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• W2120462849 endingPage "e1000356" @default.
• W2120462849 startingPage "e1000356" @default.
• W2120462849 abstract "There is considerable anticipation of future improvements in disease prevention and treatment following recent advances in genomics [1]. One aspect of genomics that is receiving considerable interest is epigenetics—the regulatory processes that control the transcription of information encoded in the DNA sequence into RNA before their translation into proteins. Programmed developmental changes and the ability of the genome to register, signal, and perpetuate environmental cues are subsumed under the epigenetic banner [2].Genes are packaged into chromatin and dynamic chromatin remodeling processes are required for the initial step in gene expression (transcription), achieved by altering the accessibility of gene promoters and regulatory regions [3]. Epigenetic factors are responsible for this regulatory process, the major components of which are DNA methylation, histone modifications, and the action of small non-coding RNAs (Figure 1). Unlike DNA sequence, which is largely fixed throughout the lifecourse, epigenetic patterns not only vary from tissue to tissue but alter with advancing age and are sensitive to environmental exposures [4]–[7]. It is this propensity for change that makes epigenetic processes the focus of such interest, as they lie at the interface of the environment and co-ordinated transcriptional control.Figure 1Epigenetic modifications.In rare developmental disorders, the role of aberrant epigenetic processes is well established [8]. Our focus here, however, is on the potential role of epigenetic processes in the context of common complex disease. Tumor-specific changes in epigenetic patterns are a hallmark of numerous cancers, with analysis of the epigenetic machinery beginning to feature prominently in emerging cancer diagnostics and therapies [9]–[11].There is an increasing body of evidence to demonstrate that epigenetic patterns are altered by environmental factors known to be associated with disease risk (e.g., diet, smoking, alcohol intake, environmental toxicants, stress) [7],[8]; however, an important question remains to be resolved in defining which epigenetic changes are a secondary outcome of either exposure or disease, and which lie on the causal pathway linking the two. Without proven causality, interventions to prevent or treat common complex diseases based upon epigenetic mechanisms will not be fruitful. Conversely, regardless of causality, defining a robust prospective relationship between epigenetic patterns and phenotypic traits may have application in diagnostics or in identifying high-risk individuals for non-epigenetic-based interventions." @default.
• W2120462849 created "2016-06-24" @default.
• W2120462849 creator A5013184354 @default.
• W2120462849 creator A5042511675 @default.
• W2120462849 date "2010-10-26" @default.
• W2120462849 modified "2023-09-26" @default.
• W2120462849 title "Epigenetic Epidemiology of Common Complex Disease: Prospects for Prediction, Prevention, and Treatment" @default.
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• W2120462849 doi "https://doi.org/10.1371/journal.pmed.1000356" @default.
• W2120462849 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2964338" @default.
• W2120462849 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21048988" @default.
• W2120462849 hasPublicationYear "2010" @default.
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