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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 (UGent), Anne De Paepe (UGent) and Franki Speleman (UGent)
(2009) Cell Death & Differentiation. 16(12). p.1563-1572
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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.
Keywords
p14ARF, MDM2, antitumor barrier, neuroblastoma, p53

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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.
@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},
}

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