Abstract
Background. Impaired changes in gastric epithelium proliferation have been described in Helicobacter pylori infection, and a progressive increase of proliferating cells has been shown with the progression of mucosal lesions. Aims. Purpose of this investigation was to study the effect of eradication on bacterium-induced proliferative changes, evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI) and its relationship to the ras oncoprotein p21, involved in early events of gastric carcinogenesis. Patients and methods. This restrospective study was performed before and after therapy in five different groups 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: complete intestinal metaplasia; IIM: incomplete intestinal metaplasia). Results. Six months after eradication, a normalization of PCNA LI was observed in the areas of gastritis, but not in those of intestinal metaplasia, which showed an unchanged type. Moreover, immunohistochemical membrane expression of ras oncoprotein p21 was only associated to intestinal metaplasia. The protein was also expressed in the cytoplasm in 3 patients with incomplete type. Conclusions. These results suggest that the development of intestinal metaplasia may be associated with an alteration in the control of gastric epithelium proliferation and could represent an initial stage in gastric carcinogenesis. Nevertheless, further genetic changes are necessary for a complete progression to neoplastic disease. A long-term follow-up on extension, type, proliferative situation and oncoprotein expression in areas of intestinal metaplasia may be helpful to explain whether the present data provide new information on the mechanism of Helicobacter pylori induced gastric carcinogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 214-219 |
| Number of pages | 6 |
| Journal | Italian Journal of Gastroenterology and Hepatology |
| Volume | 29 |
| Issue number | 3 |
| Publication status | Published - 1997 |
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Keywords
- Helicobacter pylori
- Intestinal metaplasia
- Proliferating cell nuclear antigen (PCNA)
- ras p21
ASJC Scopus subject areas
- Gastroenterology
Cite this
Effect of Helicobacter pylori eradication on gastric epithelial proliferation. Relationship with ras oncogene p21 expression. / Lerardi, E.; Francavilla, A.; Balzano, T.; Traversa, A.; Principi, M.; Monno ', R. A.; Amoruso, A.; Ingrosso, M.; Pisani, A.; Panella, C.
In: Italian Journal of Gastroenterology and Hepatology, Vol. 29, No. 3, 1997, p. 214-219.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of Helicobacter pylori eradication on gastric epithelial proliferation. Relationship with ras oncogene p21 expression
AU - Lerardi, E.
AU - Francavilla, A.
AU - Balzano, T.
AU - Traversa, A.
AU - Principi, M.
AU - Monno ', R. A.
AU - Amoruso, A.
AU - Ingrosso, M.
AU - Pisani, A.
AU - Panella, C.
PY - 1997
Y1 - 1997
N2 - Background. Impaired changes in gastric epithelium proliferation have been described in Helicobacter pylori infection, and a progressive increase of proliferating cells has been shown with the progression of mucosal lesions. Aims. Purpose of this investigation was to study the effect of eradication on bacterium-induced proliferative changes, evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI) and its relationship to the ras oncoprotein p21, involved in early events of gastric carcinogenesis. Patients and methods. This restrospective study was performed before and after therapy in five different groups 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: complete intestinal metaplasia; IIM: incomplete intestinal metaplasia). Results. Six months after eradication, a normalization of PCNA LI was observed in the areas of gastritis, but not in those of intestinal metaplasia, which showed an unchanged type. Moreover, immunohistochemical membrane expression of ras oncoprotein p21 was only associated to intestinal metaplasia. The protein was also expressed in the cytoplasm in 3 patients with incomplete type. Conclusions. These results suggest that the development of intestinal metaplasia may be associated with an alteration in the control of gastric epithelium proliferation and could represent an initial stage in gastric carcinogenesis. Nevertheless, further genetic changes are necessary for a complete progression to neoplastic disease. A long-term follow-up on extension, type, proliferative situation and oncoprotein expression in areas of intestinal metaplasia may be helpful to explain whether the present data provide new information on the mechanism of Helicobacter pylori induced gastric carcinogenesis.
AB - Background. Impaired changes in gastric epithelium proliferation have been described in Helicobacter pylori infection, and a progressive increase of proliferating cells has been shown with the progression of mucosal lesions. Aims. Purpose of this investigation was to study the effect of eradication on bacterium-induced proliferative changes, evaluated by the proliferating cell nuclear antigen labelling index (PCNA LI) and its relationship to the ras oncoprotein p21, involved in early events of gastric carcinogenesis. Patients and methods. This restrospective study was performed before and after therapy in five different groups 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: complete intestinal metaplasia; IIM: incomplete intestinal metaplasia). Results. Six months after eradication, a normalization of PCNA LI was observed in the areas of gastritis, but not in those of intestinal metaplasia, which showed an unchanged type. Moreover, immunohistochemical membrane expression of ras oncoprotein p21 was only associated to intestinal metaplasia. The protein was also expressed in the cytoplasm in 3 patients with incomplete type. Conclusions. These results suggest that the development of intestinal metaplasia may be associated with an alteration in the control of gastric epithelium proliferation and could represent an initial stage in gastric carcinogenesis. Nevertheless, further genetic changes are necessary for a complete progression to neoplastic disease. A long-term follow-up on extension, type, proliferative situation and oncoprotein expression in areas of intestinal metaplasia may be helpful to explain whether the present data provide new information on the mechanism of Helicobacter pylori induced gastric carcinogenesis.
KW - Helicobacter pylori
KW - Intestinal metaplasia
KW - Proliferating cell nuclear antigen (PCNA)
KW - ras p21
UR - http://www.scopus.com/inward/record.url?scp=0031472630&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031472630&partnerID=8YFLogxK
M3 - Article
C2 - 9646212
AN - SCOPUS:0031472630
VL - 29
SP - 214
EP - 219
JO - Digestive and Liver Disease
JF - Digestive and Liver Disease
SN - 1590-8658
IS - 3
ER -