PATTERN OF PS2 PROTEIN EXPRESSION IN PREMALIGNANT AND MALIGNANT LESIONS OF GASTRIC-MUCOSA

Citation
Jc. Machado et al., PATTERN OF PS2 PROTEIN EXPRESSION IN PREMALIGNANT AND MALIGNANT LESIONS OF GASTRIC-MUCOSA, European journal of cancer prevention, 5(3), 1996, pp. 169-179
Citations number
48
Categorie Soggetti
Oncology
ISSN journal
09598278
Volume
5
Issue
3
Year of publication
1996
Pages
169 - 179
Database
ISI
SICI code
0959-8278(1996)5:3<169:POPPEI>2.0.ZU;2-D
Abstract
The aim of this study was to evaluate the pattern of pS2 protein expre ssion in premalignant and malignant lesions of gastric epithelium, We analysed, by immunohistochemistry, the pS2 expression in six samples o f normal gastric mucosa, 18 cases of chronic atrophic gastritis with i ntestinal metaplasia (IM), 10 hyperplastic polyps, 11 adenomatous poly ps and 50 gastric carcinomas, together with the respective samples of adjacent non-neoplastic mucosa, pS2 is expressed throughout foveolar a nd superficial epithelium of normal gastric mucosa and this pattern is retained in chronic atrophic gastritis out of IM lesions, pS2 express ion is confined to goblet cells in complete rm and occurs both in gobl et and columnar cells in incomplete IM, Hyperplastic polyps displayed significantly higher pS2 expression than adenomatous polyps, In gastri c carcinomas, pS2 expression was observed in 66.0% of cases, being sig nificantly higher in diffuse (88.9%) than intestinal type carcinomas ( 53.6%), A subset of carcinomas of the latter group displayed pS2 immun oreactivity in a high percentage of cells with a pattern similar to th at of hyperplastic polyps, Our results demonstrate there are major cha nges in pS2 expression, which can be used as a marker of gastric-type differentiation during the process of gastric carcinogenesis, and supp ort the existence of at least two pathways of malignant transformation of gastric mucosa: one via intestinal metaplasia and adenomatous dysp lasia, leading to glandular carcinomas with intestinal-type differenti ation, the other via hyperplastic changes or de novo changes, leading to diffuse carcinomas and to a subset of glandular carcinomas displayi ng gastric-type differentiation.