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The epigenetics of cancer: from non-coding RNAs to chromatin and beyond.

Considerable effort has been invested in identifying genetic mutations in cancer, and with inherited cancer syndromes this approach has proved rather successful. Furthermore, genetic mutations early in the genesis of common cancers have also been identified and it is considered likely that these are associated with tumour initiation. In contrast, relatively few specific genetic mutations have been linked to tumour progression, leading to the suggestion that epigenetic changes may be involved [1]. Thus, a DNA mutation may lead to cellular transformation (cancer initiation), but then induced changes within the transformed cell’s epigenome would increase the likelihood of it metastasizing (cancer progression) [1]. In this scenario, genetic mutation initiates cancer but epigenetic change promotes its progression. In addition, in some cases the cell responsible for tumour initiation is not the cell in which the genetic mutation arises, but rather one of its progeny [2,3], suggesting that the combination between mutations and the epigenetic state of the cell might be essential for tumour initiation. It is also possible that epigenetic events directly initiate cancer themselves, or they could play a more indirect role by priming cells in such a way as to promote eventual cellular transformation. Although our knowledge of epigenetic processes and their involvement in cancer is still in its infancy, we are nevertheless excited at the prospect of developing this understanding, not least because, unlike DNA mutations, changes in the epigenome are potentially reversible. What is clear at the moment is that epigenetic processes work at multiple levels and via numerous pathways. Importantly, the concept of epigenetic cancer therapy has been established for a certain number of cancers [4,5], providing a convincing proof-of-principle for this approach. Epigenetic mechanisms can be broadly split into three groups: (i) those involving covalent modification of the DNA, (ii) those involving modification of chromatin particularly histones and (iii) those involving non-coding RNAs. This edition of BFG aims to present an up-to-date overview of our understanding of these different, but highly interdependent and inter-connected, epigenetic mechanisms in the genesis and development of cancer, with reviews from experts within these fields. The opening review in this issue is written by Halley-Stott and Gurdon, the latter a recipient of the 2012 Nobel Prize for Medicine or Physiology for his pioneering work on somatic cell reprogramming. It explores the implications for cancer based on our current knowledge of the epigenetic mechanisms relevant to cellular reprogramming into a pluripotent state. Halley-Stott and Gurdon focus on how epigenetic memory processes, which maintain cellular identity during cell divisions throughout development and which allow the transmission of imprints or traits during meiosis throughout generations, are involved in nuclear reprogramming. Similarly to cellular reprogramming, cancer formation may require destabilization of the differentiated state of adult cells, and the authors discuss how epigenetic memory may be involved in the transformation process. The review by Sproul and Meehan focuses on DNA methylation and, in particular, the authors discuss how wide-scale genomic analyses have begun to provide novel and unexpected insights into how DNA CpG island methylation is linked to the process of carcinogenesis. For instance, it is widely believed that in cancer cells the aberrant methylation of CpG islands within promoters of tumour suppressor genes leads to gene silencing. However, genome-wide studies have actually indicated that many of these genes are silenced before the CpG methylation occurs, mimicking the temporal correlation between transcriptional repression and CpG BRIEFINGS IN FUNCTIONAL GENOMICS. VOL 12. NO 3. 161^163 doi:10.1093/bfgp/elt020