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Cancer Epidemiology Biomarkers & Prevention Vol. 9, 567-573, June 2000
© 2000 American Association for Cancer Research

Glutathione S-Transferases M1, T1, and P1 and Breast Cancer1

Robert Millikan2, Gary Pittman, Chiu-Kit Tse, David A. Savitz, Beth Newman and Douglas Bell

Department of Epidemiology, School of Public Health, and Lineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599 [R. M., G. P., C-K. T., D. A. S.]; Genetic Risk Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 [G. P., D. B.]; and School of Public Health, Queensland University of Technology, Brisbane 4059, Queensland, Australia [B. N.]

We examined associations for glutathione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) genotypes and breast cancer in the Carolina Breast Cancer Study, a population-based, case-control study in North Carolina. Odds ratios were close to the null value for each GST locus among African-American women (278 cases and 271 controls) and white women (410 cases and 392 controls), as well as pre- and postmenopausal women. For women with a history of breast cancer in one or more first-degree relatives, odds ratios were 2.1 (95% confidence interval, 1.0–4.2) for GSTM1 null and 1.9 (0.8–4.6) for GSTT1 null genotypes. Among women with a family history, age at diagnosis was significantly earlier for those with the GSTM1 null genotype. We did not observe strong evidence for modification of odds ratios for smoking according to GST genotypes. There was no evidence for combined effects of GSTM1, GSTT1, and GSTP1 genotypes, and there were no combined effects for GST genotypes and the catechol O-methyltransferase genotype. We conclude that GSTM1, GSTT1, and GSTP1 genotypes do not play a strong role in susceptibility to breast cancer. However, the role of GST genotypes in age at onset and risk of breast cancer among women with a family history merits further investigation.




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