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Associations between gene polymorphisms and rheumatoid arthritis: a meta-analysis

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dc.contributor.authorLee, Young Ho-
dc.contributor.authorBae, Sang-Cheol-
dc.contributor.authorChoi, Sung Jae-
dc.contributor.authorJi, Jong Dae-
dc.contributor.authorSong, Gwan Gyu-
dc.date.accessioned2021-08-02T19:29:00Z-
dc.date.available2021-08-02T19:29:00Z-
dc.date.issued2012-06-
dc.identifier.issn1023-3830-
dc.identifier.issn1420-908X-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/27531-
dc.description.abstractObjective The aim of this study was to determine whether tumor necrosis factor alpha inducible protein 3 (TNFAIP3) polymorphisms confer susceptibility to rheumatoid arthritis (RA) in ethnically different populations. Methods The authors conducted meta-analyses on associations between the TNFAIP3 polymorphisms and RA susceptibility. Result A total of ten comparative studies were included in this meta-analysis, which showed an association between the two allele of rs6920220 and RA in all study subjects [odds ratio (OR) 1.216, 95% confidence interval (CI) 1.166–1.269, p < 1.0 × 10−9]. The two allele of rs6920220 was also significantly associated with RA in Europeans only (OR 1.227, 95% CI 1.175–1.282, p < 1.0 × 10−9). Meta-analysis revealed no association between the two allele of the rs10499194 polymorphism and RA in Europeans, but a significant association was found in Asians (OR 1.254, 95% CI 1.101–1.429, p = 6.7 × 10−4). Furthermore, an association was found between the two allele of rs2230926 and RA in all study subjects (OR 1.390, 95% CI 1.214–2.331, p = 1.9 × 10−6). Conclusions This meta-analysis confirms that the TNFAIP3 polymorphisms are associated with RA susceptibility in different ethnic groups, namely, in Europeans for rs6920220 and in Asians for rs10499194.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherBirkhauser Verlag-
dc.titleAssociations between gene polymorphisms and rheumatoid arthritis: a meta-analysis-
dc.typeArticle-
dc.publisher.location스위스-
dc.identifier.doi10.1007/s00011-012-0455-5-
dc.identifier.scopusid2-s2.0-84865137693-
dc.identifier.wosid000303820100013-
dc.identifier.bibliographicCitationInflammation Research, v.61, no.6, pp 635 - 641-
dc.citation.titleInflammation Research-
dc.citation.volume61-
dc.citation.number6-
dc.citation.startPage635-
dc.citation.endPage641-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.subject.keywordPlusSYSTEMIC-LUPUS-ERYTHEMATOSUS-
dc.subject.keywordPlusAUTOIMMUNE-DISEASES-
dc.subject.keywordPlusKAPPA-B-
dc.subject.keywordPlusTNFAIP3-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusCOMMON-
dc.subject.keywordPlus6Q23-
dc.subject.keywordPlusPOPULATION-
dc.subject.keywordPlusRESPONSES-
dc.subject.keywordPlusVARIANTS-
dc.subject.keywordAuthorTumor necrosis factor alpha inducible protein 3-
dc.subject.keywordAuthorPolymorphism-
dc.subject.keywordAuthorRheumatoid arthritis-
dc.subject.keywordAuthorMeta-analysis-
dc.identifier.urlhttps://link.springer.com/article/10.1007%2Fs00011-012-0455-5-
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