Review article: Cellular markers in the gastric precancerous process

Gastric cancer is the end result of a chronic process, which usually starts as Helicobacter pylori-associated chronic gastritis. Although some differences exist in the histological intermediary stages and in the frequency and timing of certain molecular alterations, both diffuse and intestinal cance...

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Bibliographic Details
Published in:Alimentary pharmacology & therapeutics 1998-02, Vol.12 Suppl 1, p.91
Main Author: Moss, S F
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biomarkers
Cell Division
Gene Expression Regulation, Neoplastic
Genes, p53 - genetics
Helicobacter Infections - complications
Helicobacter pylori
Humans
Intestinal Neoplasms - etiology
Intestinal Neoplasms - genetics
Intestinal Neoplasms - pathology
Mutation
Receptors, Transforming Growth Factor beta - classification
Receptors, Transforming Growth Factor beta - genetics
Receptors, Transforming Growth Factor beta - physiology
Stomach Neoplasms - etiology
Stomach Neoplasms - genetics
Stomach Neoplasms - pathology
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Summary:Gastric cancer is the end result of a chronic process, which usually starts as Helicobacter pylori-associated chronic gastritis. Although some differences exist in the histological intermediary stages and in the frequency and timing of certain molecular alterations, both diffuse and intestinal cancer are accompanied by some important common cellular changes. These include an increase in cell proliferation, and an alteration in apoptosis, which may be secondary to loss of function of p53 and loss of growth inhibition by growth factor (TGF)-beta, due to mutation of the TGF-beta receptor type II. This review examines the potential role of H. pylori in the aetiology of the molecular changes during the progression to gastric cancer, and explores the usefulness of these changes as biomarkers of increased risk of neoplasia in the intermediate steps of gastric carcinogenesis.
ISSN:0269-2813
DOI:10.1111/j.1365-2036.1998.00002.x