EFFECT OF HELICOBACTER-PYLORI ERADICATION ON GASTRIC EPITHELIAL PROLIFERATION - RELATIONSHIP WITH RAS ONCOGENE P21 EXPRESSION

Citation
E. Ierardi et al., EFFECT OF HELICOBACTER-PYLORI ERADICATION ON GASTRIC EPITHELIAL PROLIFERATION - RELATIONSHIP WITH RAS ONCOGENE P21 EXPRESSION, The Italian Journal of Gastroenterology, 29(3), 1997, pp. 214-219
Citations number
43
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
03920623
Volume
29
Issue
3
Year of publication
1997
Pages
214 - 219
Database
ISI
SICI code
0392-0623(1997)29:3<214:EOHEOG>2.0.ZU;2-K
Abstract
Background. Impaired changes in gastric epithelium proliferation have been described in Helicobacter pylori infection, and a progressive inc rease of proliferating cells has been shown with the progression of mu cosal lesions. Aims, Purpose of this investigation was to study the ef fect of eradication on bacterium-induced proliferative changes, evalua ted by the proliferating cell nuclear antigen labelling index (PCNA LI ) and its relationship to the ras oncoprotein p21, involved in early e vents of gastric carcinogenesis. Patients and methods, This restrospec tive study was performed before and after therapy in five different gr oups of patients with progressive stages of Helicobacter pylori damage (N. normality: HG: histological gastritis with normal endoscopy, EHG. histological gastritis with endoscopic chronic erosions; CIM: complet e intestinal metaplasia; IIM: incomplete intestinal metaplasia). Resul ts, Six months after eradication, a normalization of PCNA LI was obser ved in the areas of gastritis, but not in those of intestinal metaplas ia, which showed an unchanged type. Moreover immunohistochemical membr ane expression of ras oncoprotein p21 was only associated to intestina l metaplasia. The protein was also expressed in the cytoplasm in 3 pat ients with incomplete type. Conclusions. These results suggest that th e development of intestinal metaplasia may be associated with an alter ation in the control of gastric epithelium proliferation and could rep resent an initial stage in gastric carcinogenesis. Nevertheless, furth er genetic changes are necessary for a complete progression to neoplas tic disease. A long-term follow-up on extension, type, proliferative s ituation and oncoprotein expression in areas of intestinal metaplasia may be helpful to explain whether the present data provide new informa tion on the mechanism of Helicobacter pylori induced gastric carcinoge nesis.