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Helicobacter pylori infection promotes gastric carcinogenesis in a mice model
Author(s) -
HAN SANGUK,
KIM YOUNGBAE,
JOO HEEJAE,
HAHM KIBAIK,
LEE WONHEUNG,
CHO YONGKWAN,
KIM DAEYONG,
KIM MYUNGWOOK
Publication year - 2002
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2002.02684.x
Subject(s) - helicobacter pylori , carcinogenesis , medicine , gastroenterology , atrophic gastritis , adenocarcinoma , gastritis , cancer , stomach , carcinogen , gastric mucosa , incidence (geometry) , helicobacter , pathology , biology , physics , optics , genetics
Background and Aim: Debate that Helicobacter pylori might play a causative role in gastric carcinogenesis still exists in spite of the World Health Organization’s definition of H. pylori as a class I carcinogen. In order to define the exact role of H. pylori infection in gastric carcinogenesis, we established a mice model of H. pylori infection. Methods: One hundred and forty‐four female C57BL/6 mice were divided into nine groups according to N ‐methyl‐ N ‐nitrosourea (MNU) treatment and H. pylori infection. All mice were killed at the 50th or 80th week after treatment, and their histopathological changes were evaluated according to group. Results: The incidence of gastric adenocarcinoma at the 50th week was 80% in mice treated with both MNU 240 μg/L and H. pylori infection, whereas the incidence was only 27% in mice treated with only MNU 240 μg/L. Although H. pylori caused marked expansion of the proliferative zone at the surface epithelium, H. pylori infection alone caused only chronic atrophic gastritis without any evidence of carcinomas until 80 weeks. The combination of MNU and H. pylori infection also resulted in a significantly higher incidence of gastric adenoma and adenocarcinoma. Significantly higher expressions of proliferating cell nuclear antigen were noted in the gastric mucosa infected with H. pylori compared to controls. Conclusions: These results clearly demonstrated the role of H. pylori infection, rather than direct carcinogens, in promoting gastric carcinogenesis in a mice model. © 2002 Blackwell Science Asia Pty Ltd