Dietary methyl donors, methyl metabolizing enzymes, and epigenetic regulators: diet-gene interactions and promoter CpG island hypermethylation in colorectal cancer
Autor: | Ralph W.H. Gottschalk, Matty P. Weijenberg, Adriaan P. de Bruïne, Frederik J. van Schooten, R. Alexandra Goldbohm, Manon van Engeland, Kim A.D. Wouters, Stefan de Vogel, Piet A. van den Brandt, Anton F.P.M. de Goeij |
---|---|
Přispěvatelé: | RS: CAPHRI School for Public Health and Primary Care, RS: NUTRIM - R4 - Gene-environment interaction, Pathologie, Farmacologie en Toxicologie, Epidemiologie, RS: GROW - School for Oncology and Reproduction |
Jazyk: | angličtina |
Rok vydání: | 2011 |
Předmět: |
Cancer Research
Methyltransferase genetic association genotype methyl metabolizing enzyme DNA methyltransferase cancer risk LS - Life Style Polymerase Chain Reaction Epigenesis Genetic genetic heterogeneity Diet and cancer genetic variability methionine synthase reductase gene Promoter Regions Genetic cytosine Netherlands DNA methylation biology adult allele risk assessment Middle Aged cohort analysis CRC unclassified drug enzyme activity aged female Oncology CpG site priority journal Health Colorectal Neoplasms Human medicine.medical_specialty phenotype mthfr gene colorectal cancer Diet–gene interactions genetic regulation Folic Acid promoter region Gene interaction male Internal medicine DNA methyltransferase 3B gene thymine medicine methyl group Humans Genetic Predisposition to Disease Diet-gene interactions riboflavin gene pyridoxine Medical disciplines: 700 [VDP] methionine Original Paper Methyl donors epigenetics business.industry gene interaction Methyltransferases DNA methionine synthase gene MTRR heterozygote major clinical study protein intake BSS - Behavioural and Societal Sciences Vitamin B 6 digestive system diseases Diet Promoter hypermethylation enzyme Endocrinology Methylenetetrahydrofolate reductase folate metabolizing enzyme biology.protein CpG island CpG Islands methyltransferase business dietary intake |
Zdroj: | Cancer Causes and Control, 1, 22, 1-12 Cancer Causes & Control, 22(1), 1-12. Springer, Cham Cancer Causes & Control |
ISSN: | 0957-5243 |
DOI: | 10.1007/s10552-010-9659-6 |
Popis: | Dietary methyl donors might influence DNA methylation during carcinogenesis of colorectal cancer (CRC). Among 609 CRC cases and 1,663 subcohort members of the Netherlands Cohort Study on diet and cancer (n = 120,852), we estimated CRC risk according to methyl donor intake across genotypes of folate metabolizing enzymes and methyltransferases. Although diet-gene interactions were not statistically significant, methionine intake was inversely associated with CRC among subjects having both common rs2424913 and rs406193 DNMT3B C > T genotypes (highest versus lowest tertile: RR = 0.44; p trend = 0.05). Likewise, vitamin B2 was modestly inversely associated among individuals with the MTHFR c.665CC (rs1801133) genotype (RR = 0.66; p trend = 0.08), but with a significant reduced risk when ≤ 1 rare allele occurred in the combination of folate metabolizing enzymes MTHFR, MTRR and MTR (RR = 0.30; p trend = 0.005). Folate or vitamin B6 were neither inversely associated with CRC nor was methyl donor intake associated with the CpG island methylator phenotype (CIMP). Despite the absence of heterogeneity across genotypes, might an effect of methyl donors on CRC be more pronounced among individuals carrying common variants of folate metabolizing enzymes or DNA methyltransferases. Combining genotypes may assist to reveal diet associations with CRC, possibly because rare variants of related genes may collectively affect specific metabolic pathways or enzymatic functions. © 2010 The Author(s). methyltransferase, 9037-42-7; cytosine, 71-30-7; methionine, 59-51-8, 63-68-3, 7005-18-7; methyltransferase, 9033-25-4; pyridoxine, 12001-77-3, 58-56-0, 65-23-6, 8059-24-3; riboflavin, 83-88-5; thymine, 65-71-4 |
Databáze: | OpenAIRE |
Externí odkaz: |