title: XRCC1, but not APE1 and hOGG1 gene polymorphisms is a risk factor for pterygium.
abstract: OBJECTIVE
  Epidemiological evidence suggests that UV irradiation plays an important role in pterygium pathogenesis. UV irradiation can produce a wide range of DNA damage. The base excision repair (BER) pathway is considered the most important pathway involved in the repair of radiation-induced DNA damage. Based on previous studies, single-nucleotide polymorphisms (SNPs) in 8-oxoguanine glycosylase-1 (OGG1), X-ray repair cross-complementing-1 (XRCC1), and AP-endonuclease-1 (APE1) genes in the BER pathway have been found to affect the individual sensitivity to radiation exposure and induction of DNA damage. Therefore, we hypothesize that the genetic polymorphisms of these repair genes increase the risk of pterygium.
  
  
  METHODS
  XRCC1, APE1, and hOGG1 polymorphisms were studied using fluorescence-labeled Taq Man probes on 83 pterygial specimens and 206 normal controls.
  
  
  RESULTS
  There was a significant difference between the case and control groups in the XRCC1 genotype (p=0.038) but not in hOGG1 (p=0.383) and APE1 (p=0.898). The odds ratio of the XRCC1 A/G polymorphism was 2.592 (95% CI=1.225-5.484, p=0.013) and the G/G polymorphism was 1.212 (95% CI=0.914-1.607), compared to the A/A wild-type genotype. Moreover, individuals who carried at least one C-allele (A/G and G/G) had a 1.710 fold increased risk of developing pterygium compared to those who carried the A/A wild type genotype (OR=1.710; 95% CI: 1.015-2.882, p=0.044). The hOGG1 and APE1 polymorphisms did not have an increased odds ratio compared with the wild type.
  
  
  CONCLUSIONS
  XRCC1 (Arg399 Glu) is correlated with pterygium and might become a potential marker for the prediction of pterygium susceptibility.
authors.affiliation: Department of Pharmacy, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan.
authors.forename: Pei-Liang
authors.initials: PL
authors.lastname: Chen
authors.forename: Kun-Tu
authors.initials: KT
authors.lastname: Yeh
authors.forename: Yi-Yu
authors.initials: YY
authors.lastname: Tsai
authors.forename: Hank
authors.initials: H
authors.lastname: Koeh
authors.forename: Yu-Ling
authors.initials: YL
authors.lastname: Liu
authors.forename: Huei
authors.initials: H
authors.lastname: Lee
authors.forename: Ya-Wen
authors.initials: YW
authors.lastname: Cheng
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D001120:Arginine; D045647:DNA Glycosylases / Q000235:genetics*; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D018698:Glutamic Acid; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D011110:Polymorphism, Genetic; D011625:Pterygium / Q000235:genetics*; D000076105:X-ray Repair Cross Complementing Protein 1
chemical_list: D004268:DNA-Binding Proteins; D000076105:X-ray Repair Cross Complementing Protein 1; C000619371:XRCC1 protein, human; D018698:Glutamic Acid; D001120:Arginine; D045647:DNA Glycosylases; C479058:oxoguanine glycosylase 1, human; C085108:APEX1 protein, human; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase