Methylation of DNA and chromatin as a mechanism of oncogenesis and therapeutic target in neuroblastoma
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Ram Mohan Ram Kumar1 and Nina Felice Schor1,2
1Department of Pediatrics and Wilmot Cancer Center, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA
2Current affiliation: National Institute of Neurological Disorders & Stroke, National Institutes of Health, Bethesda, MD, USA
Ram Mohan Ram Kumar, email: [email protected]
Keywords: neuroblastoma; pathogenesis; epigenetics
Received: December 30, 2017 Accepted: March 21, 2018 Published: April 24, 2018
Neuroblastoma (NB), a developmental cancer, is often fatal, emphasizing the need to understand its pathogenesis and identify new therapeutic targets. The heterogeneous pathological and clinical phenotype of NB underscores the cryptic biological and genetic features of this tumor that result in outcomes ranging from rapid progression to spontaneous regression. Despite recent genome-wide mutation analyses, most primary NBs do not harbor driver mutations, implicating epigenetically-mediated gene regulatory mechanisms in the initiation and maintenance of NB. Aberrant epigenomic mechanisms, as demonstrated by global changes in DNA methylation signatures, acetylation, re-distribution of histone marks, and change in the chromatin architecture, are hypothesized to play a role in NB oncogenesis. This paper reviews the evidence for, putative mechanisms underlying, and prospects for therapeutic targeting of NB oncogenesis related to DNA methylation.
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