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The selective gene silencing which accounts for the specialization characteristic of differentiated cells is the result of reversible epigenetic modification of the genome. The process involved is heterochromatisation, a major component of which is brought about by DNA methylation with associated modifications of histones with consequent alterations in chromatin structure which control access to transcription sites. When cells divide the chromatin pattern is disturbed. To retain the differentiated state of the cell the chromatin pattern of the parent cell must be reproduced in the progeny. The mechanism involves the methylation of the replicated DNA strand to correspond with the methylation pattern of the parent strand. The complex machinery, which implicates many component elements, normally ensures that the pattern of gene silencing is accurately transmitted to the daughter cells. However, permanent derangement of the copying mechanism would result in inappropriate re-expression of previously silenced genes or failure of expression of previously active genes. It is the essence of the present proposal that the initiating event(s) of carcinogenesis are irreversible events, such as mutations, affecting the efficiency of the chromatin copying mechanism with resulting failure of fidelity of the vertical transmission of the gene activity pattern. Thus, in the affected clone, there will be a divergent range of anomalous gene expression with the emergence of sub-clones with abnormal structure and function, some of which will manifest properties characteristic of the malignant growth syndrome, such as invasiveness, metastasis and escape from proliferative control. This phase of carcinogenesis corresponds to what has been termed ‘progression’ and is characterised by genetic instability in the affected cell lineage.

Cancer is the outcome of defective epigenetic copying of the pattern of selective gene activity in differentiated cells