Volume 5 Issue 4
Apr.  2014
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David M. Roy, Logan A. Walsh, Timothy A. Chan. Driver mutations of cancer epigenomes[J]. Protein&Cell, 2014, 5(4): 265-296. doi: 10.1007/s13238-014-0031-6
Citation: David M. Roy, Logan A. Walsh, Timothy A. Chan. Driver mutations of cancer epigenomes[J]. Protein&Cell, 2014, 5(4): 265-296. doi: 10.1007/s13238-014-0031-6

Driver mutations of cancer epigenomes

doi: 10.1007/s13238-014-0031-6
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We apologize to the many authors whose work we could not cite because of space constraints. We would like to thank Deepa Ramaswami for help in reviewing the manuscript. D.M.R. was supported by the HHMI Medical Research Fellows Program and NIH MSTP grant T32GM007739. L.A.W. was supported by The Canadian Institutes of Health Research PDF. T.A.C. is a Department of Defense Era of Hope Scholar and supported in part by the Frederick Adler Fund.

  • Received Date: 2014-01-07
  • Rev Recd Date: 2014-02-03
  • Epigenetic alterations are associated with all aspects of cancer, from tumor initiation to cancer progression and metastasis. It is now well understood that both losses and gains of DNA methylation as well as altered chromatin organization contribute significantly to cancerassociated phenotypes. More recently, new sequencing technologies have allowed the identification of driver mutations in epigenetic regulators, providing a mechanistic link between the cancer epigenome and genetic alterations. Oncogenic activating mutations are now known to occur in a number of epigenetic modifiers (i.e. IDH1/2, EZH2, DNMT3A), pinpointing epigenetic pathways that are involved in tumorigenesis. Similarly, investigations into the role of inactivating mutations in chromatin modifiers (i.e. KDM6A, CREBBP/EP300, SMARCB1) implicate many of these genes as tumor suppressors. Intriguingly, a number of neoplasms are defined by a plethora of mutations in epigenetic regulators, including renal, bladder, and adenoid cystic carcinomas. Particularly striking is the discovery of frequent histone H3.3 mutations in pediatric glioma, a particularly aggressive neoplasm that has long remained poorly understood. Cancer epigenetics is a relatively new, promising frontier with much potential for improving cancer outcomes. Already, therapies such as 5-azacytidine and decitabine have proven that targeting epigenetic alterations in cancer can lead to tangible benefits. Understanding how genetic alterations give rise to the cancer epigenome will offer new possibilities for developing better prognostic and therapeutic strategies.
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