title: Base excision repair genes XRCC1 and APEX1 and the risk for prostate cancer.
abstract: Prostate cancer is the second cause of cancer death in Brazilian men. One of the relevant phenomena to the inherited susceptibility is the presence of allelic variants in genes involved with the DNA repair pathway. The aim of this study was to analyze the frequencies of prevalent, heterozygous and rare genotypes of the base excision repair genes APEX1 and XRCC1 in a case-control study and relate the genotypes with tumoral aggressiveness. DNA from peripheral blood of 172 patients and 172 controls were analyzed by RFLP-PCR method. The polymorphisms were also evaluated in relation to clinical and pathological parameters. The OR (Odds Ratio) and confidence interval (CI = 95%) were used in the association study and the Chi-square and ANOVA tests for the evaluation of histopathological parameters. The rare genotypes frequencies of the gene APEX1 increased the risk for the development of prostate cancer (OR = 1.68 95% CI 1.10-2.58). No association was found for the gene XRCC1 (OR = 0.82 95% CI 0.53-1.27). The combined analysis for both genes did not show association with this neoplasia (OR = 1.27 95% CI 0.79-20.5). The relationship of XRCC1 and APEX1 genotypes with cancer aggressiveness through the correlation with histopathological parameters, did not find any association. Our results suggest that the polymorphism in the gene APEX1 may be indicated as a potential marker for prostate cancer risk.
authors.affiliation: Department of General Biology, Biological Science Center, Londrina State University, Londrina, PR, Brazil. khellenk@yahoo.com.br
authors.forename: H
authors.initials: H
authors.lastname: Kuasne
authors.forename: I S
authors.initials: IS
authors.lastname: Rodrigues
authors.forename: R
authors.initials: R
authors.lastname: Losi-Guembarovski
authors.forename: M B
authors.initials: MB
authors.lastname: Reis
authors.forename: P E
authors.initials: PE
authors.lastname: Fuganti
authors.forename: E P
authors.initials: EP
authors.lastname: Gregório
authors.forename: F
authors.initials: F
authors.lastname: Libos Junior
authors.forename: H M
authors.initials: HM
authors.lastname: Matsuda
authors.forename: M A F
authors.initials: MA
authors.lastname: Rodrigues
authors.forename: M O
authors.initials: MO
authors.lastname: Kishima
authors.forename: I M S
authors.initials: IM
authors.lastname: Cólus
mesh_terms: D016022:Case-Control Studies; D004260:DNA Repair / Q000235:genetics*; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics*; D005787:Gene Frequency / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D009367:Neoplasm Staging; D017430:Prostate-Specific Antigen / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology; D012307:Risk Factors; 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; D017430:Prostate-Specific Antigen; C085108:APEX1 protein, human; D043603:DNA-(Apurinic or Apyrimidinic Site) Lyase