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Epigenomics. 2015 Oct;7(7):1137-53. doi: 10.2217/epi.15.49. Epub 2015 Jun 12.

DNA methylation fingerprint of neuroblastoma reveals new biological and clinical insights.

Author information

1
Developmental Tumor Biology Laboratory, Hospital Sant Joan de Déu, Edificio Docente 4th floor, C/Santa Rosa 39-57, 08950 Esplugues de Llobregat, Barcelona, Spain.
2
Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, 08036, Spain.
3
Department of Pathology, Hospital Sant Joan de Déu, Barcelona, 08950, Spain.
4
Illumina, Inc., San Diego, CA 92122, USA.
5
Center for Regenerative Medicine, Department of Chemical Physiology, The Scripps Research Institute, La Jolla, CA 92037, USA.
6
Department of Anatomic Pathology, Pharmacology & Microbiology, University of Barcelona, Barcelona, 08036, Spain.

Abstract

AIM:

To define the DNA methylation landscape of neuroblastoma and its clinicopathological impact.

MATERIALS & METHODS:

Microarray DNA methylation data were analyzed and associated with functional/regulatory genome annotation data, transcriptional profiles and clinicobiological parameters.

RESULTS:

DNA methylation changes in neuroblastoma affect not only promoters but also intragenic and intergenic regions at cytosine-phosphate-guanine (CpG) and non-CpG sites, and target functional chromatin domains of development and cancer-related genes such as CCND1. Tumors with diverse clinical risk showed differences affecting CpG and, remarkably, non-CpG sites. Non-CpG methylation observed essentially in clinically favorable cases was associated with the differentiation status of neuroblastoma and expression of key genes such as ALK.

CONCLUSION:

This epigenetic fingerprint of neuroblastoma provides new insights into the pathogenesis and clinical behavior of this pediatric tumor.

KEYWORDS:

ALK; CCND1; DNA methylome; development; neuroblastoma; non-CpG sites; nonpromoter methylation

PMID:
26067621
DOI:
10.2217/epi.15.49
[Indexed for MEDLINE]
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