Importance of changes in epithelial cell turnover during Helicobacter pylori infection in gastric carcinogenesis
M Antia, A Armuzzia, A Gasbarrinib, G Gasbarrinia
a Cattedra di Medicina Interna II, Università
Cattolica del Sacro Cuore, Largo F. Vito 1, 00168 Rome, Italy, b Istituto di Patologia Medica, Università Cattolica
del Sacro Cuore, Rome, Italy
Correspondence to: Dr Anti.
| The first 150 words of the full text of this article appear below. |
| |
Summary |
|---|
The role of Helicobacter pylori in gastric
carcinogenesis is supported almost exclusively by epidemiological data
and prospective histopathological studies. From biological and
molecular points of view, there is no evidence that H
pylori or its cytotoxic products have any mutagenic effects.
Nevertheless, this infection is associated with profound changes in the
pattern of epithelial cell turnover in gastric glands, though the
importance of these changes in gastric carcinogenesis is still
controversial. H pylori infection increases cell
proliferation and alters the distribution of cycling cells within these
glands, but these changes can be reversed by successful eradication of
the infection. Apoptosis seems to be increased in gastric epithelial
cells during H pylori infection, as shown by in vitro
studies. There is some, though no conclusive, evidence that this
finding also occurs in H pylori positive subjects. It seems that cagA status influences the effect of H
pylori on epithelial apoptosis in
This article has been cited by other articles:
-
Hofman, V., Lassalle, S., Selva, E., Kalem, K., Steff, A., Hebuterne, X., Sicard, D., Auberger, P., Hofman, P.
(2007). Involvement of mast cells in gastritis caused by Helicobacter pylori: a potential role in epithelial cell apoptosis. J. Clin. Pathol.
60: 600-607
[Abstract] [Full Text] -
Backert, S., Schwarz, T., Miehlke, S., Kirsch, C., Sommer, C., Kwok, T., Gerhard, M., Goebel, U. B., Lehn, N., Koenig, W., Meyer, T. F.
(2004). Functional Analysis of the cag Pathogenicity Island in Helicobacter pylori Isolates from Patients with Gastritis, Peptic Ulcer, and Gastric Cancer. Infect. Immun.
72: 1043-1056
[Abstract] [Full Text] -
Kwok, T., Backert, S., Schwarz, H., Berger, J., Meyer, T. F.
(2002). Specific Entry of Helicobacter pylori into Cultured Gastric Epithelial Cells via a Zipper-Like Mechanism. Infect. Immun.
70: 2108-2120
[Abstract] [Full Text] -
Kim, T. I., Lee, Y. C., Lee, K. H., Han, J. H., Chon, C. Y., Moon, Y. M., Kang, J. K., Park, I. S.
(2001). Effects of Nonsteroidal Anti-Inflammatory Drugs on Helicobacter pylori-Infected Gastric Mucosae of Mice: Apoptosis, Cell Proliferation, and Inflammatory Activity. Infect. Immun.
69: 5056-5063
[Abstract] [Full Text] -
Shirin, H., Sordillo, E. M., Kolevska, T. K., Hibshoosh, H., Kawabata, Y., Oh, S. H., Kuebler, J. F., Delohery, T., Weghorst, C. M., Weinstein, I. B., Moss, S. F.
(2000). Chronic Helicobacter pylori Infection Induces an Apoptosis-Resistant Phenotype Associated with Decreased Expression of p27kip1. Infect. Immun.
68: 5321-5328
[Abstract] [Full Text] -
Shirin, H., Sordillo, E. M., Oh, S. H., Yamamoto, H., Delohery, T., Weinstein, I. B., Moss, S. F.
(1999). Helicobacter pylori Inhibits the G1 to S Transition in AGS Gastric Epithelial Cells. Cancer Res.
59: 2277-2281
[Abstract] [Full Text]
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
