Review

Nature Reviews Cancer 2, 605-615 (August 2002) | doi:10.1038/nrc861

p73: Friend or foe in tumorigenesis

Gerry Melino1, Vincenzo De Laurenzi1 & Karen H. Vousden2  About the authors

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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 DeltaNp73 — 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?

Author affiliations

  1. Biochemistry Laboratory, IDI-IRCCS, c/o Department of Experimental Medicine and Biochemical Sciences, University of Rome 'Tor Vergata', 00133 Rome, Italy.
  2. Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick, Maryland 21702, USA.

Correspondence to: Gerry Melino1 Email: gerry.melino@uniroma2.it

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