Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2008-9-3
pubmed:abstractText
Intake of dietary factors that serve as methyl group donors may influence promoter hypermethylation in colorectal carcinogenesis. We investigated whether dietary folate, vitamin B2 and vitamin B6, methionine and alcohol were associated with mutL homologue 1 (MLH1) hypermethylation and the related molecular phenotypes of MLH1 protein expression, microsatellite instability (MSI) and BRAF mutations in patients with colorectal carcinomas. Within the Netherlands Cohort Study on diet and cancer (n = 120 852), 648 cases (367 men and 281 women) and 4059 subcohort members were available for data analyses from a follow-up period between 2.3 and 7.3 years after baseline. Gender-specific adjusted incidence rate ratios (RRs) were calculated over categories of dietary intake in case-cohort analyses. The intakes of folate, vitamin B2, methionine and alcohol were not associated with risk of tumors showing MLH1 hypermethylation, those lacking MLH1 protein expression or with MSI. Among men, we observed strong positive associations between folate and BRAF-mutated tumors (RR = 3.04 for the highest versus lowest tertile of intake, P(trend) = 0.03) and between vitamin B6 and tumors showing MLH1 hypermethylation (highest versus lowest tertile: RR = 3.23, P(trend) = 0.03). Among women, the relative risks of tumors with BRAF mutations or MLH1 hypermethylation were also increased in the highest tertiles of folate and vitamin B6 intake, respectively, but these did not reach statistical significance. The positive associations between folate intake and tumors harboring BRAF mutations and between vitamin B6 intake and those showing MLH1 hypermethylation were most pronounced among men and may suggest that these vitamins enhance colorectal cancer risk through genetic as well as epigenetic aberrations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1460-2180
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1765-73
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18339680-Adaptor Proteins, Signal Transducing, pubmed-meshheading:18339680-Aged, pubmed-meshheading:18339680-Cohort Studies, pubmed-meshheading:18339680-Colorectal Neoplasms, pubmed-meshheading:18339680-DNA, Neoplasm, pubmed-meshheading:18339680-DNA Methylation, pubmed-meshheading:18339680-Diet, pubmed-meshheading:18339680-Female, pubmed-meshheading:18339680-Folic Acid, pubmed-meshheading:18339680-Humans, pubmed-meshheading:18339680-Male, pubmed-meshheading:18339680-Methionine, pubmed-meshheading:18339680-Microsatellite Repeats, pubmed-meshheading:18339680-Middle Aged, pubmed-meshheading:18339680-Mutation, pubmed-meshheading:18339680-Netherlands, pubmed-meshheading:18339680-Nuclear Proteins, pubmed-meshheading:18339680-Phenotype, pubmed-meshheading:18339680-Promoter Regions, Genetic, pubmed-meshheading:18339680-Proto-Oncogene Proteins B-raf, pubmed-meshheading:18339680-Questionnaires, pubmed-meshheading:18339680-Riboflavin, pubmed-meshheading:18339680-Vitamin B 12, pubmed-meshheading:18339680-Vitamin B 6
pubmed:year
2008
pubmed:articleTitle
Associations of dietary methyl donor intake with MLH1 promoter hypermethylation and related molecular phenotypes in sporadic colorectal cancer.
pubmed:affiliation
Department of Epidemiology, GROW, School for Oncology and Developmental Biology, Maastricht University, Maastricht, The Netherlands. stefan.devogel@epid.unimaas.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't