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
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.