p73: Friend or foe in tumorigenesis

Gerry Melino; Vincenzo De Laurenzi; Karen H. Vousden

doi:10.1038/nrc861

p73: Friend or foe in tumorigenesis

Gerry Melino, Vincenzo De Laurenzi, Karen H. Vousden

Istituto Dermopatico dell'Immacolata , IDI

Research output: Contribution to journal › Article › peer-review

Abstract

As p53 and its homologue p73 have significant sequence and functional similarities, p73 might also be expected to act as a tumour suppressor. However, p73 is activated after DNA damage in a way that is distinct from that of p53. The existence of ΔNp73 - an isoform of p73 that is encoded by a distinct promoter and that lacks the transactivation domain - further complicates matters. It seems to function as an oncogene by inhibiting both p73- and p53-induced apoptosis. So how can these opposing functions be reconciled in human tumours?

Original language	English
Pages (from-to)	605-615
Number of pages	11
Journal	Nature Reviews Cancer
Volume	2
Issue number	8
DOIs	https://doi.org/10.1038/nrc861
Publication status	Published - Aug 2002

ASJC Scopus subject areas

Cancer Research

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AB - As p53 and its homologue p73 have significant sequence and functional similarities, p73 might also be expected to act as a tumour suppressor. However, p73 is activated after DNA damage in a way that is distinct from that of p53. The existence of ΔNp73 - an isoform of p73 that is encoded by a distinct promoter and that lacks the transactivation domain - further complicates matters. It seems to function as an oncogene by inhibiting both p73- and p53-induced apoptosis. So how can these opposing functions be reconciled in human tumours?

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p73: Friend or foe in tumorigenesis

Abstract

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