© 2002 by Oxford University Press
Journal of the National Cancer Institute, Vol. 94, No. 4, 297-306,
February 20, 2002
© 2002 Oxford University Press
ARTICLE |
A Population-Based, Case–Control Study of Polymorphisms in Carcinogen-Metabolizing Genes, Smoking, and Pancreatic Adenocarcinoma Risk
Affiliations of authors: E. J. Duell, M. Liu, K.T. Kelsey, Department of Cancer Cell Biology, Harvard School of Public Health, Boston, MA; E.A. Holly, P.M. Bracci, J.K.Wiencke, Department of Epidemiology and Biostatistics, University of California, San Francisco Department of Cancer Cell Biology, Harvard School of Public Health, Boston, MA;
Correspondence to: Karl T. Kelsey, M.D., Department of Cancer Cell Biology, Harvard School of Public Health, Bldg. 1, Rm. 207, 665 Huntington Ave., Boston, MA 02115 (e-mail: kelsey{at}hsph.harvard.edu).
Background: Cigarette smoking is associated with a twofold increased risk of pancreatic cancer. We conducted a population-based case–control study in six San Francisco Bay area counties from 1994 to 2001 to investigate associations between polymorphisms in genes for two carcinogen-metabolizing enzymes (cytochrome P450 1A1 [CYP1A1] and glutathione S-transferase [GST]), smoking, and adenocarcinoma of the exocrine pancreas. Methods: We used polymerase chain reaction–based methods to analyze blood samples obtained from 309 case subjects and 964 control subjects to determine their genotypes for three CYP1A1 polymorphisms (m1, m2, and m4) and for homozygous deletions of two GST genes, GSTM1 and GSTT1. Control subjects were frequency matched to case subjects by age and sex. All statistical tests were two-sided. Results: None of the genetic polymorphisms themselves affected the risk of pancreatic cancer among Caucasian study participants. However, we observed an interaction between GSTT1-null genotype and cigarette smoking among Caucasians that was more prominent among women than among men. Relative to never smokers with the GSTT1-present genotype, the age-adjusted odds ratios (ORs) of pancreatic cancer for heavy smokers with the GSTT1-null genotype were 5.0 (95% confidence interval [CI] = 1.8 to 14.5) for women and 3.2 (95% CI = 1.3 to 8.1) for men; for heavy smokers with the GSTT1-present genotype they were 2.0 (95% CI = 1.0 to 4.0) for women and 2.1 (95% CI = 1.1 to 3.9) for men. ORs for pancreatic cancer among heavy smokers with both GSTT1-null and GSTM1-null genotypes were similar in magnitude to those among heavy smokers with the GSTT1-null genotype alone. There was no evidence of an interaction between CYP1A1 polymorphisms and smoking. Conclusions: The combination of heavy smoking and a deletion polymorphism in GSTT1 is associated with an increased risk of pancreatic cancer among Caucasians, with the associations possibly stronger in women than in men. J Natl Cancer Inst 2002;94:297–306]
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