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Epigenomics and disease, 10th anniversary winter meeting of the UK Molecular Epidemiology Group (MEG), The Royal Statistical Society, London, UK, 8th December 2006.

Martin FL

Biomedical Sciences Unit, Department of Biological Sciences, Lancaster University, Lancaster LA1 4YQ, UK.

Meeting participants: Manel Esteller (Spanish National Cancer Research Centre, Spain), Zdenko Herceg (International Agency for Research on Cancer, France), John C. Mathers (University of Newcastle, UK), Saverio Minucci (European Institute of Oncology, Italy), Fei Ling Lim (Syngenta Central Toxicology Laboratory, UK) and James E. Trosko (Michigan State University, USA). Organizing UK MEG committee: John E. Hesketh (University of Newcastle, UK), F.L.M. (Lancaster University, UK), David H. Phillips (Institute of Cancer Research, UK), Michael N. Routledge (University of Leeds, UK), Lesley Rushton (Imperial College, UK) and Paolo Vineis (Imperial College, UK). An organism has a unique genome but may have different tissue-specific epigenomes. Distinct from the genotype, epigenomics encompasses the modulation of gene activity through particular global chromatin methylation patterns or histone modifications; these may be known as epigenetic marks. The chromatin pattern of epigenetic marks is modifiable over a lifespan and may influence disease progression at a particular site. The meeting aim was to discuss the role of epigenomics in the aetiology of disease, particularly cancer. Epigenetic marks might be modifiable through dietary intake of methyl donors and aberrant patterns may underlie phenotypical changes resulting in chronic diseases such as cancer. DNA methylation patterns or histone modifications are potentially reversible, but, in certain circumstances, such marks become imprinted and give rise to trans-generational effects. Other reversible effects influencing disease occurrence might be inhibition of gap junction intracellular communication. Environmental and/or dietary factors play a pivotal role in the aetiology of cancer. Most cancers require a mutagenic initiation step. However, it is now recognized that an aberrant pattern of epigenetic marks may link the initiating mutation to the gene expression profile of a disease phenotype. This workshop stressed the need for a human epigenomic project out of which specific aberrant patterns of epigenetic marks might be developed as novel predictors to facilitate the implementation of future disease prevention strategies, to lend new insights into aetiology of disease, to allow more exact diagnosis and to develop better-targeted therapeutic regimens.

Published 7 November 2007 in Mutagenesis, 22(6): 425-7.
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