Journal
CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
Volume 18, Issue 5, Pages 1461-1467Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1055-9965.EPI-08-0917
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Funding
- NCI NIH HHS [R01 CA072787-05, R01 CA72787, 2 T32 CA 09168, T32 CA009168, T32 CA009168-30] Funding Source: Medline
- NIEHS NIH HHS [P30ES07033, P30 ES007033, P30 ES007033-14] Funding Source: Medline
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Background: This study investigated whether single nucleotide polymorphisms (SNP) in genes within the catechol estrogen metabolism pathway altered the risk of breast cancer alone or in combination, as well as whether menopausal hormone therapy modified the effect of these SNPs on breast cancer risk. Methods: In a population-based case-control study of breast cancer, 891 cases and 878 controls were genotyped for six functional SNPs in the COMT, CYP1B1, GSTM1, GSTP1, and GSTT1 genes. Results: Women homozygous with the T allele in CYP1B1*2 (Ser(119); rs1056827) were at 1.69 (95% confidence interval, 1.17-2.46) times the risk of women homozygous with the G allele; women homozygous with the G allele in GSTP1 (Val(105); rs1695) were at 0.73 (95% confidence interval, 0.54-0.99) times the risk of breast cancer compared with women homozygous with the A allele. No other SNPs tested were associated with breast cancer to any appreciable degree. Potential gene-gene and gene-hormone therapy interactions were investigated. Conclusion: With the exception of GSTP1 and possibly CYP1B1*2, our findings do not provide support for the role of genetic variation in the catechol estrogen metabolism pathway and breast cancer risk in postmenopausal women. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1461-7)
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