p73, a member of the p53 family, exhibits activities similar to those of p53, 
including the ability to induce growth arrest and apoptosis. p73 influences 
chemotherapeutic responses in human cancer patients, in association with p53. 
Alternative splicing of the TP73 gene produces many p73 C- and N-terminal 
isoforms, which vary in their transcriptional activity towards p53-responsive 
promoters. In this paper, we show that the C-terminal spliced isoforms of the 
p73 protein differ in their DNA-binding capacity, but this is not an accurate 
predictor of transcriptional activity. In different p53-null cell lines, p73beta 
induces either mitochondrial-associated or death receptor-mediated apoptosis, 
and these differences are reflected in different gene expression profiles. In 
addition, p73 induces cell cycle arrest and p21(WAF1) expression in H1299 cells, 
but not in Saos-2. This data shows that TAp73 isoforms act differently depending 
on the tumour cell background, and have important implications for p73-mediated 
therapeutic responses in individual human cancer patients.