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Neuroblastoma epigenetics: from candidate gene approaches to genome-wide screenings

Anneleen Decock UGent, Maté Ongenaert UGent, Jo Vandesompele UGent and Franki Speleman UGent (2011) EPIGENETICS. 6(8). p.962-970
abstract
Neuroblastoma (NB) is a childhood tumor originating from sympathetic nervous system cells. Although recently new insights into genes involved in NB have emerged, the molecular basis of neuroblastoma development and progression still remains poorly understood. The best-characterized genetic alterations include amplification of the proto-oncogene MYCN, ALK activating mutations or amplification, gain of chromosome arm 17q and losses of 1p, 3p and 11q. Epigenetic alterations have been described as well: caspase-8 (CASP8) and RAS-association domain family 1 isoform A (RASSF1A) DNA-methylation are important events for the development and progression of neuroblastoma. In total, about 75 genes are described as epigenetically affected in NB cell lines and/or NB primary samples. These epigenetic alterations were either found using a candidate gene approach or based on the analysis of genome-wide screening techniques. This review gives an extensive overview of all epigenetic changes described in NB as of today, with a main focus on both prognostic use and the potential of genome-wide techniques to find epigenetic prognostic biomarkers in NB. We summarize the key findings so far and the state-of-the-art of the upcoming methods at a unique time frame in the transition towards combined genome-wide chromatin immunoprecipitation (ChIP) and DNA sequencing techniques.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
TUMOR-SUPPRESSOR RASSF1A, CELL-DEATH, PROMOTER HYPERMETHYLATION, histone modifications, APOPTOSIS, chromatin modification, DNA-methylation, apoptosis, epigenetics, neuroblastoma, HIGH-THROUGHPUT, review, CANCER CELLS, DNA METHYLATION, AMPLIFICATION, CPG ISLAND HYPERMETHYLATION, ABERRANT METHYLATION
journal title
EPIGENETICS
Epigenetics
volume
6
issue
8
pages
962 - 970
Web of Science type
Review
Web of Science id
000293344500002
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
4.318 (2011)
JCR rank
74/286 (2011)
JCR quartile
2 (2011)
ISSN
1559-2294
project
Bioinformatics: from nucleotids to networks (N2N)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1901814
handle
http://hdl.handle.net/1854/LU-1901814
date created
2011-09-15 15:22:36
date last changed
2017-02-22 14:41:47
@article{1901814,
  abstract     = {Neuroblastoma (NB) is a childhood tumor originating from sympathetic nervous system cells. Although recently new insights into genes involved in NB have emerged, the molecular basis of neuroblastoma development and progression still remains poorly understood. The best-characterized genetic alterations include amplification of the proto-oncogene MYCN, ALK activating mutations or amplification, gain of chromosome arm 17q and losses of 1p, 3p and 11q. Epigenetic alterations have been described as well: caspase-8 (CASP8) and RAS-association domain family 1 isoform A (RASSF1A) DNA-methylation are important events for the development and progression of neuroblastoma. In total, about 75 genes are described as epigenetically affected in NB cell lines and/or NB primary samples. These epigenetic alterations were either found using a candidate gene approach or based on the analysis of genome-wide screening techniques. This review gives an extensive overview of all epigenetic changes described in NB as of today, with a main focus on both prognostic use and the potential of genome-wide techniques to find epigenetic prognostic biomarkers in NB. We summarize the key findings so far and the state-of-the-art of the upcoming methods at a unique time frame in the transition towards combined genome-wide chromatin immunoprecipitation (ChIP) and DNA sequencing techniques.},
  author       = {Decock, Anneleen and Ongenaert, Mat{\'e} and Vandesompele, Jo and Speleman, Franki},
  issn         = {1559-2294},
  journal      = {EPIGENETICS},
  keyword      = {TUMOR-SUPPRESSOR RASSF1A,CELL-DEATH,PROMOTER HYPERMETHYLATION,histone modifications,APOPTOSIS,chromatin modification,DNA-methylation,apoptosis,epigenetics,neuroblastoma,HIGH-THROUGHPUT,review,CANCER CELLS,DNA METHYLATION,AMPLIFICATION,CPG ISLAND HYPERMETHYLATION,ABERRANT METHYLATION},
  language     = {eng},
  number       = {8},
  pages        = {962--970},
  title        = {Neuroblastoma epigenetics: from candidate gene approaches to genome-wide screenings},
  volume       = {6},
  year         = {2011},
}

Chicago
Decock, Anneleen, Maté Ongenaert, Jo Vandesompele, and Franki Speleman. 2011. “Neuroblastoma Epigenetics: From Candidate Gene Approaches to Genome-wide Screenings.” Epigenetics 6 (8): 962–970.
APA
Decock, A., Ongenaert, M., Vandesompele, J., & Speleman, F. (2011). Neuroblastoma epigenetics: from candidate gene approaches to genome-wide screenings. EPIGENETICS, 6(8), 962–970.
Vancouver
1.
Decock A, Ongenaert M, Vandesompele J, Speleman F. Neuroblastoma epigenetics: from candidate gene approaches to genome-wide screenings. EPIGENETICS. 2011;6(8):962–70.
MLA
Decock, Anneleen, Maté Ongenaert, Jo Vandesompele, et al. “Neuroblastoma Epigenetics: From Candidate Gene Approaches to Genome-wide Screenings.” EPIGENETICS 6.8 (2011): 962–970. Print.