PerspectiveMolecular Biology

Genetic Events That Shape the Cancer Epigenome

Science  22 Jun 2012:
Vol. 336, Issue 6088, pp. 1513-1514
DOI: 10.1126/science.1223730

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Summary

Since the discovery of the first recurrent mutations in oncogenes and tumor suppressor genes, it has been clear that cancer is, in large part, a genetic disease. Yet nearly every human neoplasm retains a phenotype reflective of its tissue of origin, thus underscoring the centrality of epigenetics in cancer biology. Indeed, there is increasing recognition that transmissible epigenetic changes—chemical modifications to the genome or its scaffold that do not involve a change in the nucleotide sequence—may be acquired de novo, and that these “epimutations” may also contribute to carcinogenesis. Aberrations of DNA methylation have epitomized this concept, largely because of the direct mechanism by which hypermethylation of a DNA locus can be faithfully transmitted through cell division. Localized hypermethylation of silenced gene promoters and global DNA hypomethylation are characteristic features of many human tumors (1, 2). However, the idea that histone modifications and other chromatin features also mediate epimutations in tumors has been more controversial, in part due to the obscurity of models for direct epigenetic transmission (3). The recent flurry of reported mutations in chromatin-related genes in human tumors indicates the need to reassess the perceived roles for chromatin and epigenetic mechanisms in cancer biology.

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