Genome-wide association analysis in primary sclerosing cholangitis identifies two non-HLA susceptibility loci.

2.50
Hdl Handle:
http://hdl.handle.net/2336/227451
Title:
Genome-wide association analysis in primary sclerosing cholangitis identifies two non-HLA susceptibility loci.
Authors:
Melum, Espen; Franke, Andre; Schramm, Christoph; Weismüller, Tobias J; Gotthardt, Daniel Nils; Offner, Felix A; Juran, Brian D; Laerdahl, Jon K; Labi, Verena; Björnsson, Einar; Weersma, Rinse K; Henckaerts, Liesbet; Teufel, Andreas; Rust, Christian; Ellinghaus, Eva; Balschun, Tobias; Boberg, Kirsten Muri; Ellinghaus, David; Bergquist, Annika; Sauer, Peter; Ryu, Euijung; Hov, Johannes Roksund; Wedemeyer, Jochen; Lindkvist, Björn; Wittig, Michael; Porte, Robert J; Holm, Kristian; Gieger, Christian; Wichmann, H-Erich; Stokkers, Pieter; Ponsioen, Cyriel Y; Runz, Heiko; Stiehl, Adolf; Wijmenga, Cisca; Sterneck, Martina; Vermeire, Severine; Beuers, Ulrich; Villunger, Andreas; Schrumpf, Erik; Lazaridis, Konstantinos N; Manns, Michael P; Schreiber, Stefan; Karlsen, Tom H
Citation:
Nat. Genet. 2011, 43(1):17-9
Issue Date:
Jan-2011
Abstract:
Primary sclerosing cholangitis (PSC) is a chronic bile duct disease affecting 2.4-7.5% of individuals with inflammatory bowel disease. We performed a genome-wide association analysis of 2,466,182 SNPs in 715 individuals with PSC and 2,962 controls, followed by replication in 1,025 PSC cases and 2,174 controls. We detected non-HLA associations at rs3197999 in MST1 and rs6720394 near BCL2L11 (combined P = 1.1 × 10⁻¹⁶ and P = 4.1 × 10⁻⁸, respectively).
Description:
To access publisher full text version of this article. Please click on the hyperlink in Additional Links field.
Additional Links:
http://dx.doi.org/10.1038/ng.728
Rights:
Archived with thanks to Nature genetics

Full metadata record

DC FieldValue Language
dc.contributor.authorMelum, Espenen_GB
dc.contributor.authorFranke, Andreen_GB
dc.contributor.authorSchramm, Christophen_GB
dc.contributor.authorWeismüller, Tobias Jen_GB
dc.contributor.authorGotthardt, Daniel Nilsen_GB
dc.contributor.authorOffner, Felix Aen_GB
dc.contributor.authorJuran, Brian Den_GB
dc.contributor.authorLaerdahl, Jon Ken_GB
dc.contributor.authorLabi, Verenaen_GB
dc.contributor.authorBjörnsson, Einaren_GB
dc.contributor.authorWeersma, Rinse Ken_GB
dc.contributor.authorHenckaerts, Liesbeten_GB
dc.contributor.authorTeufel, Andreasen_GB
dc.contributor.authorRust, Christianen_GB
dc.contributor.authorEllinghaus, Evaen_GB
dc.contributor.authorBalschun, Tobiasen_GB
dc.contributor.authorBoberg, Kirsten Murien_GB
dc.contributor.authorEllinghaus, Daviden_GB
dc.contributor.authorBergquist, Annikaen_GB
dc.contributor.authorSauer, Peteren_GB
dc.contributor.authorRyu, Euijungen_GB
dc.contributor.authorHov, Johannes Roksunden_GB
dc.contributor.authorWedemeyer, Jochenen_GB
dc.contributor.authorLindkvist, Björnen_GB
dc.contributor.authorWittig, Michaelen_GB
dc.contributor.authorPorte, Robert Jen_GB
dc.contributor.authorHolm, Kristianen_GB
dc.contributor.authorGieger, Christianen_GB
dc.contributor.authorWichmann, H-Erichen_GB
dc.contributor.authorStokkers, Pieteren_GB
dc.contributor.authorPonsioen, Cyriel Yen_GB
dc.contributor.authorRunz, Heikoen_GB
dc.contributor.authorStiehl, Adolfen_GB
dc.contributor.authorWijmenga, Ciscaen_GB
dc.contributor.authorSterneck, Martinaen_GB
dc.contributor.authorVermeire, Severineen_GB
dc.contributor.authorBeuers, Ulrichen_GB
dc.contributor.authorVillunger, Andreasen_GB
dc.contributor.authorSchrumpf, Eriken_GB
dc.contributor.authorLazaridis, Konstantinos Nen_GB
dc.contributor.authorManns, Michael Pen_GB
dc.contributor.authorSchreiber, Stefanen_GB
dc.contributor.authorKarlsen, Tom Hen_GB
dc.date.accessioned2012-06-04T15:17:47Z-
dc.date.available2012-06-04T15:17:47Z-
dc.date.issued2011-01-
dc.date.submitted2012-06-04-
dc.identifier.citationNat. Genet. 2011, 43(1):17-9en_GB
dc.identifier.issn1546-1718-
dc.identifier.pmid21151127-
dc.identifier.doi10.1038/ng.728-
dc.identifier.urihttp://hdl.handle.net/2336/227451-
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links field.en_GB
dc.description.abstractPrimary sclerosing cholangitis (PSC) is a chronic bile duct disease affecting 2.4-7.5% of individuals with inflammatory bowel disease. We performed a genome-wide association analysis of 2,466,182 SNPs in 715 individuals with PSC and 2,962 controls, followed by replication in 1,025 PSC cases and 2,174 controls. We detected non-HLA associations at rs3197999 in MST1 and rs6720394 near BCL2L11 (combined P = 1.1 × 10⁻¹⁶ and P = 4.1 × 10⁻⁸, respectively).en_GB
dc.description.sponsorshipHealth Resources and Service Administration (HRSA) of the Maternal and Child Health Bureau (MCHB) U22MC03963 Mayo Clinic College of Medicineen_GB
dc.language.isoenen
dc.publisherNature Publishing Groupen_GB
dc.relation.urlhttp://dx.doi.org/10.1038/ng.728en_GB
dc.rightsArchived with thanks to Nature geneticsen_GB
dc.subject.meshApoptosis Regulatory Proteinsen_GB
dc.subject.meshCholangitis, Sclerosingen_GB
dc.subject.meshCohort Studiesen_GB
dc.subject.meshGene Expression Profilingen_GB
dc.subject.meshGenetic Locien_GB
dc.subject.meshGenetic Predisposition to Diseaseen_GB
dc.subject.meshGenome-Wide Association Studyen_GB
dc.subject.meshHLA Antigensen_GB
dc.subject.meshHepatocyte Growth Factoren_GB
dc.subject.meshHumansen_GB
dc.subject.meshMembrane Proteinsen_GB
dc.subject.meshPolymorphism, Single Nucleotideen_GB
dc.subject.meshProto-Oncogene Proteinsen_GB
dc.titleGenome-wide association analysis in primary sclerosing cholangitis identifies two non-HLA susceptibility loci.en
dc.typeArticleen
dc.contributor.departmentNorwegian PSC Research Center, Clinic for Specialized Medicine and Surgery, Oslo University Hospital, Rikshospitalet, Oslo, Norway.en_GB
dc.identifier.journalNature geneticsen_GB

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