| pubmed-article:16652158 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0007131 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C1366475 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C1333237 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:16652158 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:16652158 | pubmed:issue | 25 | lld:pubmed |
| pubmed-article:16652158 | pubmed:dateCreated | 2006-6-15 | lld:pubmed |
| pubmed-article:16652158 | pubmed:abstractText | X-ray repair cross-complementing 1 (XRCC1) plays a key role in DNA base excision repair and cells lacking its activity are hypersensitive to DNA damage. Recently, we reported a SNP (rs3213245, -77T>C) in the XRCC1 gene 5' untranslated region (UTR) was significantly associated with the risk of developing esophageal squamous-cell carcinoma. Computer analysis predicted that this SNP was in the core of Sp1-binding motif, which suggested its functional significance. Gel shift and super shift assays confirmed that -77T>C polymorphic site in the XRCC1 promoter was within the Sp1-binding motif and the T>C substitution greatly enhanced the binding affinity of Sp1 to this region. Luciferase assays indicated that the Sp1-high-affinity C-allelic XRCC1 promoter was associated with a reduced transcriptional activity. The association between -77T>C and three other amino-acid substitution-causing polymorphisms in XRCC1 and risk of lung cancer was examined in 1024 patients and 1118 controls and the results showed that only the -77T>C polymorphism was significantly associated with an increased risk of developing lung cancer. Multivariate logistic regression analysis found that an increased risk of lung cancer was associated with the variant XRCC1 -77 genotypes (TC and CC) compared with the TT genotype (OR=1.46, 95% CI=1.18-1.82; P=0.001) and the increased risk was more pronounced in smokers (OR=1.63, 95% CI=1.20-2.21) than in non-smokers (OR=1.28, 95% CI=0.94-1.76). Taken together, these results showed that the functional SNP -77T>C in XRCC1 5'UTR was associated with cancer development owing to the decreased transcriptional activity of C-allele-containing promoter with higher affinity to Sp1 binding. | lld:pubmed |
| pubmed-article:16652158 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16652158 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16652158 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:16652158 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16652158 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16652158 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16652158 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16652158 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:LinDD | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:LUMM | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:HaoBB | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:WangHH | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:SunTT | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:FOXJ JJJ | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:ChewAA | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:TaoTT | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:ZhaiSS | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:ZhangXX | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:ZhangLL | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:ZhouYY | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:MibeMM | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:WeiQQ | lld:pubmed |
| pubmed-article:16652158 | pubmed:author | pubmed-author:LiangGG | lld:pubmed |
| pubmed-article:16652158 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16652158 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16652158 | pubmed:volume | 25 | lld:pubmed |
| pubmed-article:16652158 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16652158 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16652158 | pubmed:pagination | 3613-20 | lld:pubmed |
| pubmed-article:16652158 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:meshHeading | pubmed-meshheading:16652158... | lld:pubmed |
| pubmed-article:16652158 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16652158 | pubmed:articleTitle | A novel T-77C polymorphism in DNA repair gene XRCC1 contributes to diminished promoter activity and increased risk of non-small cell lung cancer. | lld:pubmed |
| pubmed-article:16652158 | pubmed:affiliation | Department of Biology Sciences and Biotechnology, Tsinghua University, Beijing, China. | lld:pubmed |
| pubmed-article:16652158 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16652158 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:7515 | entrezgene:pubmed | pubmed-article:16652158 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:16652158 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16652158 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16652158 | lld:pubmed |
