Document Detail

Dietary folate intake in combination with MTHFR C677T genotype and promoter methylation of tumor suppressor and DNA repair genes in sporadic colorectal adenomas.
MedLine Citation:
PMID:  17301267     Owner:  NLM     Status:  MEDLINE    
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.
Maureen van den Donk; Manon van Engeland; Linette Pellis; Ben J M Witteman; Frans J Kok; Jaap Keijer; Ellen Kampman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology     Volume:  16     ISSN:  1055-9965     ISO Abbreviation:  Cancer Epidemiol. Biomarkers Prev.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-02-15     Completed Date:  2007-04-03     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9200608     Medline TA:  Cancer Epidemiol Biomarkers Prev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  327-33     Citation Subset:  IM    
Division of Human Nutrition, Wageningen University, P.O. Box 8129, NL-6700 EV Wageningen, the Netherlands.
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MeSH Terms
Adenoma / epidemiology,  genetics*
Case-Control Studies
Colorectal Neoplasms / epidemiology,  genetics*
DNA Methylation*
DNA Repair / genetics
Folic Acid / administration & dosage*
Genes, Tumor Suppressor
Genetic Predisposition to Disease
Logistic Models
Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
Middle Aged
Netherlands / epidemiology
Polymerase Chain Reaction
Promoter Regions, Genetic
Reg. No./Substance:
59-30-3/Folic Acid; EC Reductase (NADPH2)

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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