Open AccessJournal Article
Effects of dietary folate and alcohol intake on promoter methylation in sporadic colorectal cancer: the Netherlands cohort study on diet and cancer.
Manon van Engeland,Matty P. Weijenberg,Guido M.J.M. Roemen,Mirian Brink,Adriaan P. de Bruïne,R. Alexandra Goldbohm,Piet A. van den Brandt,Stephen B. Baylin,Anton F.P.M. de Goeij,James G. Herman +9 more
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TLDR
F folate and alcohol intake may be associated with changes in promoter hypermethylation in CRC, and the number of CRCs with at least one gene methylated was higher in the low folate intake/high alcohol intake group when compared with the high folate Intake/low alcohol Intake group.Abstract:
Sporadic colorectal cancer (CRC) is characterized by genetic and epigenetic changes such as regional DNA hypermethylation and global DNA hypomethylation. Epidemiological and animal studies suggest that aherrant DNA methylation is associated with low dietary folate intake, which is aggravated by high alcohol intake. The relationship between promoter methylation of genes involved in CRC carcinogenesis and folate and alcohol intake was investigated. Methylation of the APC-1A, p14ARF, p16INK4A, hMLH1, O6-MGMT, and RASSF1A promoters was studied using methylation-specific PCR in 122 sporadic CRCs, derived from patients with folate and alcohol intake at either the lower or the higher quintiles of the distribution. Overall, promoter hypermethylation frequencies observed were: 39% for APC; 33% for p14ARF; 31% for p16INKA4A; 29% for hMLH1; 41% for O6-MGMT; and 20% for RASSF1A. For each of the tested genes, the prevalence of promoter hypermethylation was higher in CRCs derived from patients with low folate/high alcohol intake (n = 61) when compared with CRCs from patients with high folate/low alcohol intake (n = 61), but the differences were not statistically significant. The number of CRCs with at least one gene methylated was higher (84%) in the low folate intake/high alcohol intake group when compared with the high folate intake/low alcohol intake group (70%; P = 0.085). Despite the size limitations of this study, these data suggest that folate and alcohol intake may be associated with changes in promoter hypermethylation in CRC.read more
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Prenatal exposure to maternal depression, neonatal methylation of human glucocorticoid receptor gene (NR3C1) and infant cortisol stress responses
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Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands
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Vegetables, Fruit, and Cancer Prevention: A Review
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Journal Article
A Gene Hypermethylation Profile of Human Cancer
TL;DR: An unusual view of the pervasiveness of DNA alterations, in this case an epigenetic change, in human cancer is provided and a powerful set of markers are provided to outline the disruption of critical pathways in tumorigenesis and for derivation of sensitive molecular detection strategies for virtually every human tumor type.
Journal ArticleDOI
Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
James G. Herman,Asad Umar,Kornelia Polyak,Jeremy R. Graff,Nita Ahuja,Jean Pierre J. Issa,Sanford Markowitz,Sanford Markowitz,James K V Willson,Stanley R. Hamilton,Kenneth W. Kinzler,Michael F. Kane,Richard D. Kolodner,Bert Vogelstein,Thomas A. Kunkel,Stephen B. Baylin +15 more
TL;DR: The results suggest that microsatellite instability in sporadic colorectal cancer often results from epigenetic inactivation of hMLH1 in association with DNA methylation.
Journal Article
Inactivation of the DNA repair gene O6-methylguanine-DNA methyltransferase by promoter hypermethylation is a common event in primary human neoplasia
TL;DR: The presence of aberrant hypermethylation was associated with loss of MGMT protein, in contrast to retention of protein in the majority of tumors without aberrantHypermethylation, suggesting that epigenetic inactivation of MG MT plays an important role in primary human neoplasia.