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Copy number defects of G1‐Cell cycle genes in neuroblastoma are frequent and correlate with high expression of E2F target genes and a poor prognosis

The tightly controlled network of cell cycle genes consists of a core of cyclin dependent kinases (CDKs) that are activated by periodically expressed cyclins. The activity of the cyclin‐CDK complexes is regulated by cyclin dependent kinase inhibitors (CDKIs) and multiple signal transduction routes t... Full description

Journal Title: Genes Chromosomes and Cancer, January 2012, Vol.51(1), pp.10-19
Main Author: Molenaar, Jan J.
Other Authors: Koster, Jan , Ebus, Marli E. , Van Sluis, Peter , Westerhout, Ellen M. , De Preter, Katleen , Gisselsson, David , Øra, Ingrid , Speleman, Frank , Caron, Huib N. , Versteeg, Rogier
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 1045-2257 ; E-ISSN: 1098-2264 ; DOI: 10.1002/gcc.20926
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recordid: wj10.1002/gcc.20926
title: Copy number defects of G1‐Cell cycle genes in neuroblastoma are frequent and correlate with high expression of E2F target genes and a poor prognosis
format: Article
creator:
  • Molenaar, Jan J.
  • Koster, Jan
  • Ebus, Marli E.
  • Van Sluis, Peter
  • Westerhout, Ellen M.
  • De Preter, Katleen
  • Gisselsson, David
  • Øra, Ingrid
  • Speleman, Frank
  • Caron, Huib N.
  • Versteeg, Rogier
subjects:
  • Medicine
  • Biology
ispartof: Genes, Chromosomes and Cancer, January 2012, Vol.51(1), pp.10-19
description: The tightly controlled network of cell cycle genes consists of a core of cyclin dependent kinases (CDKs) that are activated by periodically expressed cyclins. The activity of the cyclin‐CDK complexes is regulated by cyclin dependent kinase inhibitors (CDKIs) and multiple signal transduction routes that converge on the cell cycle. Neuroblastoma are pediatric tumors that belong to the group of small round blue cell tumors, characterized by a fast proliferation. Here, we present high throughput analyses of cell cycle regulating genes in neuroblastoma. We analyzed a series of 82 neuroblastomas by comparative genomic hybridization arrays, single nucleotide polymorphism arrays, and Affymetrix expression arrays and analyzed the datasets in parallel with the R2 bioinformatic tool (). About 30% of the tumors had genomic amplifications, gains, or losses with shortest regions of overlap that suggested implication of a series of G1 cell cycle regulating genes. (cyclin D1) and were amplified or gained and the chromosomal regions containing the () group of CDKIs were frequently deleted. Cluster analysis showed that tumors with genomic aberrations in G1 regulating genes over‐expressed target genes, which regulate S and G2/M phase progression. These tumors have a poor prognosis. Our findings suggest that pharmacological inhibition of cell cycle genes might bear therapeutic promises for patients with high risk neuroblastoma. © 2011 Wiley Periodicals, Inc.
language: eng
source:
identifier: ISSN: 1045-2257 ; E-ISSN: 1098-2264 ; DOI: 10.1002/gcc.20926
fulltext: fulltext
issn:
  • 1045-2257
  • 10452257
  • 1098-2264
  • 10982264
url: Link


