Abstract
It is now well-established that the majority of the aberrant gene
expression profiles described in human cancers are due to #epigeneticchanges. These patterns reflect #DNAmethylation 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-suppressorgenes 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.
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