| pubmed-article:11597790 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0684249 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0080103 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0026027 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0017837 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C1882417 | lld:lifeskim |
| pubmed-article:11597790 | lifeskim:mentions | umls-concept:C0205195 | lld:lifeskim |
| pubmed-article:11597790 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:11597790 | pubmed:dateCreated | 2001-10-12 | lld:pubmed |
| pubmed-article:11597790 | pubmed:abstractText | Human microsomal epoxide hydrolase (mEH) catalyzes a key step in the biotransformation of benzo[a]pyrene that yields the highly mutagenic (+)-anti-7,8-diol-9,10 epoxide (BPDE). Two polymorphisms have been described in the coding region of the mEH gene (EPHX1) that produce two protein variants: 113Tyr-->113His (exon 3) and 139His-->139Arg (exon 4). We performed a case-control study among Northwestern Mediterranean Caucasians to investigate a possible association between these EPHX1 variants and lung cancer risk. Both EPHX1 polymorphisms were analyzed in a group of lung cancer patients (n=176) and in a control group of healthy smokers (n=187). The results showed a significantly decreased risk for the rare homozygous 113His/113His (adjusted odds ratio (OR): 0.44, 95% confidence interval (CI): 0.27-0.71) and 139Arg/139Arg (adjusted OR: 0.55, 95% CI: 0.33-0.91) compared with the major wild-types 113Tyr/113Tyr and 139His/139His, respectively, as the references. Thereafter, we analyzed the EPHX1 variants in combination with three glutathione S-transferase polymorphic genes (GSTM1, GSTT1, and GSTP1) and we found a significant overepresentation of cancer patients with a combination of exon 3 113Tyr/113Tyr EPHX1 and exon 5 105Ile/105Ile GSTP1 (adjusted OR: 2.34, 95% CI: 1.21-4.52). The polymorphic site within the exon 5 of GSTP1 results in a Ile-->Val substitution, and the isoleucine GSTpi isoform has been found in vitro to be less active than the valine isoform towards the conjugation of BPDE. The 113 Tyr/Tyr EPHX1 encodes for a high-activity mEH. Our results agree with these observations in vitro and suggest that a genetically determined combination of a high-activity mEH and a low-activity GSTpi may increase lung cancer risk among smokers. | lld:pubmed |
| pubmed-article:11597790 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11597790 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11597790 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11597790 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11597790 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11597790 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11597790 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11597790 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:11597790 | pubmed:issn | 0304-3835 | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:GeriAA | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:CorbellaJJ | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:To-FiguerasJJ | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:Gómez-Catalán... | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:PiquéEE | lld:pubmed |
| pubmed-article:11597790 | pubmed:author | pubmed-author:BorregoNN | lld:pubmed |
| pubmed-article:11597790 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11597790 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:11597790 | pubmed:volume | 173 | lld:pubmed |
| pubmed-article:11597790 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11597790 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11597790 | pubmed:pagination | 155-62 | lld:pubmed |
| pubmed-article:11597790 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11597790 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11597790 | pubmed:articleTitle | Lung cancer susceptibility in relation to combined polymorphisms of microsomal epoxide hydrolase and glutathione S-transferase P1. | lld:pubmed |
| pubmed-article:11597790 | pubmed:affiliation | Toxicology Unit, Hospital Clínic, IDIBAPS, Departament de Salut Pública, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain. jtofigue@medicina.ub.es | lld:pubmed |
| pubmed-article:11597790 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11597790 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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