Abstract
We assessed the association between genetic variants of XPG, XPA, XPD, CSB, XPC and CCNH in the nucleotide excision repair (NER) pathway and risk of prostate cancer. We genotyped the XPG, XPA, XPD, CSB, XPC and CCNH polymorphisms by a 384-well plate format on the MassARRAY® platform. Multivariate logistical regression analysis was used to assess the associations between the six gene polymorphisms and risk of prostate cancer. Individuals carrying the XPG rs229614 TT (OR=2.01, 95%CI=1.35-3.27) genotype and T allele (OR=1.73, 95%CI=1.37-2.57) were moderately significantly associated with a higher risk of prostate cancer. Subjects with XPD rs13181 G allele had a marginally increased risk of prostate cancer, with adjusted OR(95%CI) of 1.53 (1.04-2.37). Moreover, individuals carrying with CSB rs2228526 GG genotype (OR=2.05, 95% CI=1.23-3.52) and G allele (OR=1.56, 95%CI=1.17-2.05) were associated with a higher increased risk of prostate cancer. The combination genotype of XPG rs2296147 T and CSB rs2228526 G allele had accumulative effect on the risk of this cancer, with an OR (95% CI) of 2.23(1.37-3.59). Our study indicates that XPG rs2296147 and CSB rs2228526 polymorphisms are significantly associated with increased risk of prostate cancer, and that combination of XPG rs2296147 T allele and CSB rs2228526 G allele is strongly associated with an increased risk.
Highlights
Prostate cancer is the second most commonly diagnosed solid tumor in males, accounting for 10% of male cancer related death (Globocan, 2008)
Our study indicates that XPG rs2296147 and CSB rs2228526 polymorphisms are significantly associated with increased risk of prostate cancer, and that combination of XPG rs2296147 T allele and CSB rs2228526 G allele is strongly associated with an increased risk
A total of 241 prostate cancer patients and 264 controls gene polymorphisms are associated with prostate cancer were recruited in our study
Summary
Prostate cancer is the second most commonly diagnosed solid tumor in males, accounting for 10% of male cancer related death (Globocan, 2008). Genomic stability and integrity are important in maintaining accurate DNA replication. DNA disruptions could induce gene rearrangements, translocations, amplifications and deletions, which could play an important role in the carcinogenesis. DNA repair system plays a vital role in maintaining the stability of cellular functions and genomic integrity through the reversal of the damaged DNA induced by various endogenous and/or exogenous factors. There are four well known DNA repair pathways which are responsible for repairing various of DNA damage, including base excision repair (BER), nucleotide excision repair (NER), double-strand break repair (SSBR) and homologous recombination repair (HRR). Nucleotide excision repair (NER) pathway is an important mechanism that maintains genomic integrity by removing DNA bulky lesions or interstrand adducts induced by exogenous and/ or endogenous factors (Neumann et al, 2005; Wu et al., 2005). The variation of DNA repair genes in the NER pathway may affect the capacity of encoded DNA repair enzymes, and subsequently enhance the risk of cancer (Goode et al, 2002; Hu et al, 2002; Hu et al, 2004)
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