title: Association of DNA double-strand break gene XRCC6 genotypes and lung cancer in Taiwan.
abstract: OBJECTIVE
  The DNA repair gene X-ray repair complementing defective repair in Chinese hamster cells 6 (XRCC6) is thought to play an important role in the repair of DNA double-strand breaks. It is known that defects in double-strand break repair capacity can lead to irreversible genomic instability. However, the association of polymorphic variants of XRCC6 with lung cancer susceptibility has never been reported. In this hospital-based case-control study, the association of XRCC6 promoter T-991C (rs5751129), promoter G-57C (rs2267437), promoter G-31A (rs132770), and intron 3 (rs132774) polymorphisms with lung cancer risk in a Taiwanese population, was studied.
  
  
  METHODS
  In total, 358 patients with lung cancer and 716 healthy controls recruited from the China Medical Hospital in Taiwan were genotyped.
  
  
  RESULTS
  The results showed that there were significant differences between lung cancer and control groups in the distribution of their genotypic (p=3.7×10(-4)) and allelic frequency (p=2.7×10(-5)) in the XRCC6 promoter T-991C polymorphism. Individuals who carried at least one C allele (TC or CC) had a 2.03-fold increased odds ratio of developing lung cancer compared to those who carried the wild-type TT genotype (95% conference internal=1.42-2.91, p=0.0001). For the other three polymorphisms, there was no difference between the case and control groups in the distribution of either genotypic or allelic frequency.
  
  
  CONCLUSIONS
  In conclusion, the XRCC6 promoter T-991C, but not the promoter C-57G, promoter G-31A or intron 3, is associated with lung cancer susceptibility.
authors.affiliation: Terry Fox Cancer Research Laboratory, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan, R.O.C.
authors.forename: Te-Chun
authors.initials: TC
authors.lastname: Hsia
authors.forename: Chin-Jung
authors.initials: CJ
authors.lastname: Liu
authors.forename: Chia-Chen
authors.initials: CC
authors.lastname: Chu
authors.forename: Liang-Wen
authors.initials: LW
authors.lastname: Hang
authors.forename: Wen-Shin
authors.initials: WS
authors.lastname: Chang
authors.forename: Chia-Wen
authors.initials: CW
authors.lastname: Tsai
authors.forename: Chao-I
authors.initials: CI
authors.lastname: Wu
authors.forename: Chi-Shun
authors.initials: CS
authors.lastname: Lien
authors.forename: Wen-Ling
authors.initials: WL
authors.lastname: Liao
authors.forename: Chien-Yi
authors.initials: CY
authors.lastname: Ho
authors.forename: Da-Tian
authors.initials: DT
authors.lastname: Bau
mesh_terms: D000368:Aged; D034961:Antigens, Nuclear / Q000235:genetics*; D001483:Base Sequence; D016022:Case-Control Studies; D004249:DNA Damage; D017931:DNA Primers; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D000072200:Ku Autoantigen; D008175:Lung Neoplasms / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011401:Promoter Regions, Genetic; D013624:Taiwan
chemical_list: D034961:Antigens, Nuclear; D017931:DNA Primers; D004268:DNA-Binding Proteins; C000606509:Xrcc6 protein, human; D000072200:Ku Autoantigen