Source:http://linkedlifedata.com/resource/pubmed/id/18268116
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2008-2-12
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| pubmed:abstractText |
Disturbances in DNA methylation are a characteristic of colorectal carcinogenesis. Folate-mediated one-carbon metabolism is essential for providing one-carbon groups for DNA methylation via DNA methyltransferases (DNMTs). Alcohol, a folate antagonist, could adversely affect one-carbon metabolism. In a case-control study of colorectal polyps, we evaluated three single nucleotide polymorphisms (-149C>T, -283T>C, -579G>T) in the promoter region of the DNMT3b gene, and a functional polymorphism in the coding region of the alcohol dehydrogenase ADH1C gene, ADH1C *2. Cases had a first diagnosis of colorectal adenomatous (n = 530) or hyperplastic (n = 202) polyps at the time of colonoscopy, whereas controls were polyp-free (n = 649). Multivariate logistic regression analysis was used to estimate odds ratios (OR) and corresponding 95% confidence intervals (CI). There were no significant main associations between the DNMT3b or ADH1C polymorphisms and polyp risk. However, DNMT3b -149TT was associated with an increase in adenoma risk among individuals with low folate and methionine intake (OR, 2.00; 95% CI, 1.06-3.78, P interaction = 0.10). The ADH1C *2/*2 genotype was associated with a possibly elevated risk for adenomatous polyps among individuals who consumed >26 g of alcohol/d (OR, 1.95; 95% CI, 0.60-6.30), whereas individuals who were wild-type for ADH1C were not at increased risk of adenoma (P interaction = 0.01). These gene-diet interactions suggest that polymorphisms relevant to DNA methylation or alcohol metabolism may play a role in colorectal carcinogenesis in conjunction with a high-risk diet.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
1055-9965
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
17
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
330-8
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| pubmed:dateRevised |
2010-5-21
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| pubmed:meshHeading |
pubmed-meshheading:18268116-Adenomatous Polyps,
pubmed-meshheading:18268116-Adult,
pubmed-meshheading:18268116-Aged,
pubmed-meshheading:18268116-Alcohol Dehydrogenase,
pubmed-meshheading:18268116-Colonic Polyps,
pubmed-meshheading:18268116-Colonoscopy,
pubmed-meshheading:18268116-DNA (Cytosine-5-)-Methyltransferase,
pubmed-meshheading:18268116-DNA Methylation,
pubmed-meshheading:18268116-Female,
pubmed-meshheading:18268116-Genetic Predisposition to Disease,
pubmed-meshheading:18268116-Genotype,
pubmed-meshheading:18268116-Haplotypes,
pubmed-meshheading:18268116-Humans,
pubmed-meshheading:18268116-Logistic Models,
pubmed-meshheading:18268116-Male,
pubmed-meshheading:18268116-Middle Aged,
pubmed-meshheading:18268116-Polymorphism, Single Nucleotide,
pubmed-meshheading:18268116-Promoter Regions, Genetic
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| pubmed:year |
2008
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| pubmed:articleTitle |
DNA methyltransferase and alcohol dehydrogenase: gene-nutrient interactions in relation to risk of colorectal polyps.
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| pubmed:affiliation |
Cancer Prevention Program, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, M4-B402, Seattle, WA 98109-1024, USA.
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| pubmed:publicationType |
Journal Article
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