The importance and role of the cellular epigenome in cell fating and development have been studied for decades. The epigenome encompasses a range of attributes including DNA methylation, histone modifications, and chromatin remodelers; together these components define the cellular transcriptome, identity, and function. The cellular epigenome is dynamic in response to environmental signals, modifiable during normal cell differentiation and is heritable in daughter cells. This plasticity, however, poses a risk for misregulation and may underlie a number of hereditary disorders, development defects, and cancer. Although the first epigenetic change described in cancer was gene hypomethylation [Holliday R, Jeggo PA: Mechanisms for changing gene expression and their possible relationship to carcinogenesis.Cancer Surv 1985, 4:557-581; Feinberg AP, Vogelstein B: Hypomethylation distinguishes genes of some human cancers from their normal counterparts.Nature 1983, 301:89-92], we know that cancers not only display global hypomethylation, but also, site-specific gene hypermethylation in addition to changes in chromatin modifications. Mechanisms explaining the sometimes paradoxical epigenetic changes observed in cancer, their contributions to tumor initiation and progression and how epigenetics relate to genetic events are poorly understood. In this review we will briefly discuss recent findings on the epigenomic states observed in colon cancer, in particular, how perturbations to the genome and epigenome together may contribute to initiation and progression of colon cancer.
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