Biological and clinical role of p73 in neuroblastoma

• Published in: Cancer letters Vol. 197; no. 1; pp. 111 - 117
• Main Authors: Romani, M., Tonini, G.P., Banelli, B., Allemanni, G., Mazzocco, K., Scaruffi, P., Boni, L., Ponzoni, M., Pagnan, G., Raffaghello, L., Ferrini, S., Croce, M., Casciano, I.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 18.07.2003; Elsevier Limited
• Subjects: Alternative Splicing; Apoptosis; Apoptosis - physiology; Binding sites; Cancer; Chromosomes; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; DNA-Binding Proteins - physiology; Genes; Genes, Tumor Suppressor; Humans; Methylation; Neuroblastoma; Neuroblastoma - genetics; Neuroblastoma - metabolism; Neuroblastoma - pathology; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Nuclear Proteins - physiology; p73; Prognosis; Survival Rate; Tumor Protein p73; Tumor suppressor gene; Tumor Suppressor Proteins; Tumors; Neuroblastoma; Methylation; p73; Apoptosis; Tumor suppressor gene
• ISSN: 0304-3835; 1872-7980
• DOI: 10.1016/S0304-3835(03)00092-2

The p73 gene is a p53 homologue localized at 1p36.3, a chromosomal region frequently deleted in neuroblastoma. p73 was originally considered an oncosuppressor gene. However, it was soon realized that its mode of action did not resemble that of a classic anti-oncogene. The recent discovery of N-terminal truncated isoforms, with oncogenic properties, showed that p73 has a ‘two in one’ structure. Indeed, the full-length variants are strong inducers of apoptosis while the truncated isoforms inhibit the pro-apoptotic activity of p53 and of the full-length p73. This review summarizes some aspects of p73 biology with particular reference to its possible role in neuroblastoma.