BACKGROUND: The p73 gene is a p53 homologue that induces apoptosis and inhibits 
cell proliferation. N-terminal truncated isoforms of p73 (DeltaNp73) act as 
dominant-negative inhibitors of wild-type p53 and TAp73 and result in tumour 
growth in nude mice.
AIMS: To detect DeltaNp73 expression in 24 benign prostatic hyperplasia samples, 
33 prostate carcinomas, and five normal samples and to evaluate the relation 
between DeltaNp73, TAp73 concentrations, and the clinicopathological 
characteristics of patients with prostate cancer.
METHODS: TAp73 was determined by real time polymerase chain reaction (PCR); 
DeltaNp73 and DeltaN'p73 were assessed using reverse transcription PCR. western 
blotting was used to analyse protein expression. p53 mutation was determined by 
immunohistochemistry.
RESULTS: A significant increase of DeltaNp73 was seen in 20 of 33 carcinomas and 
17 of 24 benign prostate hyperplasia tissues, but in none of the normal samples. 
None of the specimens expressed DeltaN'p73. No significant relation was found 
between TAp73 expression and clinical parameters. The incidence of positive 
expression of DeltaNp73 correlated with the Gleason score in prostate 
carcinomas. Cancer samples with wild-type p53 had significantly higher 
expression of DeltaNp73 than p53 mutant cancers.
CONCLUSION: These data suggest a potential role for DeltaNp73 in prostate cancer 
progression.