© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 22, 1960-1964,
November 17, 1999
© 1999 Oxford University Press
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Glutathione S-Transferase Mu and Theta Polymorphisms and Breast Cancer Susceptibility
Affiliation of authors: M. García-Closas, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; K. T. Kelsey, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, and Department of Environmental Health, Department of Cancer Cell Biology, and Harvard Center for Cancer Prevention, Harvard School of Public Health, Boston; S. E. Hankinson, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, and Department of Epidemiology, Harvard School of Public Health; D. Spiegelman, Department of Epidemiology and Department of Biostatistics, Harvard School of Public Health; K. Springer, Department of Cancer Cell Biology, Harvard Center for Cancer Prevention, Harvard School of Public Health; W. C. Willett, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, and Department of Nutrition and Harvard Center for Cancer Prevention, Harvard School of Public Health; F. E. Speizer, Department of Environment Health, Harvard School of Public Health; D. J. Hunter, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, and Harvard Center for Cancer Prevention, Harvard School of Public Health.
Correspondence to: David J. Hunter, M.B.B.S., Sc.D., Channing Laboratory, 181 Longwood Ave., Boston, MA 02115 (e-mail: nhdjh{at}gauss.med.harvard.edu).
BACKGROUND: The enzymes encoded by the glutathione S-transferase mu 1 (GSTM1) and theta 1 (GSTT1) genes are involved in the metabolism (mainly inactivation, but activation is possible) of a wide range of carcinogens that are ubiquitous in the environment; the enzyme encoded by the GSTT1 gene may also be active in endogenous mutagenic processes. Homozygous deletions of the GSTM1 and GSTT1 genes are commonly found in the population and result in a lack of enzyme activity. This study was undertaken to evaluate the association between GSTM1 and GSTT1 gene polymorphisms and breast cancer risk. METHODS: Our study included 466 women with incident cases of breast cancer occurring from May 1989 through May 1994 and 466 matched control subjects. These individuals were part of a prospective cohort of U.S. women (i.e., the Nurses' Health Study). Odds ratios (ORs) and 95% confidence intervals (CIs) from conditional logistic regression models were used to estimate the association between genetic polymorphisms and breast cancer risk. RESULTS: The GSTM1 and GSTT1 null genotypes were not associated with an increased risk of breast cancer (OR = 1.05 [95% CI = 0.80-1.37] for GSTM1 null; OR = 0.86 [95% CI = 0.61-1.21] for GSTT1 null). On the contrary, a suggestion of a decreased risk of breast cancer associated with the GSTT1 null genotype was observed among premenopausal women. When considered together, no combination of the GSTM1 and GSTT1 genotypes was associated with an increased risk of breast cancer. The relationship between GSTM1 and GSTT1 gene deletions and breast cancer risk was not substantially modified by cigarette smoking. CONCLUSIONS: Our data provide evidence against a substantially increased risk of breast cancer associated with GSTM1 and/or GSTT1 homozygous gene deletions.
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