Source:http://linkedlifedata.com/resource/pubmed/id/16195240
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2006-2-27
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| pubmed:abstractText |
Common polymorphisms in genes encoding phase I and phase II enzymes are considered to modify lung cancer risk due to changes in enzyme activity. Candidates include genetic variants of glutathione S-transferases (GSTM1, GSTT1 and GSTP1) and myeloperoxidase (MPO). We performed a large case-control study of these candidate genes in 1103 patients with non-small cell lung cancer (NSCLC) and 627 controls without NSCLC. Associations between deletion genotypes of GSTM1 and GSTT1 and between single nucleotide polymorphisms (SNPs) of GSTP1 Ile105Val and MPO G-463A were first tested by adjusted logistic regression. Then we analysed gene-gene interactions, also incorporating our published data on the Ile462Val SNP in the phase I enzyme, cytochrome P450 CYP1A1. The homozygous GSTP1 105Val genotype was significantly under-represented in NSCLC compared with controls (OR = 0.73; 95%CI 0.53-1.00; P = 0.050), especially in females (OR = 0.57; 95%CI 0.34-0.98; P = 0.04). The GSTT1-null genotype was significantly over-represented in adenocarcinomas (OR = 1.41; 95%CI 1.06-1.90; P = 0.02) but not in squamous cell carcinomas (OR = 1.03; 95%CI 0.76-1.41; P = 0.84). There was weak risk reduction associated with GSTM1 null in heavy smokers (OR = 0.71; 95%CI 0.54-0.94; P = 0.02), but neither GSTM1 nor MPO genotypes affected the overall risk of NSCLC. The MPO and CYP1A1 risk genotypes interacted to increase the overall risk of NSCLC (OR = 2.88; 95%CI 1.70-5.00; P < 0.001). The data are consistent with the concept that multiple genes of modest effect interact to confer genomic-based susceptibility to lung cancer.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytochrome P-450 CYP1A1,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Transferase,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/glutathione S-transferase M1,
http://linkedlifedata.com/resource/pubmed/chemical/glutathione S-transferase T1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0143-3334
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
27
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
525-32
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16195240-Adenocarcinoma,
pubmed-meshheading:16195240-Aged,
pubmed-meshheading:16195240-Carcinoma, Non-Small-Cell Lung,
pubmed-meshheading:16195240-Carcinoma, Squamous Cell,
pubmed-meshheading:16195240-Case-Control Studies,
pubmed-meshheading:16195240-Cytochrome P-450 CYP1A1,
pubmed-meshheading:16195240-Female,
pubmed-meshheading:16195240-Genetic Predisposition to Disease,
pubmed-meshheading:16195240-Genotype,
pubmed-meshheading:16195240-Glutathione Transferase,
pubmed-meshheading:16195240-Humans,
pubmed-meshheading:16195240-Lung Neoplasms,
pubmed-meshheading:16195240-Male,
pubmed-meshheading:16195240-Middle Aged,
pubmed-meshheading:16195240-Odds Ratio,
pubmed-meshheading:16195240-Peroxidase,
pubmed-meshheading:16195240-Polymorphism, Single Nucleotide,
pubmed-meshheading:16195240-Smoking
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| pubmed:year |
2006
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| pubmed:articleTitle |
CYP1A1 Ile462Val and MPO G-463A interact to increase risk of adenocarcinoma but not squamous cell carcinoma of the lung.
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| pubmed:affiliation |
Department of Thoracic Medicine, The Prince Charles Hospital, Brisbane, Australia.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|