Journal
CANCER LETTERS
Volume 197, Issue 1-2, Pages 93-98Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0304-3835(03)00088-0
Keywords
neuroblastoma; p53; mutation; MYCN; MDM2; drug resistance; therapy; survival; cytotoxic; relapse
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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 G, 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. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.
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