***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: We propose a hypothesis that differences in base excision repair capacity modulate the effect of dietary antioxidant intake  on  prostate cancer risk .  As a preliminary test of this hypothesis , we conducted a pilot case-control study to evaluate  prostate cancer risk in men with polymorphisms in the XRCC1 gene , a key player in base excision repair , across different strata of antioxidant intake .  Seventy-seven prostate cancer patients and 183 community controls , for whom we have detailed dietary information , were frequency matched on age and race . We found a somewhat lower prostate cancer risk for men with one or two copies of the variant alleles at the XRCC1 codons 194 and 399 than for those who were homozygous for the common allele [ codon 194 : odds ratio ( OR ) = 0.8 ; 95 % confidence interval ( CI ) , 0.4 - 1.8 and codon 399 : OR = 0.8 ; 95 % CI , 0.5 - 1.3 ] . The variant at codon 280 was associated with a slightly increased prostate cancer risk ( OR = 1.5 ; 95 % CI , 0.7 - 3.6 ) . Only the codon 399 polymorphism occurred frequently enough to investigate its joint effect with  antioxidant  intake . Prostate cancer risk was highest among men who were homozygous for the common allele at codon 399 and had low dietary intake of vitamin E ( OR = 2.4 ; 95 % CI , 1.0 - 5.6 ) or lycopene ( OR = 2.0 ; 95 % CI , 0.8 - 4.9 ) , whereas low intake of these antioxidants in men without this genotype hardly increased prostate cancer risk . The polymorphism did not modulate risk associated with low intake of vitamin C , A , or beta-carotene . The data give some support for our hypothesis but should be regarded as preliminary , because it is limited by small sample size . We discuss what kind of data and what kind of studies are needed for future evaluation of this hypothesis As part of a population -based case-control study in Shanghai , China , we investigated whether variants in several DNA repair genes , either alone or in conjunction with other risk factors , are associated with prostate cancer risk .  Genomic DNA from 162 patients newly diagnosed with prostate cancer and 251 healthy men r and omly selected from the population were typed for five nonsynonymous DNA repair markers . We found that the XRCC1-Arg399Gln AA and the MGMT-Leu84Phe CT+TT genotypes were associated with an increased risk of prostate cancer [ odds ratio ( OR ) , 2.18 ; 95 % confidence interval ( CI ) , 0.99 - 4.81 and OR , 1.99 ; 95 % CI , 1.19 - 3.34 , respectively ] . In contrast , XRCC3-Thr241Met , XPD-Lys751Gln , and MGMT-Ile143Val markers showed no significant associations with risk , although due to the much lower frequency of their variant alleles in this population we can not rule out small to modest effects . There was a significant interaction between the MGMT-84 marker and insulin resistance ( Pinteraction = 0.046 ) . Relative to men with the MGMT-84 CC genotype and a low insulin resistance ( < 0.097 ) , those having the CT-TT genotype and a greater insulin resistance had a 5.4-fold risk ( OR , 5.39 ; 95 % CI , 2.46 - 11.82 ) . In addition , for the XRCC3 - 241 marker , relative to men with the CC genotype and a low intake of preserved foods ( < 12.7 g/d ) , those harboring the CT+TT genotype and having a higher intake of preserved foods ( > 12.7 g/d ) , which contain nitrosamines and nitrosamine precursors , had a significantly increased risk of prostate cancer risk ( OR , 2.62 ; 95 % CI , 1.13 - 6.06 ) . In contrast , men with the CT+TT genotype and a low intake of preserved foods had a 69 % reduction in risk ( OR , 0.31 ; 95 % CI , 0.10 - 0.96 ; Pinteraction = 0.005 ) . These results suggest that genetic variants in the DNA repair pathways may be involved in prostate cancer etiology and that other risk factors , including preserved foods and insulin resistance , may modulate prostate cancer risk in combination with genetic susceptibility in these repair pathways . Replication in larger studies is necessary