pubmed-article:17425776 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17425776 | lifeskim:mentions | umls-concept:C0005684 | lld:lifeskim |
pubmed-article:17425776 | lifeskim:mentions | umls-concept:C0596244 | lld:lifeskim |
pubmed-article:17425776 | lifeskim:mentions | umls-concept:C1366475 | lld:lifeskim |
pubmed-article:17425776 | lifeskim:mentions | umls-concept:C1333237 | lld:lifeskim |
pubmed-article:17425776 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
pubmed-article:17425776 | pubmed:dateCreated | 2007-5-7 | lld:pubmed |
pubmed-article:17425776 | pubmed:abstractText | Cigarette smoking and chemical occupational exposure are the main known risk factors for bladder transitional cell carcinoma (TCC). Oxidative DNA damage induced by carcinogens present in these exposures requires accurate base excision repair (BER). The XRCC1 protein plays a crucial role in BER by acting as a scaffold for other BER enzymes. Variants in the XRCC1 gene might alter protein structure or function or create alternatively spliced proteins which may influence BER efficiency and hence affect individual susceptibility to bladder cancer. Recent epidemiological studies have shown inconsistent associations between these polymorphisms and bladder cancer. To clarify the situation, we conducted a comprehensive analysis of 14 XRCC1 polymorphisms in a case-control study involving more than 1100 subjects. | lld:pubmed |
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pubmed-article:17425776 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17425776 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17425776 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17425776 | pubmed:issn | 1471-2156 | lld:pubmed |
pubmed-article:17425776 | pubmed:author | pubmed-author:BarrettJennif... | lld:pubmed |
pubmed-article:17425776 | pubmed:author | pubmed-author:BishopD... | lld:pubmed |
pubmed-article:17425776 | pubmed:author | pubmed-author:KiltieAnne... | lld:pubmed |
pubmed-article:17425776 | pubmed:author | pubmed-author:PaulAlan BAB | lld:pubmed |
pubmed-article:17425776 | pubmed:author | pubmed-author:SakSei... | lld:pubmed |
pubmed-article:17425776 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17425776 | pubmed:volume | 8 | lld:pubmed |
pubmed-article:17425776 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17425776 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17425776 | pubmed:pagination | 13 | lld:pubmed |
pubmed-article:17425776 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17425776 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17425776 | pubmed:articleTitle | DNA repair gene XRCC1 polymorphisms and bladder cancer risk. | lld:pubmed |
pubmed-article:17425776 | pubmed:affiliation | Molecular Radiobiology Group, Section of Oncology, Leeds Institute of Molecular Medicine, St James's University Hospital, Leeds, UK. seichungsak@yahoo.com <seichungsak@yahoo.com> | lld:pubmed |
pubmed-article:17425776 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17425776 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:17425776 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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