Association between common genetic variation in Cockayne syndrome A and B genes and nucleotide excision repair capacity among smokers

Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology
Shuguang LengSteven A Belinsky

Abstract

Mutagen sensitivity in in vitro cultured lymphocytes challenged by benzo[a]pyrene diolepoxide (BPDE) has been validated as an intrinsic susceptibility factor for several cancers. Bulky BPDE-DNA adducts are repaired via either transcription-coupled repair or global genome nucleotide excision repair depending on the location of lesions. Cockayne syndrome A (CSA) and B (CSB) play essential roles in integrating the recognition of damage, chromatin remodeling, and the core nucleotide excision repair proteins. This study evaluated the hypothesis that common genetic variation in CSA and CSB is associated with mutagen sensitivity induced by BPDE in 276 cancer-free smokers. Tag single nucleotide polymorphisms (SNP; n = 37) selected across the entire coding and putative regulatory regions of CSA and CSB based on a high-density SNP database were genotyped by the Illumina Golden Gate assay. Major principal components of CSA and CSB that captured the linkage disequilibrium from multiple SNPs were globally associated with the number of breaks per cell at the threshold of 80% (P < or = 0.02 for both genes). Haplotype H125 in CSA and H97 in CSB as well as SNPs in high linkage disequilibrium with these two haplotypes were significantly associat...Continue Reading

References

Mar 15, 1989·International Journal of Cancer. Journal International Du Cancer·T C HsuC Furlong
Jan 30, 1995·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·D BootsmaJ Hoeijmakers
Apr 10, 1999·Genes & Development·W L de LaatJ H Hoeijmakers
Jan 11, 2000·Nucleic Acids Research·E WingenderS Urbach
Mar 20, 2001·American Journal of Human Genetics·M StephensP Donnelly
Oct 24, 2003·American Journal of Human Genetics·Matthew Stephens, Peter Donnelly
Nov 26, 2003·American Journal of Human Genetics·Cecilie Löe LichtVilhelm A Bohr
Mar 5, 2005·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Jian GuXifeng Wu
Jun 7, 2006·Genetic Epidemiology·Bingshu E ChenPhilip S Rosenberg
Jun 17, 2006·Cancer Research·Xifeng WuGary E Swan
Jul 18, 2006·Nucleic Acids Research·Lucía CondeJoaquín Dopazo
Dec 21, 2006·Cancer Research·Veronica Wendy SetiawanChristopher A Haiman
Apr 6, 2007·Genetic Epidemiology·W James GaudermanDavid V Conti
Apr 19, 2007·Biomarkers : Biochemical Indicators of Exposure, Response, and Susceptibility to Chemicals·J ChengY Zheng
Oct 13, 2007·Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology·Jie LinXifeng Wu

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Citations

Jan 15, 2011·Journal of Nucleic Acids·Bo Hang
Dec 14, 2016·British Journal of Cancer·Barbara PardiniGiuseppe Matullo
Feb 26, 2009·Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology·Juan ChengYuxin Zheng

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