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lüll Escape from p53-mediated tumor surveillance in neuroblastoma: switching off the p14(ARF)-MDM2-p53 axis Van Maerken T; Vandesompele J; Rihani A; De Paepe A; Speleman FCell Death Differ 2009[Dec]; 16 (12): 1563-72A 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.|Animals[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Humans[MESH]|Neuroblastoma/genetics/*metabolism/pathology/*therapy[MESH]|Proto-Oncogene Proteins c-mdm2/genetics/*metabolism[MESH]|Signal Transduction[MESH]|Tumor Suppressor Protein p14ARF/*metabolism[MESH]|Tumor Suppressor Protein p53/*metabolism[MESH] |