SHORT REPORT

p73 gene mutations in gastric adenocarcinomas

E Pilozzi¹, C Talerico¹, A Platt², C Fidler² and L Ruco¹

¹ Department of Experimental Medicine and Pathology, II Facoltà di Medicina e Chirurgia, Ospedale Sant’Andrea, Università "La Sapienza", Roma, Italy
² Department of Cellular Science, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, UK

Correspondence to:
Correspondence to:
Dr E Pilozzi, Servizio di Istopatologia, Ospedale Sant’Andrea, Via di Grottarossa 1035–39, 00189 Roma, Italy;
emanuela.pilozzi{at}uniroma1.it

Background/Aims: The p73 gene encodes a protein that shares structural and functional homology with the p53 gene product. The highest degree of homology is in the DNA binding domain, which is the region of p53 that is most frequently mutated in cancer. In contrast to p53 there is little evidence that p73 acts as a classic tumour suppressor gene. Because of the similarities between the p53 and p73 genes and the high frequency of mutation of p53, this study was designed to investigate the p73 gene in patients with gastric adenocarcinoma.

Methods: The mutational status of the p73 gene was investigated in a series of 13 cases of gastric adenocarcinoma from the antro–pyloric region and the gastro–oesophageal junction, using the polymerase chain reaction, single strand conformational polymorphism, and direct DNA sequencing.

Results: A glutamine to arginine mutation was detected in exon 5 of the p73 gene in a case of adenocarcinoma at the gastro–oesophageal junction.

Conclusion: Although limited to a small series of cases, these results suggest that p73 may have a potential pathogenetic role in this tumour.

Keywords: p73 gene; gastric adenocarcinomas; DNA mutation

Abbreviations: PCR, polymerase chain reaction; SCCP, single strand conformational polymorphism

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