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The p53 pathway and its inactivation in neuroblastoma

Lookup NU author(s): Professor Deborah Tweddle, Professor Andrew Pearson, Professor John Lunec

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Abstract

Early studies of p53 in neuroblastoma reported infrequent mutations in tumours and cell lines. Cytoplasmic sequestration was later proposed as an alternative mechanism of inactivation, but many studies have since reported an intact p53 pathway in neuroblastoma cell lines, as detected by nuclear p53 accumulation after DNA damage, intact DNA binding, transcriptional activation of target genes and the induction of apoptosis. In some MYCN amplified cell lines however, an irradiation induced G1 arrest does not occur, despite the presence of normal p53. Neuroblastoma usually responds to chemotherapy but frequently relapses, and there is evidence from tumours, and cell lines that p53 inactivation via mutation or MDM2amplification occurs at relapse and is sometimes associated with multidrug resistance. If p53 inactivation occurs frequently in relapsed tumours it may be appropriate to include p53 independent therapies in the initial management of high-risk neuroblastoma. © 2003 Elsevier Science Ireland Ltd. All rights reserved.


Publication metadata

Author(s): Tweddle, D.A., Pearson, A.D.J., Haber, M., Norris, M., Xue, C., Flemming, C., Lunec, J.

Publication type: Article

Publication status: Published

Journal: Cancer Letters

Year: 2003

Volume: 197

Issue: 1-2

Pages: 93-98

Print publication date: 18/07/2003

ISSN (print): 0304-3835

ISSN (electronic):

URL: http://dx.doi.org/10.1016/S0304-3835(03)00088-0

DOI: 10.1016/S0304-3835(03)00088-0

PubMed id: 12880966


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