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Open AccessEditorial

5-Methylcytosine and 5-Hydroxymethylcytosine Signatures Underlying Pediatric Cancers

by Shalu Jhanwar 1,2,* and Ajinkya Deogade 2,3
1
Developmental Genetics, Department of Biomedicine, University of Basel, 4058 Basel, Switzerland
2
Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Universitat Pompeu Fabra (UPF), 08003 Barcelona, Spain
3
Department of Molecular, Cellular and Developmental Biology, University of California, Santa Barbara, Santa Barbara, CA 93106, USA
*
Author to whom correspondence should be addressed.
Epigenomes 2019, 3(2), 9; https://doi.org/10.3390/epigenomes3020009
Received: 30 April 2019 / Accepted: 6 May 2019 / Published: 9 May 2019
(This article belongs to the Special Issue Biological Methylation in Development and Cancer)
In addition to the genetic variations, recent evidence has shown that DNA methylation of both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) underlies the pathogenesis of pediatric cancer. Given the high mortality rate, there is an urgent need to study the mechanisms contributing to the pathogenicity of pediatric cancer. Over the past decades, next-generation sequencing (NGS) has enabled us to perform genome-wide screening to study the complex regulatory mechanisms of 5mC and 5hmC underlying pediatric tumorigenesis. To shed light on recent developments on pediatric cancer predisposition and tumor progression, here we discuss the role of both genome-wide and locus-specific dysregulation of 5mC and 5hmC in hematopoiesis malignancy and neuroblastoma, the most common types of pediatric cancer, together with their therapeutic potential. View Full-Text
Keywords: epigenetics; DNA methylation; pediatric cancer; 5mC; 5hmC; acute lymphoblastic leukaemia; neuroblastoma epigenetics; DNA methylation; pediatric cancer; 5mC; 5hmC; acute lymphoblastic leukaemia; neuroblastoma
MDPI and ACS Style

Jhanwar, S.; Deogade, A. 5-Methylcytosine and 5-Hydroxymethylcytosine Signatures Underlying Pediatric Cancers . Epigenomes 2019, 3, 9.

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