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[Cancer Research 66, 2483-2487, February 15, 2006]
© 2006 American Association for Cancer Research


Epidemiology and Prevention

A Prospective Study of Serum C-Reactive Protein and Colorectal Cancer Risk in Men

Marc J. Gunter1, Rachael Stolzenberg-Solomon1, Amanda J. Cross1, Michael F. Leitzmann1, Stephanie Weinstein1, Richard J. Wood2, Jarmo Virtamo3, Philip R. Taylor1, Demetrius Albanes1 and Rashmi Sinha1

1 Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Rockville, Maryland; 2 Mineral Bioavailability Laboratory, USDA, Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts; and 3 Department of Epidemiology and Health Promotion, National Public Health Institute, Helsinki, Finland

Requests for reprints: Marc Gunter, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, Rockville, MD 20852. Phone: 301-451-9581; E-mail: gunterm{at}mail.nih.gov.

Chronic inflammation has been implicated in the etiology of colorectal cancer. C-reactive protein (CRP), a sensitive marker of inflammation, has been investigated with regard to colorectal cancer in only three previous studies, and the results from these investigations were inconsistent. We examined serum CRP levels in relation to colorectal cancer incidence in a nested case-control study within the Alpha Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study, a cohort of 29,133 Finnish males enrolled from 1985 to 1988 with follow-up through April 2002. Colorectal cancer cases were ascertained by the Finnish Cancer Registry; this analysis included 130 cases of colorectal cancer (with available blood), which occurred between 1990 and April 30, 2002, and 260 matched controls. Baseline median CRP levels were ~25% higher among colorectal cancer cases (3.4 mg/L) than controls (2.6 mg/L; P = 0.04). Relative to men in the lowest quartile of CRP concentration, men in the highest quartile had an odds ratio of 2.9 (95% confidence interval, 1.4-6.0) for developing colorectal cancer with a dose-response relationship supported (Ptrend = 0.006). The relation between CRP and incident colorectal cancer was modified by body mass index such that the association was stronger among lean individuals than in heavier individuals (Pinteraction = 0.018). These results support the notion that chronic low-grade inflammation is a marker for increased risk of colorectal cancer. (Cancer Res 2006; 66(4): 2483-7)




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