to preclude chance findings , particularly those among subgroups , and clarify the mechanisms involved DNA repair gene alterations have been shown to cause a reduction in DNA repair capacity and may influence an individual 's susceptibility to carcinogenesis . Single nucleotide polymorphisms ( SNPs ) of DNA repair genes have been shown to cause a reduction in repair activity . We hypothesized that SNPs of DNA repair genes may be a risk factor for renal cell carcinoma ( RCC ) . To test this hypothesis , DNA sample s from 112 cases of renal cell cancer and healthy controls ( n=180 ) were analyzed by PCR-RFLP to determine the genotypic frequency of six different polymorphic loci on five DNA repair genes ( XRCC1 , XPC , ERCC1 , XRCC3 , and XRCC7 ) . The chi(2 ) test was applied to compare the genotype frequency between patients and controls . We found that the frequency of 399Gln variant at XRCC1 Arg399Gln was significantly higher in RCC cases than in controls ( OR=2.83 , 95%CI=1.24 - 6.49 , P=0.01 ) . The frequency of T-A haplotype of XRCC1 194 Trp and XRCC1 399Gln was significantly higher in RCC than controls . No differences in genotypes were observed at the other sites . This is the first report on SNPs of DNA repair genes in renal cell carcinoma that suggests XRCC1 399Gln polymorphism may be a risk factor for RCC . Our present data suggest that the XRCC1 399Gln allele may be linked to susceptibility for RCC Environmental carcinogens contained in air pollution , such as polycyclic aromatic hydrocarbons , aromatic amines or N-nitroso compounds , predominantly form DNA adducts but can also generate interstr and cross-links and reactive oxygen species . If unrepaired , such lesions increase the risk of somatic mutations and cancer . Our study investigated the relationships between 22 polymorphisms ( and their haplotypes ) in 16 DNA repair genes belonging to different repair pathways in 1094 controls and 567 cancer cases ( bladder cancer , 131 ; lung cancer , 134 ; oral-pharyngeal cancer , 41 ; laryngeal cancer , 47 ; leukaemia , 179 ; death from emphysema and chronic obstructive pulmonary disease , 84 ) . The design was a case-control study nested within a prospect i ve investigation . Among the many comparisons , few polymorphisms were associated with the diseases at the univariate analysis : XRCC1 - 399 Gln/Gln variant homozygotes [ odds ratios ( OR ) = 2.20 , 95 % confidence intervals ( CI ) = 1.16 - 4.17 ] and XRCC3 - 241 Met/Met homozygotes ( OR = 0.51 , 95 % CI = 0.27 - 0.96 ) and leukaemia . The recessive model in the stepwise multivariate analysis revealed a possible protective effect of XRCC1 - 399Gln/Gln in lung cancer ( OR = 0.22 , 95 % CI = 0.05 - 0.98 ) , and confirmed an opposite effect ( OR = 2.47 , 95 % CI = 1.02 - 6.02 ) in the leukaemia group . Our results also suggest that the XPD/ERCC1-GAT haplotype may modulate leukaemia ( OR = 1.28 , 95 % CI = 1.02 - 1.61 ) , bladder cancer ( OR = 1.38 , 95 % CI = 1.06 - 1.79 ) and possibly other cancer risks . Further investigations of the combined effects of polymorphisms within these DNA repair genes , smoking and other risk factors may help to clarify the influence of genetic variation in the carcinogenic process 
    Output:
    
We identified that XRCC1-rs25489 polymorphism was associated with an increased risk of urological neoplasms in heterozygote and dominant models .
Moreover , in the subgroup analysis by cancer type , we found that XRCC1-rs25489 polymorphism was associated with an increased risk of bladder cancer ( BC ) in heterozygote model .
Although overall analyses suggested a null result for XRCC1-rs25487 polymorphism , in the stratified analysis by ethnicity , an increased risk of urological neoplasms for Asians in allelic and homozygote models was identified .
While for other polymorphisms in XRCC genes , no significant association was uncovered .
To sum up , our results indicated that XRCC1-rs25489 polymorphism is a risk factor for urological neoplasms , particularly for BC .