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Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis

Tom Van Maerken UGent, Jo Vandesompele UGent, Ali Rihani, Anne De Paepe UGent and Franki Speleman UGent (2009) Cell Death & Differentiation. 16(12). p.1563-1572
abstract
A primary failsafe program against unrestrained proliferation and oncogenesis is provided by the p53 tumor suppressor protein, inactivation of which is considered as a hallmark of cancer. Intriguingly, mutations of the TP53 gene are rarely encountered in neuroblastoma tumors, suggesting that alternative p53-inactivating lesions account for escape from p53 control in this childhood malignancy. Several recent studies have shed light on the mechanisms by which neuroblastoma cells circumvent the p53-driven antitumor barrier. We review here these mechanisms for evasion of p53-mediated growth control and conclude that deregulation of the p14(ARF)-MDM2-p53 axis seems to be the principal mode of p53 inactivation in neuroblastoma, opening new perspectives for targeted therapeutic intervention.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
p14ARF, MDM2, antitumor barrier, neuroblastoma, p53
journal title
Cell Death & Differentiation
Cell Death Differ.
volume
16
issue
12
pages
1563 - 1572
Web of Science type
Review
Web of Science id
000271783600001
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
8.24 (2009)
JCR rank
23/281 (2009)
JCR quartile
1 (2009)
ISSN
1350-9047
DOI
10.1038/cdd.2009.138
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
835726
handle
http://hdl.handle.net/1854/LU-835726
date created
2010-01-23 22:27:50
date last changed
2016-12-19 15:40:55
@article{835726,
  abstract     = {A primary failsafe program against unrestrained proliferation and oncogenesis is provided by the p53 tumor suppressor protein, inactivation of which is considered as a hallmark of cancer. Intriguingly, mutations of the TP53 gene are rarely encountered in neuroblastoma tumors, suggesting that alternative p53-inactivating lesions account for escape from p53 control in this childhood malignancy. Several recent studies have shed light on the mechanisms by which neuroblastoma cells circumvent the p53-driven antitumor barrier. We review here these mechanisms for evasion of p53-mediated growth control and conclude that deregulation of the p14(ARF)-MDM2-p53 axis seems to be the principal mode of p53 inactivation in neuroblastoma, opening new perspectives for targeted therapeutic intervention.},
  author       = {Van Maerken, Tom and Vandesompele, Jo and Rihani, Ali and De Paepe, Anne and Speleman, Franki},
  issn         = {1350-9047},
  journal      = {Cell Death \& Differentiation},
  keyword      = {p14ARF,MDM2,antitumor barrier,neuroblastoma,p53},
  language     = {eng},
  number       = {12},
  pages        = {1563--1572},
  title        = {Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis},
  url          = {http://dx.doi.org/10.1038/cdd.2009.138},
  volume       = {16},
  year         = {2009},
}

Chicago
Van Maerken, Tom, Jo Vandesompele, Ali Rihani, Anne De Paepe, and Franki Speleman. 2009. “Escape from P53-mediated Tumor Surveillance in Neuroblastoma: Switching Off the p14(ARF)-MDM2-p53 Axis.” Cell Death & Differentiation 16 (12): 1563–1572.
APA
Van Maerken, T., Vandesompele, J., Rihani, A., De Paepe, A., & Speleman, F. (2009). Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis. Cell Death & Differentiation, 16(12), 1563–1572.
Vancouver
1.
Van Maerken T, Vandesompele J, Rihani A, De Paepe A, Speleman F. Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis. Cell Death & Differentiation. 2009;16(12):1563–72.
MLA
Van Maerken, Tom, Jo Vandesompele, Ali Rihani, et al. “Escape from P53-mediated Tumor Surveillance in Neuroblastoma: Switching Off the p14(ARF)-MDM2-p53 Axis.” Cell Death & Differentiation 16.12 (2009): 1563–1572. Print.