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Article: H. pylori genotypes and cytokine gene polymorphisms influence the development of gastric intestinal metaplasia in a chinese population

TitleH. pylori genotypes and cytokine gene polymorphisms influence the development of gastric intestinal metaplasia in a chinese population
Authors
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ajg/index.html
Citation
American Journal Of Gastroenterology, 2006, v. 101 n. 4, p. 714-720 How to Cite?
AbstractBACKGROUND: Cytokine gene polymorphisms and Helicobacter pylori (HP) genotypes have been linked to gastric cancer development in Western countries. We determined the role of host cytokine polymorphisms and bacterial virulent factors in the development of gastric intestinal metaplasia (IM) in a Chinese population with a high background gastric cancer incidence. METHODS: Three hundred two HP-infected noncancer individuals living in Shandong province of China with available DNA were studied. Polymorphisms in different loci of inflammatory cytokines Interleukin IL-1B, IL-1RN, Interleukin IL-8, IL-10, IL-18, tumor necrosis factor-A (TNF-A), and Transforming growth factor (TGF-B), were determined by allelic discriminating TaqMan polymerase chain reaction (PCR) or a variable number of tandem repeats. Presence of HP virulence factors in cagA, vacA, and babA2 were determined by PCR. Baseline gastric biopsies were assessed for the presence of IM. RESULTS: Among HP-infected subjects, carriers of the IL-1B-511 T allele were associated with a modestly greater prevalence of IM (adjusted OR 2.0, 95% CI 1.0-3.7). There was no association between the presence of IM and polymorphisms in other inflammatory cytokines. Although most subjects from this region harbored the virulent HP strains, carriage of the vacA m1 strain was associated with a significantly higher prevalence of IM (adjusted OR 1.8, 1.1-3.0). The presence of both host (IL-1B-511 T) and HP (vacA m1) genotypes further increased the risk of IM (OR 5.7, 2.0-16) when compared with individuals with the low-risk genotype. CONCLUSION: The carriage of proinflammatory IL-1B-511 and HP vacA m1 genotypes was associated with the development of gastric IM in the Chinese. © 2006 by Am. Coll. of Gastroenterology.
Persistent Identifierhttp://hdl.handle.net/10722/162956
ISSN
2015 Impact Factor: 10.383
2015 SCImago Journal Rankings: 3.946
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_US
dc.contributor.authorChan, MCWen_US
dc.contributor.authorTo, KFen_US
dc.contributor.authorMan, EPSen_US
dc.contributor.authorNg, EKWen_US
dc.contributor.authorChu, ESHen_US
dc.contributor.authorLau, JYWen_US
dc.contributor.authorLin, SRen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:25:53Z-
dc.date.available2012-09-05T05:25:53Z-
dc.date.issued2006en_US
dc.identifier.citationAmerican Journal Of Gastroenterology, 2006, v. 101 n. 4, p. 714-720en_US
dc.identifier.issn0002-9270en_US
dc.identifier.urihttp://hdl.handle.net/10722/162956-
dc.description.abstractBACKGROUND: Cytokine gene polymorphisms and Helicobacter pylori (HP) genotypes have been linked to gastric cancer development in Western countries. We determined the role of host cytokine polymorphisms and bacterial virulent factors in the development of gastric intestinal metaplasia (IM) in a Chinese population with a high background gastric cancer incidence. METHODS: Three hundred two HP-infected noncancer individuals living in Shandong province of China with available DNA were studied. Polymorphisms in different loci of inflammatory cytokines Interleukin IL-1B, IL-1RN, Interleukin IL-8, IL-10, IL-18, tumor necrosis factor-A (TNF-A), and Transforming growth factor (TGF-B), were determined by allelic discriminating TaqMan polymerase chain reaction (PCR) or a variable number of tandem repeats. Presence of HP virulence factors in cagA, vacA, and babA2 were determined by PCR. Baseline gastric biopsies were assessed for the presence of IM. RESULTS: Among HP-infected subjects, carriers of the IL-1B-511 T allele were associated with a modestly greater prevalence of IM (adjusted OR 2.0, 95% CI 1.0-3.7). There was no association between the presence of IM and polymorphisms in other inflammatory cytokines. Although most subjects from this region harbored the virulent HP strains, carriage of the vacA m1 strain was associated with a significantly higher prevalence of IM (adjusted OR 1.8, 1.1-3.0). The presence of both host (IL-1B-511 T) and HP (vacA m1) genotypes further increased the risk of IM (OR 5.7, 2.0-16) when compared with individuals with the low-risk genotype. CONCLUSION: The carriage of proinflammatory IL-1B-511 and HP vacA m1 genotypes was associated with the development of gastric IM in the Chinese. © 2006 by Am. Coll. of Gastroenterology.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ajg/index.htmlen_US
dc.relation.ispartofAmerican Journal of Gastroenterologyen_US
dc.subject.meshChinaen_US
dc.subject.meshCytokines - Geneticsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGastric Mucosa - Pathology - Virologyen_US
dc.subject.meshGenes, Viralen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHelicobacter Infections - Pathologyen_US
dc.subject.meshHelicobacter Pylori - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshInterleukins - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMetaplasiaen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshPolymorphism, Geneticen_US
dc.subject.meshPrecancerous Conditions - Genetics - Pathology - Virologyen_US
dc.subject.meshStomach Neoplasms - Genetics - Pathology - Virologyen_US
dc.subject.meshTransforming Growth Factor Beta - Geneticsen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Geneticsen_US
dc.subject.meshVirulence Factors - Metabolismen_US
dc.titleH. pylori genotypes and cytokine gene polymorphisms influence the development of gastric intestinal metaplasia in a chinese populationen_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.doi10.1111/j.1572-0241.2006.00560.xen_US
dc.identifier.pmid16635219-
dc.identifier.scopuseid_2-s2.0-33645452011en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645452011&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume101en_US
dc.identifier.issue4en_US
dc.identifier.spage714en_US
dc.identifier.epage720en_US
dc.identifier.isiWOS:000236666800008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridChan, MCW=36941299700en_US
dc.identifier.scopusauthoridTo, KF=7101911940en_US
dc.identifier.scopusauthoridMan, EPS=7004439159en_US
dc.identifier.scopusauthoridNg, EKW=7201647539en_US
dc.identifier.scopusauthoridChu, ESH=8631130300en_US
dc.identifier.scopusauthoridLau, JYW=13907867100en_US
dc.identifier.scopusauthoridLin, SR=7407614017en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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