The context and potential of epigenetics in oncology

Abstract

Cancer has long been known to be a disease caused by alterations in the genetic blueprint of cells. In the past decade it has become evident that epigenetic processes have a function, at least equally important, in neoplasia. Epigenetics describes the mechanisms that result in heritable alterations in gene expression profiles without an accompanying change in DNA sequence. Genetics and epigenetics intricately interact in the pathogenesis of cancer (Esteller, 2007). In this review, we paint a broad picture of current understanding of epigenetic changes in cancer cells and reflect on the immense clinical potential of emerging knowledge of epigenetics in the diagnosis, prognostic assessment, treatment, and screening of cancer.

Figure 1

Current understanding of some of the changes to DNA and chromatin that occur in cancer cells. In the normal cell, promoters of actively transcribed genes are unmethylated and found within regions of euchromatin. Expression of other genes is repressed by promoter methylation and heterochromatin formation. In cancer, this is deregulated, resulting in the aberrant expression of normally silent genes and repression of tumour suppressor genes. Abbreviations: HAT, histone acetyltransferase; SWI/SNF, switch/sucrose nonfermentable nucleosome remodelling complex; MeCP2, methyl CpG-binding protein 2; HDAC, histone deacetylase.