ArticleEpigenomics2012
Gene × environment interaction by a longitudinal epigenome-wide association study (LEWAS) overcomes limitations of genome-wide association study (GWAS).
Article in Epigenomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Gene-environment interactions in Alzheimer disease: the emerging role of epigenetics.Nature reviews. Neurology · 2022Review
- Epigenetic dysregulation of brainstem nuclei in the pathogenesis of Alzheimer's disease: looking in the correct place at the right time?Cellular and molecular life sciences : CMLS · 2017Review
- Transgenerational latent early-life associated regulation unites environment and genetics across generations.Epigenomics · 2016Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The goal of genome-wide association studies is to identify SNPs unique to disease. It usually involves a single sampling from subjects' lifetimes. While primary DNA sequence variation influences gene-expression levels, expression is also influenced by epigenetics, including the 'somatic epitype' (G(SE)), an epigenotype acquired postnatally. While genes are inherited, and novel polymorphisms do not routinely appear, G(SE) is fluid. Furthermore, G(SE) could respond to environmental factors (such as heavy metals) and to differences in exercise, maternal care and dietary supplements - all of which postnatally modify oxidation or methylation of DNA, leading to altered gene expression. Change in epigenetic status may be critical for the development of many diseases. We propose a 'longitudinal epigenome-wide association study', wherein G(SE) are measured at multiple time points along with subjects' histories. This Longitudinal epigenome-wide association study, based on the 'dynamic' somatic epitype over the 'static' genotype, merits further investigation.
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Registered trials
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