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titleCopy number defects of G1‐Cell cycle genes in neuroblastoma are frequent and correlate with high expression of E2F target genes and a poor prognosis
creatorMolenaar, Jan J. ; Koster, Jan ; Ebus, Marli E. ; Van Sluis, Peter ; Westerhout, Ellen M. ; De Preter, Katleen ; Gisselsson, David ; Øra, Ingrid ; Speleman, Frank ; Caron, Huib N. ; Versteeg, Rogier
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descriptionThe tightly controlled network of cell cycle genes consists of a core of cyclin dependent kinases (CDKs) that are activated by periodically expressed cyclins. The activity of the cyclin‐CDK complexes is regulated by cyclin dependent kinase inhibitors (CDKIs) and multiple signal transduction routes that converge on the cell cycle. Neuroblastoma are pediatric tumors that belong to the group of small round blue cell tumors, characterized by a fast proliferation. Here, we present high throughput analyses of cell cycle regulating genes in neuroblastoma. We analyzed a series of 82 neuroblastomas by comparative genomic hybridization arrays, single nucleotide polymorphism arrays, and Affymetrix expression arrays and analyzed the datasets in parallel with the R2 bioinformatic tool (). About 30% of the tumors had genomic amplifications, gains, or losses with shortest regions of overlap that suggested implication of a series of G1 cell cycle regulating genes. (cyclin D1) and were amplified or gained and the chromosomal regions containing the () group of CDKIs were frequently deleted. Cluster analysis showed that tumors with genomic aberrations in G1 regulating genes over‐expressed target genes, which regulate S and G2/M phase progression. These tumors have a poor prognosis. Our findings suggest that pharmacological inhibition of cell cycle genes might bear therapeutic promises for patients with high risk neuroblastoma. © 2011 Wiley Periodicals, Inc.
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descriptionThe tightly controlled network of cell cycle genes consists of a core of cyclin dependent kinases (CDKs) that are activated by periodically expressed cyclins. The activity of the cyclin‐CDK complexes is regulated by cyclin dependent kinase inhibitors (CDKIs) and multiple signal transduction routes that converge on the cell cycle. Neuroblastoma are pediatric tumors that belong to the group of small round blue cell tumors, characterized by a fast proliferation. Here, we present high throughput analyses of cell cycle regulating genes in neuroblastoma. We analyzed a series of 82 neuroblastomas by comparative genomic hybridization arrays, single nucleotide polymorphism arrays, and Affymetrix expression arrays and analyzed the datasets in parallel with the R2 bioinformatic tool (). About 30% of the tumors had genomic amplifications, gains, or losses with shortest regions of overlap that suggested implication of a series of G1 cell cycle regulating genes. (cyclin D1) and were amplified or gained and the chromosomal regions containing the () group of CDKIs were frequently deleted. Cluster analysis showed that tumors with genomic aberrations in G1 regulating genes over‐expressed target genes, which regulate S and G2/M phase progression. These tumors have a poor prognosis. Our findings suggest that pharmacological inhibition of cell cycle genes might bear therapeutic promises for patients with high risk neuroblastoma. © 2011 Wiley Periodicals, Inc.
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abstractThe tightly controlled network of cell cycle genes consists of a core of cyclin dependent kinases (CDKs) that are activated by periodically expressed cyclins. The activity of the cyclin‐CDK complexes is regulated by cyclin dependent kinase inhibitors (CDKIs) and multiple signal transduction routes that converge on the cell cycle. Neuroblastoma are pediatric tumors that belong to the group of small round blue cell tumors, characterized by a fast proliferation. Here, we present high throughput analyses of cell cycle regulating genes in neuroblastoma. We analyzed a series of 82 neuroblastomas by comparative genomic hybridization arrays, single nucleotide polymorphism arrays, and Affymetrix expression arrays and analyzed the datasets in parallel with the R2 bioinformatic tool (). About 30% of the tumors had genomic amplifications, gains, or losses with shortest regions of overlap that suggested implication of a series of G1 cell cycle regulating genes. (cyclin D1) and were amplified or gained and the chromosomal regions containing the () group of CDKIs were frequently deleted. Cluster analysis showed that tumors with genomic aberrations in G1 regulating genes over‐expressed target genes, which regulate S and G2/M phase progression. These tumors have a poor prognosis. Our findings suggest that pharmacological inhibition of cell cycle genes might bear therapeutic promises for patients with high risk neuroblastoma. © 2011 Wiley Periodicals, Inc.
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pubWiley Subscription Services, Inc., A Wiley Company
doi10.1002/gcc.20926
pages10-19
date2012-01