© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 11, 961-966,
June 2, 1999
© 1999 Oxford University Press
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Androgen Receptor Exon 1 CAG Repeat Length and Breast Cancer in Women Before Age Forty Years
Affiliations of authors: A. B. Spurdle, X. Chen, G. Chenevix-Trench (Cancer Unit), C. Mayne (Epidemiology Unit), Joint Experimental Oncology Programme, Queensland Institute of Medical Research, and The University of Queensland, Brisbane, Australia; G. S. Dite, J. L. Hopper, Centre for Genetic Epidemiology, The University of Melbourne, Carlton, Australia; M. C. Southey, L. E. Batten, H. Chy, L. Trute, Department of Pathology and Research, Peter MacCallum Cancer Institute, Melbourne; M. R. E. McCredie, Cancer Epidemiology Research Unit, NSW Cancer Council, Kings Cross, Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand; G. G. Giles, Cancer Epidemiology Centre, Anti-Cancer Council of Victoria, Australia; J. Armes, Victorian Breast Cancer Research Consortium and Department of Pathology, Peter MacCallum Cancer Institute, Melbourne; D. J. Venter, Department of Pathology and Research, Peter MacCallum Cancer Institute, and Department of Pathology, The University of Melbourne.
Correspondence to: Amanda B. Spurdle, Ph.D., Cancer Unit, Queensland Institute of Medical Research, P.O. Royal Brisbane Hospital, Queensland, 4029, Australia (e-mail: mandyS{at}qimr.edu.au).
BACKGROUND: We conducted a population-based, case-control-family study to determine whether androgen receptor (AR) exon 1 polymorphic CAG repeat length (CAGn) was a risk factor for early-onset breast cancer in the Australian population. METHODS: Case subjects under 40 years of age at diagnosis of a first primary breast cancer and age-matched control subjects were interviewed to assess family history and other risk factors. AR CAGn length was determined for 368 case subjects and 284 control subjects. Distributions in the two groups were compared by linear and logistic regression, allowing adjustment for measured risk factors. All statistical tests were two-tailed. RESULTS: When analyzed as either a continuous or a dichotomous variable, there was no association between CAGn length and breast cancer risk, before or after adjustment for risk factors. Mean (95% confidence interval [CI]) CAGn lengths were 22.0 (21.8-22.2) for case subjects and 22.0 (21.7-22.3) for control subjects (P = .9). The frequency (95% CI) of alleles with 22 or more CAGn repeats was 0.531 (0.494-0.568) for case subjects and 0.507 (0.465-0.549) for control subjects (P = .4). After adjustment, the average effect on log OR (odds ratio) per allele was 0.16 (95% CI = -0.03 to 0.40; P = .2), and the effect of any allele was equivalent to an OR of 1.40 (95% CI = 0.94-2.09; P = .1). Stratification by family history also failed to reveal any association. Similar results were obtained when alleles were defined by other cutoff points. CONCLUSION: We found no evidence for an association between AR exon 1 CAGn length and breast cancer risk in women under the age of 40, despite having 80% power to detect modest effects.
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