumors.
Conclusion: Refined carbohydrate and red meat consumption may promote development of MSI-H tumors, whereas β-carotene may be associated with lower risk.
Footnotes
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- Accepted September 23, 2004.
- Received June 30, 2004.
- Revision received August 19, 2004.
