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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-6-18
pubmed:abstractText
DNA damaged by exposure to exogenous and endogenous carcinogens could be removed effectively by the base excision repair pathway, in which the XRCC1, APE1, and ADPRT genes play a key role. Genetic variations in these important genes may alter repair function and contribute to cancer risk. We hypothesized that XRCC1, APE1, and ADPRT polymorphisms are associated with risk of bladder cancer. In a hospital-based case-control study of 234 patients with bladder cancer and 253 cancer-free controls, we genotyped the XRCC1-77T>C, Arg194Trp, Arg280His, Arg399Gln, APE1-656T>G, Asp148Glu, ADPRT-442G>A, and Val762Ala polymorphisms using polymerase chain reaction-restriction fragment length polymorphism method. We found an increased risk of bladder cancer associated with the XRCC1 194Trp/Trp and 280Arg/His genotypes (adjusted odds ratio = 3.90, 95% confidence interval = 1.69-8.98 for 194Trp/Trp and 2.53, 1.67-3.83 for 280Arg/His) compared with the 194Arg/Arg and 280Arg/Arg genotypes, respectively. In contrast, the APE1-656GG genotype was associated with a decreased risk of bladder cancer (0.57, 0.33-0.98) compared with the TT genotype. When we evaluated these eight polymorphisms together, we found that the combined genotypes with 9-13 variant (risk) alleles were associated with an increased risk of bladder cancer (2.25, 1.48-3.40) compared with those with 3-8 variants. These findings suggest that the XRCC1 and APE1 polymorphisms may contribute to susceptibility to bladder cancer. Larger studies are warranted to verify these findings.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1557-7430
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
303-11
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Genetic variants of XRCC1, APE1, and ADPRT genes and risk of bladder cancer.
pubmed:affiliation
Department of Molecular and Genetic Toxicology, Cancer Center of Nanjing Medical University, Nanjing, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't