Metabolic, hormonal and immunological associations with global DNA methylation among postmenopausal women

Ulrich, Cornelia M.; Toriola, Adetunji T.; Koepl, Lisel; Sandifer, T.G.; Poole, Elizabeth M.; Duggan, Catherine; McTiernan, Anne; Issa, Jean–Pierre J.

doi:10.4161/epi.21464

Cited by 41 publications

(36 citation statements)

References 71 publications

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“…All of the studies used BMI or changes in BMI to classify obesity, and two studies also used percentage body fat 32 33 . The majority of these investigations, including a large study combining four study populations, including up to 1254 individuals 34 , did not find an association between obesity and global methylation 33,[35][36][37][38][39][40] . Two studies that included only women 32 41 , found reduced global methylation with increasing BMI, however in one of these studies this only occurred in the presence of low concentrations of the methyl donor folate 32 .…”

Section: Global Methylation and Obesitymentioning

confidence: 99%

Epigenetics and human obesity

Molloy

Varinli³

et al. 2014

Int J Obes

295

214

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Section: Global Methylation and Obesitymentioning

confidence: 99%

Epigenetics and human obesity

Molloy

Varinli³

et al. 2014

Int J Obes

295

214

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show abstract

“…However, in blood, L1 methylation displays little variability (109), and it remains unclear how sensitive such assays are to detect subtle DNA methylation variability. Methylation of TEs, particularly L1, is often reported as genome-wide or "global" DNA methylation.…”

Section: Assay Measurementmentioning

confidence: 99%

Is There a Link Between Genome-Wide Hypomethylation in Blood and Cancer Risk?

Brennan

Flanagan

2012

Cancer Prevention Research

103

104

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Cancer cells display widespread genetic and epigenetic abnormalities, but the contribution to disease risk, particularly in normal tissue before disease, is not yet established. Genome-wide hypomethylation occurs frequently in tumors and may facilitate chromosome instability, aberrant transcription and transposable elements reactivation. Several epidemiologic case-control studies have reported genomic hypomethylation in peripheral blood of cancer patients, suggesting a systemic effect of hypomethylation on disease predisposition, which may be exploited for biomarker development. However, more recent studies have failed to reproduce this. Here, we report a meta-analysis, indicating a consistent inverse association between genomic 5-methylcytosine levels and cancer risk [95% confidence interval (CI), 1.2-6.1], but no overall risk association for studies using surrogates for genomic methylation, including methylation at the LINE-1 repetitive element (95% CI, 0.8-1.7). However, studies have been highly heterogeneous in terms of experimental design, assay type, and analytical methods. We discuss the limitations of the current approaches, including the low interindividual variability of surrogate assays such as LINE1 and the importance of using prospective studies to investigate DNA methylation in disease risk. Insights into genomic location of hypomethylation, from recent whole genome, highresolution methylome maps, will help address this interesting and clinically important question. Cancer Prev Res; 5(12); 1345-57. Ó2012 AACR.

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“…In a cross-sectional study, postmenopausal women exhibited an inverse relationship between lymphocyte LINE-1 methylation and sex hormone concentrations when stratifi ed by serum folate levels (Ulrich et al 2012 ). LINE-1 methylation was positively associated with immune markers in those with high serum folate levels (Ulrich et al 2012 ). Furthermore, there was a nonsignifi cant inverse trend with supplemental vitamin B 6 intakes and LINE-1 methylation (Jin et al 2009 ).…”

Section: Human Studiesmentioning

confidence: 99%

“…However, after folate-repletion, global DNA methylation levels were restored in postmenopausal (Jacob et al 1998 ) but not in elderly (Rampersaud et al 2000 ) women. In a cross-sectional study, postmenopausal women exhibited an inverse relationship between lymphocyte LINE-1 methylation and sex hormone concentrations when stratifi ed by serum folate levels (Ulrich et al 2012 ). LINE-1 methylation was positively associated with immune markers in those with high serum folate levels (Ulrich et al 2012 ).…”

Section: Human Studiesmentioning

confidence: 99%

One-Carbon Metabolism Nutrients and Epigenetics: A Mechanistic Link Between Aberrant One-Carbon Metabolism and Cancer Risk?

Masih

Plumptre

Kim

2014

Molecular Mechanisms and Physiology of Disease

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In relation to the genome, investigation of the epigenome is emerging as an equal, if not more infl uential factor in modulating human health and disease. Since epigenetic modifi cations are gradual in onset and potentially reversible, determining factors that modulate the epigenome is critical for possible preventive and therapeutic interventions. The development and progression of cancer is mechanistically linked to a number of epigenetic changes, including global DNA hypomethylation and genespecifi c CpG promoter DNA hypermethylation. Environmental factors, including diet, have been shown to affect cancer risk, via epigenetic and non-epigenetic mechanisms. In this regard, one-carbon nutrients are prototypic dietary factors that may modulate cancer risk via epigenetic mechanisms. This chapter will discuss the role of nutrients involved in one-carbon metabolism and their effect on cancer risk via epigenetic modifi cations with a particular focus on DNA methylation.

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Metabolic, hormonal and immunological associations with global DNA methylation among postmenopausal women

Cited by 41 publications

References 71 publications

Epigenetics and human obesity

Epigenetics and human obesity

Is There a Link Between Genome-Wide Hypomethylation in Blood and Cancer Risk?

One-Carbon Metabolism Nutrients and Epigenetics: A Mechanistic Link Between Aberrant One-Carbon Metabolism and Cancer Risk?

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