DNA methylation fingerprint of neuroblastoma reveals new biological and clinical insights

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anaplastic Lymphoma Kinase
  • Brain Neoplasms / diagnosis
  • Brain Neoplasms / genetics*
  • Brain Neoplasms / metabolism
  • Brain Neoplasms / mortality
  • Cell Line, Tumor
  • Child
  • Child, Preschool
  • Chromatin / chemistry
  • Chromatin / metabolism
  • CpG Islands
  • Cyclin D1 / genetics*
  • Cyclin D1 / metabolism
  • DNA Fingerprinting
  • DNA Methylation
  • DNA, Intergenic
  • Epigenesis, Genetic*
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic*
  • Genome, Human
  • Humans
  • Infant
  • Male
  • Neuroblastoma / diagnosis
  • Neuroblastoma / genetics*
  • Neuroblastoma / metabolism
  • Neuroblastoma / mortality
  • Oligonucleotide Array Sequence Analysis
  • Prognosis
  • Promoter Regions, Genetic
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Survival Analysis

Substances

  • CCND1 protein, human
  • Chromatin
  • DNA, Intergenic
  • Cyclin D1
  • ALK protein, human
  • Anaplastic Lymphoma Kinase
  • Receptor Protein-Tyrosine Kinases