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Article: Pathogenesis of pre-neoplastic lesions of the stomach: Targets for prevention

TitlePathogenesis of pre-neoplastic lesions of the stomach: Targets for prevention
Authors
Issue Date2004
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/DDI
Citation
Digestive Diseases, 2004, v. 22 n. 4, p. 306-312 How to Cite?
AbstractGastric atrophy and intestinal metaplasia are generally considered to be precancerous lesions of the stomach. Chronic Helicobacter pylori infection is one the most important factors in the development of these pre-malignant gastric lesions. In addition to bacterial factors, polymorphisms in the cytokine genes of the host that modulate inflammatory responses are found to have a synergistic effect in the development of gastric cancer as well as pre-neoplastic lesions. Recently, inappropriate activation of the intestine-specific transcription factor like the homeobox gene complex CDX1 and CDX2 are found to be an important contributing factor in the induction of intestinal metaplasia in the stomach. Aberrant expression of cyclooxygenase-2 and epigenetic changes are also frequently detected in pre-neoplastic gastric lesions. One of the most important questions relating to these pre-neoplastic gastric lesions is that whether H. pylori eradication could reverse these changes. However, most controlled studies showed no or just modest improvement in intestinal metaplasia after H. pylori eradication. Further studies should evaluate the role of other chemopreventive agents, particularly cyclooxygenase-2 inhibitor, on regression of pre-neoplastic lesions. Copyright © 2004 S. Karger AG.
Persistent Identifierhttp://hdl.handle.net/10722/162860
ISSN
2015 Impact Factor: 1.777
2015 SCImago Journal Rankings: 0.877
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:24:30Z-
dc.date.available2012-09-05T05:24:30Z-
dc.date.issued2004en_US
dc.identifier.citationDigestive Diseases, 2004, v. 22 n. 4, p. 306-312en_US
dc.identifier.issn0257-2753en_US
dc.identifier.urihttp://hdl.handle.net/10722/162860-
dc.description.abstractGastric atrophy and intestinal metaplasia are generally considered to be precancerous lesions of the stomach. Chronic Helicobacter pylori infection is one the most important factors in the development of these pre-malignant gastric lesions. In addition to bacterial factors, polymorphisms in the cytokine genes of the host that modulate inflammatory responses are found to have a synergistic effect in the development of gastric cancer as well as pre-neoplastic lesions. Recently, inappropriate activation of the intestine-specific transcription factor like the homeobox gene complex CDX1 and CDX2 are found to be an important contributing factor in the induction of intestinal metaplasia in the stomach. Aberrant expression of cyclooxygenase-2 and epigenetic changes are also frequently detected in pre-neoplastic gastric lesions. One of the most important questions relating to these pre-neoplastic gastric lesions is that whether H. pylori eradication could reverse these changes. However, most controlled studies showed no or just modest improvement in intestinal metaplasia after H. pylori eradication. Further studies should evaluate the role of other chemopreventive agents, particularly cyclooxygenase-2 inhibitor, on regression of pre-neoplastic lesions. Copyright © 2004 S. Karger AG.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/DDIen_US
dc.relation.ispartofDigestive Diseasesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCyclooxygenase Inhibitors - Therapeutic Useen_US
dc.subject.meshHumansen_US
dc.subject.meshPrecancerous Conditions - Etiology - Prevention & Controlen_US
dc.subject.meshRisk Factorsen_US
dc.subject.meshStomach Neoplasms - Etiology - Prevention & Controlen_US
dc.titlePathogenesis of pre-neoplastic lesions of the stomach: Targets for preventionen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000083591en_US
dc.identifier.pmid15812152-
dc.identifier.scopuseid_2-s2.0-21844439018en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21844439018&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue4en_US
dc.identifier.spage306en_US
dc.identifier.epage312en_US
dc.identifier.isiWOS:000228072200003-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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