Open AccessGastric and intestinal phenotypes and histogenesis of advanced glandular stomach cancers in carcinogen‐treated, Helicobacter pylori ‐infected Mongolian gerbils
Author(s) -
Mizoshita Tsutomu,
Tsukamoto Tetsuya,
Takenaka Yoshiharu,
Cao Xueyuan,
Kato Sosuke,
Kaminishi Michio,
Tatematsu Masae
Publication year - 2006
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/j.1349-7006.2006.00135.x
Subject(s) - intestinal metaplasia , stomach , helicobacter pylori , histogenesis , cancer , gastric mucosa , pathology , biology , phenotype , stomach cancer , gastritis , gastroenterology , chronic gastritis , adenocarcinoma , medicine , immunohistochemistry , gene , biochemistry
The Helicobacter pylori ‐infected Mongolian gerbil (MG) has been established as an appropriate animal model for studies of stomach cancer development. However, there have hitherto been no data on the phenotypic classification of glandular stomach cancers in H. pylori ‐infected and non‐infected MG. We therefore examined the phenotypes of 50 and six advanced glandular stomach cancers in H. pylori ‐infected and non‐infected MG, respectively, as well as adjacent non‐neoplastic mucosa, using several gastrointestinal epithelial phenotypic markers. The lesions were divided phenotypically into 21 gastric, 24 gastric‐and‐intestinal mixed, four intestinal and one null types, with 90.0% of the lesions harboring gastric elements and 56.0% demonstrating intestinal phenotypic expression in H. pylori ‐infected MG. All six lesions were classified as gastric type in non‐infected MG. There was no clear correlation with the presence of intestinal metaplasia in surrounding mucosa. In conclusion, our data suggest that most advanced adenocarcinomas retain a gastric cellular phenotype in the glandular MG stomach. Thus, it might be proposed that intestinal metaplasia is a paracancerous phenomenon rather than a premalignant condition. H. pylori infection may trigger intestinalization of both stomach cancers and non‐neoplastic mucosa. ( Cancer Sci 2006; 97: 38 – 44)