1993
DOI: 10.1136/gut.34.10.1339
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Systemic and mucosal humoral responses to Helicobacter pylori in gastric cancer.

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Cited by 208 publications
(108 citation statements)
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“…In agreement with the results obtained in other western populations (Crabtree et al 1993, Klaamas et al 1996, Holtmann et al 1998, in the present study, serum antiCagA antibodies were detected more frequently in gastric carcinoma and duodenal ulcer patients than in H. pyloripositive patients without these diseases. Infection with cagA-positive strains has been associated with higher degree of gastric mucosa inflammation, a risk for the development of the diseases associated with infection.…”
Section: Discussionsupporting
confidence: 93%
“…In agreement with the results obtained in other western populations (Crabtree et al 1993, Klaamas et al 1996, Holtmann et al 1998, in the present study, serum antiCagA antibodies were detected more frequently in gastric carcinoma and duodenal ulcer patients than in H. pyloripositive patients without these diseases. Infection with cagA-positive strains has been associated with higher degree of gastric mucosa inflammation, a risk for the development of the diseases associated with infection.…”
Section: Discussionsupporting
confidence: 93%
“…There is evidence that H. pylori is frequently found in gastric biopsy specimens from individuals with atrophic gastritis, intestinal metaplasia and gastric cancer, and that with the development of advanced gastric tumors, the bacteria can be lost from the stomach (20,21) . With loss of infection, the level of circulating anti-H. pylori antibodies will fall, so that patients with gastric cancer may be H. pylori seronegative even though they have been infected in the past (10) . Most researchers believe that the pathogenesis of human gastric cancer is a multifactorial and multistage process (13,19,22) .…”
Section: Introductionmentioning
confidence: 99%
“…CagA, a 120-to 145-kDa bacterial protein, is recognized as a major etiologic determinant of Helicobacter pylori-associated gastric disease found to increase the risk for peptic ulceration (14,15,23), atrophic gastritis (20) and non-cardia gastric adenocarcinoma (12,25). After H. pylori binding to the gastric epithelium, CagA has been shown to translocate into the gastric epithelial cell cytoplasm via the H. pylori type IV secretion system (24).…”
mentioning
confidence: 99%