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The Steroid 5-Reductase Type II TA Repeat Polymorphism Is Not Associated with Risk of Breast or Ovarian Cancer in Australian Women¹

Oncology Division, Joint Experimental Oncology Programme, The Queensland Institute of Medical Research, and The University of Queensland, Brisbane, QLD 4029 Australia [A. B. S., X. C., G. C-T.]); Centre for Genetic Epidemiology, The University of Melbourne, Carlton, VIC 3053 Australia [J. L. H., G. S.]; The New South Wales Cancer Council, Kings Cross, NSW 2011 Australia, and Department of Preventive and Social Medicine, University of Otago, Dunedin, New Zealand [M. R. E. M.]; The Anti-Cancer Council of Victoria, Carlton, VIC 3053 Australia [G. G. G.]; Peter MacCallum Cancer Institute, Melbourne, Australia, and Department of Pathology, The University of Melbourne, Parkville, VIC 3052 Australia [D. J. V., M. C. S.], Population and Clinical Sciences Division, The Queensland Institute of Medical Research, Brisbane, QLD 4029 Australia [D. P.]

The enzyme 5-reductase type II (SRD5A2) converts testosterone to its more active form 5-dihydroxytestosterone. The 3' untranslated region of the gene contains a (TA)_n length polymorphism. The (TA)₉ allele has been reported to be associated with higher serum prostate-specific antigen levels in breast tumors and lower risk of relapse in breast cancer patients and more recently has also been reported to be linked to the codon 89 valine variant, which is itself associated with higher serum prostate-specific antigen levels in breast tumors and a more favorable breast cancer prognosis. We investigated whether the SRD5A2 (TA)_n polymorphism was associated with risk of breast or ovarian cancer in Australian women by studying 946 breast cancer cases and 509 age-matched controls, and 544 ovarian cancer cases and 298 controls of similar age distribution. The (TA)₉ allele frequency was similar in breast cancer cases (0.110), breast cancer controls (0.125), ovarian cancer cases (0.106), and ovarian cancer controls (0.117). There was no difference in genotype distribution between breast cancer cases and controls (P = 0.5), ovarian cancer cases and controls (P = 0.7), or between the two control groups (P = 0.9). Genotypes containing at least one (TA)₉ allele were not significantly associated with risk of breast cancer overall (odds ratio, 0.86; 95% confidence interval, 0.67–1.12; P = 0.3) or in women stratified by age, menopausal status, or family history. Similarly, the (TA)₉ allele was not associated with risk of ovarian cancer (odds ratio, 0.87; 95% confidence interval, 0.61–1.23; P = 0.4) or with ovarian tumor behavior (invasive or low malignant potential), histology, stage, or grade. Given that this study had sufficient power to detect altered risks in the order of 1.4- to 1.7-fold, our results suggest that the SRD5A2 (TA)₉ allele is unlikely to be associated with moderate alterations in breast or ovarian cancer risk.

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