*Corresponding author:Patrick A Riley, Totteridge Institute for Advanced Studies, The Grange, Grange Avenue, London
Received: February 07, 2018; Published: February 19, 2018
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It is now well-established that the majority of the aberrant gene expression profiles described in human cancers are due to epigenetic changes. These patterns reflect DNA methylation changes, including both hypo- and hypermethylation. There is evidence to suggest that, in general, hypomethylation is associated with the expression of previously silenced genes whereas DNA hypermethylation is involved in the silencing of previously transcribed genes and there has been much interest in the inhibition of tumour-suppressor genes as a possible carcinogenic mechanism. This brief overview discusses the possible origins of the observed anomalies of DNA methylation and proposes that the initiating carcinogenic mechanism lies in the failure of accurate copying of the epigenetic pattern during stem cell proliferation.
Keywords: DNA Methylation; Cancer; Epigenetics