Brief Reports
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 28, 2005; 11(28): 4400-4403
Published online Jul 28, 2005. doi: 10.3748/wjg.v11.i28.4400
Relationship between β-catenin expression and epithelial cell proliferation in gastric mucosa with intestinal metaplasia
Adriana Romiti, Angelo Zullo, Francesco Borrini, Ida Sarcina, Cesare Hassan, Simon Winn, Silverio Tomao, Aldo Vecchione, Sergio Morini, Pietro Mingazzini
Adriana Romiti, Ida Sarcina, Aldo Vecchione, Medical Oncology, “Sant’Andrea” Hospital, Rome, Italy
Angelo Zullo, Cesare Hassan, Simon Winn, Sergio Morini, Gastroenterology and Digestive Endoscopy, “Nuovo Regina Margherita” Hospital, Rome, Italy
Francesco Borrini, Pietro Mingazzini, Department of Experimental Medicine and Pathology, “La Sapienza” University, Rome, Italy
Silverio Tomao, Oncology, IRCCS “Regina Elena”, Rome, Italy
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Adriana Romiti, Ospedale “S. Andrea”, Oncologia Medica, Via di Grottarossa 1035, Rome 00189, Italy. sanoncol@libero.it
Telephone: +39-6-80345338 Fax: +39-6-80345001
Received: March 23, 2004
Revised: January 1, 2005
Accepted: January 5, 2005
Published online: July 28, 2005
Abstract

AIM: To investigate β-catenin expression in patients with intestinal metaplasia, and to look for a possible relationship between β-catenin expression and either epithelial proliferation values or Helicobacter pylori (H pylori) infection.

METHODS: Twenty patients with complete type intestinal metaplasia were studied. β-catenin expression and epithelial cell proliferation in antral mucosa were assessed using an immunohistochemical analysis. H pylori infection was detected by histology and a rapid urease test.

RESULTS: Reduced β-catenin expression on the surface of metaplastic cells was detected in 13 (65%) out of 20 patients. Moreover, in eight (40%) patients intranuclear expression of β-catenin was found. When patients were analyzed according to H pylori infection, the prevalence of both β-catenin reduction at the cell surface and its intranuclear localization did not significantly differ between infected and uninfected patients. Cell proliferation was higher in patients with intranuclear β-catenin expression as compared to the remaining patients, although the difference failed to reach the statistical significance (36 ± 8.9 vs 27.2 ± 11.4, P = 0.06). On the contrary, a similar cell proliferation value was observed between patients with reduced expression of β-catenin on cell surface and those with a normal expression (28.1 ± 11.8 vs 26.1 ± 8.8, P = 0.7). H pylori infection significantly increased cell proliferation (33.3 ± 10.2% vs 24.6 ± 7.4%, respectively, P = 0.04).

CONCLUSION: Both cell surface reduction and intranuclear accumulation of β-catenin were detected in intestinal metaplasia. The intranuclear localization of β-catenin increases cell proliferation. H pylori infection does not seem to play a direct role in β-catenin alterations, whilst it significantly increases cell proliferation.

Keywords: β-catenin; Intestinal metaplasia; Proliferation; Helicobacter pylori