Environment and Breast Cancer: Science Review
About
Polymorphism in the DNA repair gene XPD, polycyclic aromatic hydrocarbon-DNA adducts, cigarette smoking, and breast cancer risk
Terry, M. B., Gammon, M. D., Zhang, F. F., Eng, S. M., Sagiv, S. K., Paykin, A. B., Wang, Q., Hayes, S., Teitelbaum, S. L., Neugut, A. I., Santella, R. M. Cancer Epidemiol Biomarkers Prev. 2004. 13:12, 2053-8.
Topic area
Environmental pollutant - PAH
Environmental pollutant - PAH
Study design
Population based case-control
Population based case-control
Study Participants
Number of Cases
1,053
1,053
Menopausal Status
Post menopausal
The menopausal status of women included in this study is listed here.
Pre menopausalPost menopausal
Number of Controls
Controls: 1,102
Controls: 1,102
Participant selection: Inclusion and exclusion criteria
Criteria used to select participants in the study.
Participants in the Long Island Breast Cancer Study Project who donated blood
Exposures investigated
Self-reported smoking, PAH-DNA adducts, XPD
Self-reported smoking, PAH-DNA adducts, XPD
How exposure was measured
Biological Questionnaire, in person
Biological Questionnaire, in person
Statistical Analysis
Ethnic groups with separate analysis
If this study provided a separate analysis by ethnic or racial group, the groups are listed here.
No
Confounders considered
Other breast cancer risk factors, such as family history, age at first birth, and hormone replacement therapy use, that were taken into account in the study.
Adequately controlled
Genetic characterization included
If the study analyzed relationships between environmental factors and inherited genetic variations, this field will be marked “Yes.” “No”, if not.
Yes
Description of major analysis
Chi-square, ANOVA, logistic regression.
Chi-square, ANOVA, logistic regression.
Strength of associations reported
Detectable vs. nondetectable PAH-DNA adducts OR=1.32; 95% CI 1.00-1.74
XPD Gln/Gln allele and PAH-DNA adduct level > median OR 1.61; 95% CI 0.99-2.63. Risk was not elevated for Gln/Gln allele and adducts < median. Increased risk for Gln/Gln was also seen for current smokers, but not never smokers.
Joint effect of Gln/Gln genotype and adducts > median OR 1.9; 95% CI 1.15-3.15 versus Lys/Lys genotype and adducts < median
Frequency of Glyn allele in controls was 36%
Detectable vs. nondetectable PAH-DNA adducts OR=1.32; 95% CI 1.00-1.74
XPD Gln/Gln allele and PAH-DNA adduct level > median OR 1.61; 95% CI 0.99-2.63. Risk was not elevated for Gln/Gln allele and adducts < median. Increased risk for Gln/Gln was also seen for current smokers, but not never smokers.
Joint effect of Gln/Gln genotype and adducts > median OR 1.9; 95% CI 1.15-3.15 versus Lys/Lys genotype and adducts < median
Frequency of Glyn allele in controls was 36%
Results Comments
Nucleotide excision repair is a pathway of DNA repair involved in removal of bulky DNA adducts, such as those formed by PAH. XPD is a gene involved in nucleotide excision repair. Gln allele is associated with suboptimal repair. Results provide evidence of increased risk associated with PAH in women with poor DNA repair.
Nucleotide excision repair is a pathway of DNA repair involved in removal of bulky DNA adducts, such as those formed by PAH. XPD is a gene involved in nucleotide excision repair. Gln allele is associated with suboptimal repair. Results provide evidence of increased risk associated with PAH in women with poor DNA repair.
Author address
Department of Epidemiology, Mailman School of Public Health, Columbia University, PH 18-102, 600 West 168th Street, New York, NY 10032, USA. mt146@columbia.edu
Department of Epidemiology, Mailman School of Public Health, Columbia University, PH 18-102, 600 West 168th Street, New York, NY 10032, USA. mt146@columbia.edu
Controls participation rate
Less than 70%
Less than 70%