NDLI: DNA double-strand break repair genotype and phenotype and breast cancer risk within sisters from the New York site of the Breast Cancer Family Registry (BCFR)

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DNA double-strand break repair genotype and phenotype and breast cancer risk within sisters from the New York site of the Breast Cancer Family Registry (BCFR)

Content Provider	Springer Nature Link
Author	Wu, Hui Chen Delgado Cruzata, Lissette Machella, Nicola Wang, Qiao Santella, Regina M. Terry, Mary Beth
Copyright Year	2013
Abstract	We previously observed that poor DNA repair phenotype is associated with increased breast cancer (BC) risk within families. Here, we examined whether genetic variation in double-strand break repair (DSBR) genes is associated with BC risk and if genotypes are related to phenotype in unaffected women. Using data from the New York site of the Breast Cancer Family Registry, we investigated 25 single-nucleotide polymorphism (SNPs) involved in DSBR using biospecimens from 337 BC cases and 410 unaffected sister controls.Genotypes in XRCC4 were associated with BC risk, with ORs of 1.67 (95 % CI 1.01–2.76) for the combined GA/AA of rs1805377 and 1.69 (95 % CI 1.03–2.77) for rs1056503 TG/GG; these associations were no longer statistically significant in multivariable conditional logistic regression models. When examining the association of SNPs with phenotype, we found that genotypes of XRCC5 rs3834 and rs1051685, which were highly correlated with each other, were associated with end-joining (EJ) capacity; women with the XRCC5 rs3834 GA genotype had better DNA repair as measured by higher levels of EJ capacity (37.8 ± 14.1 % for GA vs. 27.9 ± 11.8 % for GG carriers p = 0.0006). Women with the AA genotype of BRCA1 rs799917 also had higher EJ capacity (35.1 ± 9.2 %) than those with GG (26.4 ± 10.1 %, p = 0.02).Overall, we found that selected DSBR genotypes were associated with phenotype, although they were not associated with BC risk itself, suggesting that phenotypic measures are influenced by endogenous and exogenous factors across the life course and may be better markers than genotypic measures for ascertaining BC risk.
Starting Page	2157
Ending Page	2168
Page Count	12
File Format	PDF
ISSN	09575243
Journal	Cancer Causes & Control
Volume Number	24
Issue Number	12
e-ISSN	15737225
Language	English
Publisher	Springer Netherlands
Publisher Date	2013-09-24
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Breast cancer Double-strand break End-joining capacity Polymorphism Cancer Research Biomedicine general Oncology Public Health Epidemiology Hematology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Oncology

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