Double-strand break repair gene polymorphisms and risk of breast or ovarian cancer

Webb, Penelope, Hopper, John L., Newman, Beth, Chen, Xiaoqing, Kelemen, Livia, Giles, Graham G., Southey, Melissa C., Chenevix-Trench, Georgia and Spurdle, Amanda B. (2005) Double-strand break repair gene polymorphisms and risk of breast or ovarian cancer. Cancer Epidemiology Biomarkers and Prevention, 14 2: 319-323. doi:10.1158/1055-9965.EPI-04-0335

Author Webb, Penelope
Hopper, John L.
Newman, Beth
Chen, Xiaoqing
Kelemen, Livia
Giles, Graham G.
Southey, Melissa C.
Chenevix-Trench, Georgia
Spurdle, Amanda B.
Title Double-strand break repair gene polymorphisms and risk of breast or ovarian cancer
Journal name Cancer Epidemiology Biomarkers and Prevention   Check publisher's open access policy
ISSN 1055-9965
Publication date 2005-01-01
Sub-type Article (original research)
DOI 10.1158/1055-9965.EPI-04-0335
Open Access Status Not yet assessed
Volume 14
Issue 2
Start page 319
End page 323
Total pages 5
Place of publication Philadelphia, PA, United States
Publisher American Association for Cancer Research
Language eng
Subject C1
Abstract Deficiencies in DNA repair have been hypothesized to increase cancer risk and excess cancer incidence is a feature of inherited diseases caused by defects in DNA damage recognition and repair. We investigated, using a case-control design, whether the double-strand break repair gene polymorphisms RAD51 5' untranslated region -135 G > C, XRCC2 R188H G > A, and XRCC3 T241M C > T were associated with risk of breast or ovarian cancer in Australian women. Sample sets included 1,456 breast cancer cases and 793 age-matched controls ages under 60 years of age, 549 incident ovarian cancer cases, and 335 controls of similar age distribution. For the total sample and the subsample of Caucasian women, there were no significant differences in genotype distribution between breast cancer cases and controls or between ovarian cancer cases and combined control groups. The crude odds ratios (OR) and 95% confidence intervals (95% CI) associated with the RAD51 GC/CC genotype frequency was OR, 1.10; 95% CI, 0.80-1.41 for breast cancer and OR, 1.22; 95% CI, 0.92-1.62 for ovarian cancer. Similarly, there were no increased risks associated with the XRCC2 GA/AA genotype (OR, 0.98; 95% CI, 0.76-1.26 for breast cancer and OR, 0.93; 95% CI, 0.69-1.25 for ovarian cancer) or the XRCC3 CT/TT genotype (OR, 0.92; 95% Cl, 0.77-1.10 for breast cancer and OR, 0.87; 95% CI, 0.71-1.08 for ovarian cancer). Results were little changed after adjustment for age and other measured risk factors. Although there was little statistical power to detect modest increases in risk for the homozygote variant genotypes, particularly for the rare RAD51 and XRCC2 variants, the data suggest that none of these variants play a major role in the etiology of breast or ovarian cancer.
Keyword Oncology
Public, Environmental and Occupational Health
Single Nucleotide Polymorphism
Diagnostic X-rays
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2006 Higher Education Research Data Collection
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School of Medicine Publications
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