This Article Full Text Full Text (PDF) 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 Potter, J. D. Articles by Grambsch, P. Search for Related Content PubMed PubMed Citation Articles by Potter, J. D. Articles by Grambsch, P.

Colorectal Adenomatous and Hyperplastic Polyps: Smoking and N-Acetyltransferase 2 Polymorphisms

Fred Hutchinson Cancer Research Center, Seattle, Washington 98109 [J. D. P., J. B., C. C.]; University of Minnesota, Minneapolis, Minnesota 55454 [L. F., T. A. L., P. G.]; South Carolina Cancer Center, University of South Carolina, Columbia, South Carolina 29203 [R. M. B.]; and Wageningen Agricultural University, Wageningen, the Netherlands [E. K.]

Arylamine N-acetyltransferase 2 (NAT2) is involved in both the detoxification and bioactivation of carcinogenic arylamines and other mutagens. This enzyme is polymorphic, and the fast and slow phenotypes are thought to be risk factors for colon and bladder cancer, respectively. Here, we report on a case-control study of adenomatous and hyperplastic polyps, with particular attention to tobacco smoking, a known risk factor for adenomas, and polymorphisms of NAT2. All participants underwent complete colonoscopy and were subsequently divided into case and control groups on the basis of pathology. Cases were diagnosed with confirmed adenomas (n = 527) or hyperplastic polyps (n = 200); controls (n = 633) had no history of colonic neoplasia and no polyps at colonoscopy. NAT2 genotype was determined using an oligonucleotide ligation assay and fast, intermediate, or slow phenotype imputed. Multivariate-adjusted odds ratios (ORs) and 95% confidence intervals were computed using logistic regression adjusting for age, sex, nonsteroidal anti-inflammatory drug use, and hormone replacement therapy use. Smoking was associated with an increased risk of adenomas [current versus never smoking OR = 2.0 (95% confidence interval, 1.4–2.9)] and hyperplastic polyps [current versus never smoking OR = 4.1 (2.6–6.5)]. NAT2 status among adenomatous polyp patients and hyperplastic polyp patients, respectively, showed ORs of 1.1 (0.8–1.4) and 1.2 (0.8–1.6; intermediate versus slow) and 1.1 (0.6–1.9) and 0.9 (0.4–1.9; fast versus slow). There were no differences in risk when adenoma patients were stratified on multiplicity, size, or histopathological subtype of polyps. Never-smokers showed no variation in risk across acetylator status for either species of polyp, whereas current smokers showed ORs of 2.0 (1.2–3.2) and 2.3 (1.4–3.9) for adenomas and 3.9 (2.1–7.1) and 4.9 (2.6–9.4) for hyperplastic polyps for slow and intermediate/fast NAT2, respectively, compared with slow-NAT2 never-smokers. Risks of both multiple [OR = 4.3 (2.1–8.8)] and large [OR = 3.8 (1.9–7.5)] adenomas were somewhat elevated in current smokers with an intermediate/fast phenotype compared with smokers with a slow NAT2 phenotype, but the interaction was not statistically significant. Risk of hyperplastic polyps and adenomatous polyps is strongly related to smoking. There is little suggestion of interaction between NAT2 status and smoking and no relationship with NAT2 genotype alone.

This article has been cited by other articles:

				A. Shin, M. J. Shrubsole, J. M. Rice, Q. Cai, M. A. Doll, J. Long, W. E. Smalley, Y. Shyr, R. Sinha, R. M. Ness, et al. Meat Intake, Heterocyclic Amine Exposure, and Metabolizing Enzyme Polymorphisms in Relation to Colorectal Polyp Risk Cancer Epidemiol. Biomarkers Prev., February 1, 2008; 17(2): 320 - 329. [Abstract] [Full Text] [PDF]

				E. D. Paskett, K. W. Reeves, T. E. Rohan, M. A. Allison, C. D. Williams, C. R. Messina, E. Whitlock, A. Sato, and J. R. Hunt Association Between Cigarette Smoking and Colorectal Cancer in the Women's Health Initiative J Natl Cancer Inst, November 21, 2007; 99(22): 1729 - 1735. [Abstract] [Full Text] [PDF]

				E. L. Goode, J. D. Potter, W. R. Bamlet, D. N. Rider, and J. Bigler Inherited variation in carcinogen-metabolizing enzymes and risk of colorectal polyps Carcinogenesis, February 1, 2007; 28(2): 328 - 341. [Abstract] [Full Text] [PDF]

				B.-T. Ji, J. L. Weissfeld, W.-H. Chow, W.-Y. Huang, R. E. Schoen, R. B. Hayes, and for the Prostate, Lung, Colorectal, and Ovarian Tr Tobacco smoking and colorectal hyperplastic and adenomatous polyps. Cancer Epidemiol. Biomarkers Prev., May 1, 2006; 15(5): 897 - 901. [Abstract] [Full Text] [PDF]

