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 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.
Department of Medicine, St Luke's-Roosevelt Hospital Center/Columbia University, New York, NY 10025, USA.
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D000818:Animals; D017209:Apoptosis; D015415:Biomarkers; D002455:Cell Division; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53 / Q000235:genetics; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori; D006801:Humans; D007414:Intestinal Neoplasms / Q000209:etiology / Q000235:genetics / Q000473:pathology*; D009154:Mutation; D018125:Receptors, Transforming Growth Factor beta / Q000145:classification / Q000235:genetics / Q000502:physiology; D013274:Stomach Neoplasms / Q000209:etiology / Q000235:genetics / Q000473:pathology*
D015415:Biomarkers; D018125:Receptors, Transforming Growth Factor beta