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Article: Three SNPs in chromosome 11q23.3 are independently associated with systemic lupus erythematosus in Asians

TitleThree SNPs in chromosome 11q23.3 are independently associated with systemic lupus erythematosus in Asians
Authors
Issue Date2014
Citation
Human Molecular Genetics, 2014, v. 23, n. 2, p. 524-533 How to Cite?
AbstractSystemic lupus erythematosus (SLE) has a complex etiology and is affected by both genetic and environmental factors. Althoughmorethan 40 loci haveshownrobust association withSLE, the details of these loci,suchas the independent contributors and the genes involved, are still unclear. In this study, we performed meta-analysis of two existing genome-wide association studies (GWASs) on Chinese Han populations from Hong Kong and Anhui, China, and followed the findings by further replication on three additional Chinese and Thailand cohorts with a total of 4254 cases and 6262 controls matched geographically and ethnically. We discovered multiple susceptibility variants for SLE in the 11q23.3 region, including variants in/near PHLDB1 (rs11603023, P_combined 5 1.25E208, OR 5 1.20), DDX6 (rs638893, P_combined 5 5.19E207, OR 5 1.22) and CXCR5 (rs10892301, P_combined 5 2.51E208, OR 5 0.85). Genetic contributions from the newly identified variants were all independent of SNP rs4639966, whose association was reported from the previous GWAS. In addition, the three newly identified variants all showed independent association with the disease through modeling by both stepwise and conditional logistic regression. The presence of multiple independent variants in this region emphasizes its role in SLE susceptibility, and also hints the possibility that distinct biological mechanisms might be involved in the disease involving this genomic region. © The Author 2013. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/220760
ISSN
2015 Impact Factor: 5.985
2015 SCImago Journal Rankings: 4.288
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, Jing-
dc.contributor.authorZhang, Yan-
dc.contributor.authorYang, Jing-
dc.contributor.authorZhang, Lu-
dc.contributor.authorSun, Liangdan-
dc.contributor.authorPan, Hai Feng-
dc.contributor.authorHirankarn, Nattiya-
dc.contributor.authorYing, Dingge-
dc.contributor.authorZeng, Shuai-
dc.contributor.authorLee, Tsz Leung-
dc.contributor.authorLau, Chak Sing-
dc.contributor.authorChan, Tak Mao-
dc.contributor.authorLeung, Alexander Moon Ho-
dc.contributor.authorMok, Chi Chiu-
dc.contributor.authorWong, Sik Nin-
dc.contributor.authorLee, Ka Wing-
dc.contributor.authorHo, Marco Hok Kung-
dc.contributor.authorLee, Pamela Pui Wah-
dc.contributor.authorChung, Brian Hon Yin-
dc.contributor.authorChong, Chun Yin-
dc.contributor.authorWong, Raymond Woon Sing-
dc.contributor.authorMok, Mo Yin-
dc.contributor.authorWong, Wilfred Hing Sang-
dc.contributor.authorTong, Kwok Lung-
dc.contributor.authorTse, Niko Kei Chiu-
dc.contributor.authorLi, Xiang Pei-
dc.contributor.authorAvihingsanon, Yingyos-
dc.contributor.authorRianthavorn, Pornpimol-
dc.contributor.authorDeekajorndej, Thavatchai-
dc.contributor.authorSuphapeetiporn, Kanya-
dc.contributor.authorShotelersuk, Vorasuk-
dc.contributor.authorYing, Shirley King Yee-
dc.contributor.authorFung, Samuel Ka Shun-
dc.contributor.authorLai, Wai Ming-
dc.contributor.authorGarcia-Barceló, Maria Mercè-
dc.contributor.authorCherny, Stacey S.-
dc.contributor.authorTam, Paul Kwong Hang-
dc.contributor.authorCui, Yong-
dc.contributor.authorSham, Pak Chung-
dc.contributor.authorYang, Sen-
dc.contributor.authorYe, Dong Qing-
dc.contributor.authorZhang, Xue Jun-
dc.contributor.authorLau, Yu Lung-
dc.contributor.authorYang, Wanling-
dc.date.accessioned2015-10-16T06:50:28Z-
dc.date.available2015-10-16T06:50:28Z-
dc.date.issued2014-
dc.identifier.citationHuman Molecular Genetics, 2014, v. 23, n. 2, p. 524-533-
dc.identifier.issn0964-6906-
dc.identifier.urihttp://hdl.handle.net/10722/220760-
dc.description.abstractSystemic lupus erythematosus (SLE) has a complex etiology and is affected by both genetic and environmental factors. Althoughmorethan 40 loci haveshownrobust association withSLE, the details of these loci,suchas the independent contributors and the genes involved, are still unclear. In this study, we performed meta-analysis of two existing genome-wide association studies (GWASs) on Chinese Han populations from Hong Kong and Anhui, China, and followed the findings by further replication on three additional Chinese and Thailand cohorts with a total of 4254 cases and 6262 controls matched geographically and ethnically. We discovered multiple susceptibility variants for SLE in the 11q23.3 region, including variants in/near PHLDB1 (rs11603023, P_combined 5 1.25E208, OR 5 1.20), DDX6 (rs638893, P_combined 5 5.19E207, OR 5 1.22) and CXCR5 (rs10892301, P_combined 5 2.51E208, OR 5 0.85). Genetic contributions from the newly identified variants were all independent of SNP rs4639966, whose association was reported from the previous GWAS. In addition, the three newly identified variants all showed independent association with the disease through modeling by both stepwise and conditional logistic regression. The presence of multiple independent variants in this region emphasizes its role in SLE susceptibility, and also hints the possibility that distinct biological mechanisms might be involved in the disease involving this genomic region. © The Author 2013. Published by Oxford University Press. All rights reserved.-
dc.languageeng-
dc.relation.ispartofHuman Molecular Genetics-
dc.titleThree SNPs in chromosome 11q23.3 are independently associated with systemic lupus erythematosus in Asians-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1093/hmg/ddt424-
dc.identifier.pmid24001599-
dc.identifier.scopuseid_2-s2.0-84903373728-
dc.identifier.hkuros227307-
dc.identifier.volume23-
dc.identifier.issue2-
dc.identifier.spage524-
dc.identifier.epage533-
dc.identifier.eissn1460-2083-
dc.identifier.isiWOS:000330840400020-

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