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dc.contributor.authorMatysiak-Budnik, Tamara
dc.contributor.authorMégraud, Francis
dc.date.accessioned2009-04-14T07:54:58Z
dc.date.available2009-04-14T07:54:58Z
dc.date.issued2006-04
dc.identifier.citationEur. J. Cancer 2006, 42 (6):708-716en
dc.identifier.issn0959-8049
dc.identifier.pmid16556496
dc.identifier.doi10.1016/j.ejca.2006.01.020
dc.identifier.urihttp://hdl.handle.net/10146/64817
dc.descriptionKEYWORDS CLASSIFICATION: analysis;Animals;complications;Cell Transformation,Neoplastic;dietary modulation of cancer & cancer biomarkers;Diet;Evaluation;France;genetics;Gastritis;Helicobacter Infections;Helicobacter pylori;Humans;lifestyle modulation of cancer & cancer biomarkers;mechanisms of carcinogenesis;microbiology;Models,Animal;pathogenicity;pathology;Paris;Precancerous Conditions;secretion;Stomach Neoplasms;Virulence.en
dc.description.abstractThe pathogenesis of gastric cancer (GC) includes a sequence of events that begins with Helicobacter pylori-induced chronic superficial gastritis, progressing towards atrophic gastritis, intestinal metaplasia, dysplasia and eventually GC. The association between H. pylori and GC is supported by experimental data showing a capacity of H. pylori to induce GC in animals, and the results of interventional studies showing that H. pylori eradication can lower the risk of GC and prevent development of pre-cancerous lesions in humans and in experimental animals. The "driving force" of gastric carcinogenesis is a chronic gastric inflammation, whose intensity and localisation depending on bacterial, host and environmental factors, determines the risk of GC. The mechanisms by which chronic inflammation lead to epithelial and pre-cancerous lesions include induction of oxidative stress, perturbation of the epithelial cells proliferation/apoptosis ratio, and cytokine secretion. Several molecular alterations associated with gastric carcinogenesis have also been described.
dc.language.isoenen
dc.relation.urlhttp://www.ejcancer.info/article/S0959-8049(06)00125-0/abstracten
dc.subjectVirulenceen
dc.subjectcagAen
dc.subjectVacAen
dc.subjectInflammationen
dc.subjectAnimal modelen
dc.subjectPre-cancerous lesionsen
dc.subjectHost factoren
dc.subjectGastritisen
dc.subject.meshAnimals
dc.subject.meshCell Transformation, Neoplastic
dc.subject.meshDiet
dc.subject.meshGastritis
dc.subject.meshHelicobacter Infections
dc.subject.meshHelicobacter pylori
dc.subject.meshHumans
dc.subject.meshModels, Animal
dc.subject.meshPrecancerous Conditions
dc.subject.meshStomach Neoplasms
dc.subject.meshVirulence
dc.titleHelicobacter pylori infection and gastric cancer.en
dc.typeArticleen
dc.identifier.journalEuropean journal of cancer (Oxford, England : 1990)en
html.description.abstractThe pathogenesis of gastric cancer (GC) includes a sequence of events that begins with Helicobacter pylori-induced chronic superficial gastritis, progressing towards atrophic gastritis, intestinal metaplasia, dysplasia and eventually GC. The association between H. pylori and GC is supported by experimental data showing a capacity of H. pylori to induce GC in animals, and the results of interventional studies showing that H. pylori eradication can lower the risk of GC and prevent development of pre-cancerous lesions in humans and in experimental animals. The "driving force" of gastric carcinogenesis is a chronic gastric inflammation, whose intensity and localisation depending on bacterial, host and environmental factors, determines the risk of GC. The mechanisms by which chronic inflammation lead to epithelial and pre-cancerous lesions include induction of oxidative stress, perturbation of the epithelial cells proliferation/apoptosis ratio, and cytokine secretion. Several molecular alterations associated with gastric carcinogenesis have also been described.


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