Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-2-15
pubmed:abstractText
Methylation of the promoter region of tumor suppressor genes is increasingly recognized to play a role in cancer development through silencing of gene transcription. We examined the associations between dietary folate intake, MTHFR C677T genotype, and promoter methylation of six tumor suppressor and DNA repair genes. Patients with colorectal adenoma (n = 149) and controls (n = 286) with folate intake in the upper or lower tertile with the CC or TT genotype were selected from a case-control study. Methylation-specific PCRs were conducted on colorectal adenoma specimens. The percentages of promoter methylation ranged from 15.7% to 64.2%. In case-case comparisons, folate was inversely associated with promoter methylation, especially among TT homozygotes. Case-control comparisons suggested that folate was not associated with the occurrence of adenomas with promoter methylation, and increased the risk of unmethylated adenomas, especially in TT homozygotes. The interactions between folate and MTHFR genotype were most pronounced for O(6)-MGMT: compared with CC homozygotes with low folate intake, the adjusted odds ratios (95% confidence interval) of having a methylated O(6)-MGMT promoter were 3.39 (0.82-13.93) for TT homozygotes with low folate intake and 0.37 (0.11-1.29) for TT homozygotes with high folate intake (P interaction = 0.02); the odds ratios for the occurrence of adenomas without methylation were 0.57 (0.16-2.11) for TT homozygotes with low folate intake and 3.37 (1.17-9.68) for TT homozygotes with high folate intake (P interaction = 0.03). In conclusion, folate intake seems to be inversely associated with promoter methylation in colorectal adenomas in case-case comparisons, and was positively associated with the occurrence of adenomas without promoter methylation in case-control comparisons, especially for TT homozygotes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1055-9965
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
327-33
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17301267-Adenoma, pubmed-meshheading:17301267-Adolescent, pubmed-meshheading:17301267-Adult, pubmed-meshheading:17301267-Aged, pubmed-meshheading:17301267-Case-Control Studies, pubmed-meshheading:17301267-Colorectal Neoplasms, pubmed-meshheading:17301267-DNA Methylation, pubmed-meshheading:17301267-DNA Repair, pubmed-meshheading:17301267-Female, pubmed-meshheading:17301267-Folic Acid, pubmed-meshheading:17301267-Genes, Tumor Suppressor, pubmed-meshheading:17301267-Genetic Predisposition to Disease, pubmed-meshheading:17301267-Genotype, pubmed-meshheading:17301267-Humans, pubmed-meshheading:17301267-Logistic Models, pubmed-meshheading:17301267-Male, pubmed-meshheading:17301267-Methylenetetrahydrofolate Reductase (NADPH2), pubmed-meshheading:17301267-Middle Aged, pubmed-meshheading:17301267-Netherlands, pubmed-meshheading:17301267-Polymerase Chain Reaction, pubmed-meshheading:17301267-Promoter Regions, Genetic, pubmed-meshheading:17301267-Questionnaires
pubmed:year
2007
pubmed:articleTitle
Dietary folate intake in combination with MTHFR C677T genotype and promoter methylation of tumor suppressor and DNA repair genes in sporadic colorectal adenomas.
pubmed:affiliation
Division of Human Nutrition, Wageningen University, P.O. Box 8129, NL-6700 EV Wageningen, the Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't