				C. Lilla, E. Verla-Tebit, A. Risch, B. Jager, M. Hoffmeister, H. Brenner, and J. Chang-Claude Effect of NAT1 and NAT2 Genetic Polymorphisms on Colorectal Cancer Risk Associated with Exposure to Tobacco Smoke and Meat Consumption Cancer Epidemiol. Biomarkers Prev., January 1, 2006; 15(1): 99 - 107. [Abstract] [Full Text] [PDF]

				L. E. Moore, W.-Y. Huang, N. Chatterjee, M. Gunter, S. Chanock, M. Yeager, B. Welch, P. Pinsky, J. Weissfeld, and R. B. Hayes GSTM1, GSTT1, and GSTP1 Polymorphisms and Risk of Advanced Colorectal Adenoma Cancer Epidemiol. Biomarkers Prev., July 1, 2005; 14(7): 1823 - 1827. [Abstract] [Full Text] [PDF]

				K. Robien, K. Curtin, C. M. Ulrich, J. Bigler, W. Samowitz, B. Caan, J. D. Potter, and M. L. Slattery Microsomal Epoxide Hydrolase Polymorphisms Are Not Associated with Colon Cancer Risk Cancer Epidemiol. Biomarkers Prev., May 1, 2005; 14(5): 1350 - 1352. [Full Text] [PDF]

				R. Sparks, J. Bigler, J. G Sibert, J. D Potter, Y. Yasui, and C. M Ulrich TGF{beta}1 polymorphism (L10P) and risk of colorectal adenomatous and hyperplastic polyps Int. J. Epidemiol., October 1, 2004; 33(5): 955 - 961. [Abstract] [Full Text] [PDF]

				M. M. de Jong, I. M. Nolte, G. J. te Meerman, W. T. A. van der Graaf, E. G. E. de Vries, R. H. Sijmons, R. M. W. Hofstra, and J. H. Kleibeuker Low-penetrance Genes and Their Involvement in Colorectal Cancer Susceptibility Cancer Epidemiol. Biomarkers Prev., November 1, 2002; 11(11): 1332 - 1352. [Abstract] [Full Text] [PDF]

				L. M. Morimoto, P. A. Newcomb, C. M. Ulrich, R. M. Bostick, C. J. Lais, and J. D. Potter Risk Factors for Hyperplastic and Adenomatous Polyps: Evidence for Malignant Potential? Cancer Epidemiol. Biomarkers Prev., October 1, 2002; 11(10): 1012 - 1018. [Abstract] [Full Text] [PDF]

				M. B. Terry, A. I. Neugut, R. M. Bostick, R. S. Sandler, R. W. Haile, J. S. Jacobson, C. M. Fenoglio-Preiser, and J. D. Potter Risk Factors for Advanced Colorectal Adenomas: A Pooled Analysis Cancer Epidemiol. Biomarkers Prev., July 1, 2002; 11(7): 622 - 629. [Abstract] [Full Text] [PDF]

				C. Chen, S. Ricks, D. R. Doody, E.D. Fitzgibbons, P. L. Porter, and S. M. Schwartz N-Acetyltransferase 2 polymorphisms, cigarette smoking and alcohol consumption, and oral squamous cell cancer risk Carcinogenesis, December 1, 2001; 22(12): 1993 - 1999. [Abstract] [Full Text] [PDF]

				C. M. Ulrich and J. D. Potter Testing for Colon Neoplasia Susceptibility Variants at the Human COX2 Locus J Natl Cancer Inst, October 17, 2001; 93(20): 1572a - 1573a. [Full Text] [PDF]

				E. Giovannucci An Updated Review of the Epidemiological Evidence that Cigarette Smoking Increases Risk of Colorectal Cancer Cancer Epidemiol. Biomarkers Prev., July 1, 2001; 10(7): 725 - 731. [Abstract] [Full Text] [PDF]

				S. De Flora, A. Izzotti, F. D'Agostini, and R. M. Balansky Mechanisms of N-acetylcysteine in the prevention of DNA damage and cancer, with special reference to smoking-related end-points Carcinogenesis, July 1, 2001; 22(7): 999 - 1013. [Abstract] [Full Text] [PDF]

				J. D. Potter Colorectal Cancer: Molecules and Populations J Natl Cancer Inst, June 2, 1999; 91(11): 916 - 932. [Abstract] [Full Text] [PDF]

				E. Kampman, M. L. Slattery, J. Bigler, M. Leppert, W. Samowitz, B. J. Caan, and J. D. Potter Meat Consumption, Genetic Susceptibility, and Colon Cancer Risk: A United States Multicenter Case-Control Study Cancer Epidemiol. Biomarkers Prev., January 1, 1999; 8(1): 15 - 24. [Abstract] [Full Text]