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Lookup NU author(s): Dr Jane Carr-Wilkinson, Dr Emma Bell, Professor Andrew Pearson, Professor John LunecORCiD, Professor Deborah Tweddle
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p53 mutations have been reported in cell lines derived from relapsed neuroblastoma tumors. We hypothesize that functional inactivation of p53 by mutation or other mechanisms is common in relapsed neuroblastoma and can contribute to chemoresistance. Our aim was to determine the frequency of p53 mutations, p14ARF methylation, or deletion and MDM2 amplification in 23 neuroblastoma cell lines (6 derived at diagnosis and 17 derived at relapse). One cell line was p53 mutant (BE2c) and two cell lines were deleted for p14 ARF (LAN-6 and SHEP). Two cell lines were methylated for p14 ARF (GIMEN and pER-108), one of which had low levels of p14 ARF mRNA expression which increased following demethylation with 5-aza-2/deoxycytidine treatment (GIMEN), and four cell lines were confirmed to be MDM2 -amplified. All these cell lines were derived from neuroblastomas at relapse. Inactivation of the p53 pathway was observed in 9 out of 17 neuroblastoma cell lines (53%) established at relapse and in none of the cell lines established from pretreatment tumors. If these data are confirmed in neuroblastoma tumors, this suggests that p53-independent therapy and reactivation of inactive p53 approaches would be useful in the management of relapsed neuroblastoma. ©2006 American Association for Cancer Research.
Author(s): Carr J, Bell E, Pearson ADJ, Kees U, Beris H, Lunec J, Tweddle DA
Publication type: Article
Publication status: Published
Journal: Cancer Research
Year: 2006
Volume: 66
Issue: 4
Pages: 2138-2145
Print publication date: 15/02/2006
ISSN (print): 0008-5472
ISSN (electronic): 1538-7445
URL: http://dx.doi.org/10.1158/0008-5472.CAN-05-2623
DOI: 10.1158/0008-5472.CAN-05-2623
PubMed id: 16489014
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