Low presence of p53 abnormalities in H. pylori-infected gastric mucosa and in gastric adenocarcinoma |
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Authors: | Pasquale Berloco Francesco Russo Filomena Cariola Mattia Gentile Piero Giorgio Maria Lucia Caruso Anna Maria Valentini Giovanni Di Matteo Alfredo Di Leo |
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Affiliation: | (1) Laboratory of Biochemistry, Scientific Institute for Digestive Diseases, IRCCS “Saverio de Bellis”, 70013 Castellana Grotte (Bari), Italy, IT;(2) Laboratory of Genetics, Scientific Institute for Digestive Diseases, IRCCS “Saverio de Bellis”, Castellana Grotte (Bari), Italy, IT;(3) Endoscopy Unit, Scientific Institute for Digestive Diseases, IRCCS “Saverio de Bellis”, Castellana Grotte (Bari), Italy, IT;(4) Department of Pathology, Scientific Institute for Digestive Diseases, IRCCS “Saverio de Bellis”, Castellana Grotte (Bari), Italy, IT |
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Abstract: | Background: Alterations of the p53 gene and/or its abnormal protein accumulation have been observed in gastric cancer and preneoplastic lesions. Our aim was to assess possible associations between different H. pylori strains and p53 abnormalities in patients with dyspepsia and with gastric cancer. Methods: Seventy-five dyspeptic patients and 40 patients with gastric adenocarcinoma entered the study. H. pylori status was determined by the rapid urease test, histology, and polymerase chain reaction (PCR) analysis. Overexpression of the p53 protein was evaluated by immunohistochemistry. Detection of p53 mutations was done by direct DNA sequencing. Results: Fifty-four of the 75 (72.0%) dyspeptic patients and 27 of the 40 (67.5%) gastric cancer patients showed H. pylori infection. Cytotoxin-associated gene (cagA)-positive strains were found in 31 of the 54 (58%) dyspeptic patients and in 25 of the 27 (92.6%) neoplastic patients. As regards vacA, s2 strains showed the highest prevalence among dyspeptic patients (24 of 54 patients; 44.4%), whereas s1 strains were more expressed among cancer patients (23 of 27; 85.2%). Among the dyspeptic patients, 1 patient with duodenal ulcer showed p53 overexpression. Three mutations were identified by DNA sequencing: one in a patient with normal endoscopic findings and two in patients suffering from gastritis. Among the neoplastic patients, 16 subjects (40%) showed p53 overexpression (9 had diffuse-type and 7 intestinal-type cancer). Four mutations (10%) occurred in patients with intestinal-type gastric cancer. No association between p53 abnormalities (overexpression/mutation) and H. pylori infection was found in either group of patients. Conclusions: These results lead us to hypothesize that H. pylori infection does not affect the p53 pattern in gastric mucosa. Moreover, mutations of the p53 gene do not seem to be a predominant event in gastric carcinogenesis, at least in our populations. Received: December 14, 2001 / Accepted: May 17, 2002 RID="*" ID="*" These authors contributed equally to the work RID="*" ID="*" These authors contributed equally to the work Acknowledgments. The authors would like to thank Mrs B. D'Attoma and Mrs P. Fiorente for their valuable technical assistance, and Mrs M.V.C. Pragnell, B.A., for her help in revising the English. Reprint requests to: A. Di Leo |
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Keywords: | : dyspepsia H. pylori gastric cancer p53 |
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