Methylenetetrahydrofolate reductase polymorphism, plasma homocysteine and age

Todesco, Liliane; Angst, Christian P.; Litynski, Piotr; Loehrer, F.; Fowler, Brian; Haefeli, Walter E.

doi:10.1046/j.1365-2362.1999.00578.x

Cited by 50 publications

(26 citation statements)

References 49 publications

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“…There was significant heterogeneity between the pooled estimates of prospective and ret- Other Tokgozoglu et al 67 Gulec et al 66 Inbal et al 65 Morita et al 62 Nakai et al 63 Ou et al 64 Silberberg et al Van Bockxmeer et al 61 Thogersen et al 49 Todesco et al 50 …”

Section: Prospective Vs Retrospective Studiesmentioning

confidence: 99%

MTHFR 677C→T Polymorphism and Risk of Coronary Heart Disease

Klerk

Verhoef²,

Clarke³

et al. 2002

JAMA

855

481

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Section: Prospective Vs Retrospective Studiesmentioning

confidence: 99%

MTHFR 677C→T Polymorphism and Risk of Coronary Heart Disease

Klerk

Verhoef²,

Clarke³

et al. 2002

JAMA

855

481

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“…54 Each variant homozygote has a decreased enzyme activity, which would result in an increased pool of methylene-THF at the expense of a decreased pool of methyl-THF. [72][73][74][75][76][77][78] A study by Rosenberg et al 79 addressed the question of whether the MTHFR 677CT alteration has an ancestral origin or has occurred repeatedly. 79 Stern and colleagues 80 investigated whether a common 677CT mutation in the MTHFR gene, which results in reduced enzyme activity in vitro, affects genomic DNA methylation.…”

Section: Methylenetetrahydrofolate Reductase (Mthfr)mentioning

confidence: 99%

Folic acid, polymorphism of methyl-group metabolism genes, and DNA methylation in relation to GI carcinogenesis

Fang

Xiao

2003

Journal of Gastroenterology

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DNA methylation is the main epigenetic modification after replication in humans. DNA (cytosine-5)-methyltransferase (DNMT) catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to C5 of cytosine within CpG dinucleotide sequences in the genomic DNA of higher eukaryotes. There is considerable evidence that aberrant DNA methylation plays an integral role in carcinogenesis. Folic acid or folate is crucial for normal DNA synthesis and can regulate DNA methylation, and through this, it affects cellular SAM levels. Folate deficiency results in DNA hypomethylation. Epidemiological studies have indicated that folic acid protects against gastrointestinal (GI) cancers. Methylene-tetrahydrofolate reductase (MTHFR) and methionine synthase (MS) are the enzymes involved in folate metabolism and are thought to influence DNA methylation. MTHFR is highly polymorphic, and the variant genotypes result in decreased MTHFR enzyme activity and lower plasma folate level. Two common MTHFR polymorphisms, 677CT (or 677TT) and A1298C, and an MS polymorphism, A-->G at 2756, have been identified. Most studies support an inverse association between folate status and the rate of colorectal adenomas and carcinomas. During human GI carcinogenesis, MTHFR is highly polymorphic, and the variant genotypes result in decreased MTHFR enzyme activity and lower plasma folate level, as well as aberrant methylation.

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“…Finally, we examined three genes not belonging to any of these biological processes but still considered reliable candidates in previous studies: the highly discussed candidate gene angiotensin I-converting enzyme (ACE), for which the I/D insertion/deletion (tagged by rs4343 (Abdollahi et al 2008)) has been reported by several authors to be associated with longevity (Arias-Vasquez et al 2005;Cellini et al 2005;Frederiksen et al 2003;Luft 1999;Novelli et al 2008;Schachter et al 1994;Zajc et al 2012); the iron absorption regulatory protein hfe, for which the Cys282Tyr variation (rs1800562) was found to decrease with age Lio et al 2002); and, finally, MTHFR, which is of importance for the essential remethylation of homocysteine to methionine, where the C677T (rs1801133) polymorphism has been suggested as associated with longevity (Stessman et al 2005;Todesco et al 1999).…”

Section: Introductionmentioning

confidence: 99%