The present study was designed to explore the role of p73 in response to cisplatin. In contrast to cisplatin-resistant ovarian carcinoma cells, pharmacological drug concentrations, which caused induction of p53, induced a marginal increase of p73 in sensitive cells. The effect was more marked at high concentrations, with no evidence of p21(WAF1) induction. This behaviour, associated with substantial apoptosis, suggests cell inability to activate DNA damage checkpoint following extensive stress. Although p73 appears to be implicated mainly in response to high stress conditions, the available results support a cooperation between p53 and p73 in cisplatin-induced apoptosis in sensitive cells.