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 Jiao, L. Articles by Li, D. Search for Related Content PubMed PubMed Citation Articles by Jiao, L. Articles by Li, D.

Haplotype of N-Acetyltransferase 1 and 2 and Risk of Pancreatic Cancer

Departments of ¹ Gastrointestinal Medical Oncology and ² Epidemiology, The University of Texas M. D. Anderson Cancer Center; ³ Human Genetics Center, The University of Texas School of Public Health, Houston, Texas; and ⁴ Department of Pharmacology and Toxicology and Brown Cancer Center, University of Louisville School of Medicine, Louisville, Kentucky

Requests for reprints: Donghui Li, Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Unit 426, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: 713-834-6690; Fax: 713-834-6153. E-mail: dli{at}mdanderson.org

We examined the association between N-acetyltransferase 1 and 2 (NAT1 and NAT2) haplotype and risk of pancreatic cancer by genotyping eight NAT1 and seven NAT2 single nucleotide polymorphisms in 532 patients and in 581 healthy controls (all non-Hispanic white) who were recruited at M. D. Anderson Cancer Center from January 2000 to December 2006. Haplotypes were reconstructed by using an expectation-maximization algorithm. Odds ratios and 95% confidence intervals were estimated by using unconditional logistic regression models. Covariates included age (continuous variable), sex, pack-year of smoking (categorical), and history of diabetes when appropriate. NAT1 and NAT2 genotype was mutually adjusted. The prevalence of haplotype NAT1*10-NAT2*6A was 4.3% versus 2.7% (P = 0.06) and NAT1*11-NAT2*6A was 1.2% versus 0.4% (P = 0.05) in patients and controls, respectively. The diplotype NAT1*10/*10 or NAT1*10/*11 and NAT2*6A/any slow allele was associated with a higher risk of pancreatic cancer compared with other diplotypes (multivariate odds ratio, 4.15; 95% confidence interval, 1.15-15.00; P = 0.03). NAT2 slow genotype were associated with increased risk of pancreatic cancer among heavy smokers and among individuals with a history of diabetes. We for the first time found that rare NAT1*10 or NAT1*11-NAT2*6A diplotype may be an "at-risk" genetic variant for pancreatic cancer. The NAT2*6A/any slow acetylation genotype may be a predisposing factor for pancreatic cancer among diabetics with smoking exposure. Our observations must be confirmed in larger independent studies. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2379–86)

This article has been cited by other articles:

				H. Suzuki, J. S. Morris, Y. Li, M. A. Doll, D. W. Hein, J. Liu, L. Jiao, M. M. Hassan, R. S. Day, M. L. Bondy, et al. Interaction of the cytochrome P4501A2, SULT1A1 and NAT gene polymorphisms with smoking and dietary mutagen intake in modification of the risk of pancreatic cancer Carcinogenesis, June 1, 2008; 29(6): 1184 - 1191. [Abstract] [Full Text] [PDF]