Germline variation of TNFAIP3 in primary Sjögren's syndrome-associated lymphoma
Background and objectiveA germline and coding polymorphism (rs2230926) of TNFAIP3 (A20), a central gatekeeper of nuclear factor-kappa B (NF-kB) activation, was recently found associated with primary Sjögren's syndrome (pSS)-associated lymphoma in a French cohort. We aimed to replicate this asso...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2016-04, Vol.75 (4), p.780-783 |
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| creator | Nocturne, Gaetane Tarn, Jessica Boudaoud, Saida Locke, James Miceli-Richard, Corinne Hachulla, Eric Dubost, Jean-Jacques Bowman, Simon Gottenberg, Jacques-Eric Criswell, Lindsey A Lessard, Christopher J Sivils, Kathy L Carapito, Raphael Bahram, Siamak Seror, Raphaèle Ng, Wan-Fai Mariette, Xavier |
| description | Background and objectiveA germline and coding polymorphism (rs2230926) of TNFAIP3 (A20), a central gatekeeper of nuclear factor-kappa B (NF-kB) activation, was recently found associated with primary Sjögren's syndrome (pSS)-associated lymphoma in a French cohort. We aimed to replicate this association.Patients and methodsThe rs2230926 polymorphism was genotyped in cases and controls of European ancestry from two independent cohorts from UK and France. Case control association tests were performed (Fisher's test) in the two cohorts, followed by a meta-analysis of the two cohorts.ResultsThe UK cohort included 308 controls and 590 patients with pSS including 31 with a history of lymphoma. The French cohort consisted of 448 controls and 589 patients with pSS including 47 with lymphoma. In both cohorts, the rs2230926 missense polymorphism was not associated with pSS. However, in the UK cohort, the rs2230926G variant was significantly associated with pSS-associated lymphoma (OR=2.74, 95% CI (1.07 to 7.03), p=0.0423, compared with patients with pSS without lymphoma, and OR=3.12, 95% CI (1.16 to 8.41), p=0.0314, compared with healthy controls) as observed in the French cohort. The meta-analysis of the two cohorts confirmed these results (OR=2.48, 95% CI (1.87 to 3.28) p=0.0037 and OR=2.60, 95% CI (1.91 to 3.53) p=0.0031, respectively).ConclusionsThis study confirms the role of A20 impairment in pSS-associated lymphoma. Subtle germline abnormalities of genes leading to impaired control of NF-kB activation in B cells continuously stimulated by autoimmunity enhance the risk of lymphoma. |
| doi_str_mv | 10.1136/annrheumdis-2015-207731 |
| format | Article |
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We aimed to replicate this association.Patients and methodsThe rs2230926 polymorphism was genotyped in cases and controls of European ancestry from two independent cohorts from UK and France. Case control association tests were performed (Fisher's test) in the two cohorts, followed by a meta-analysis of the two cohorts.ResultsThe UK cohort included 308 controls and 590 patients with pSS including 31 with a history of lymphoma. The French cohort consisted of 448 controls and 589 patients with pSS including 47 with lymphoma. In both cohorts, the rs2230926 missense polymorphism was not associated with pSS. However, in the UK cohort, the rs2230926G variant was significantly associated with pSS-associated lymphoma (OR=2.74, 95% CI (1.07 to 7.03), p=0.0423, compared with patients with pSS without lymphoma, and OR=3.12, 95% CI (1.16 to 8.41), p=0.0314, compared with healthy controls) as observed in the French cohort. The meta-analysis of the two cohorts confirmed these results (OR=2.48, 95% CI (1.87 to 3.28) p=0.0037 and OR=2.60, 95% CI (1.91 to 3.53) p=0.0031, respectively).ConclusionsThis study confirms the role of A20 impairment in pSS-associated lymphoma. Subtle germline abnormalities of genes leading to impaired control of NF-kB activation in B cells continuously stimulated by autoimmunity enhance the risk of lymphoma.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/annrheumdis-2015-207731</identifier><identifier>PMID: 26338037</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>England: Elsevier Limited</publisher><subject>Blood & organ donations ; Case-Control Studies ; Cohort Studies ; DNA-Binding Proteins - genetics ; France ; Germ-Line Mutation - genetics ; Hodgkin Disease - genetics ; Humans ; Hypotheses ; Intracellular Signaling Peptides and Proteins - genetics ; Logistic Models ; Lymphoma ; Lymphoma - complications ; Lymphoma - genetics ; Lymphoma, B-Cell - genetics ; Meta-analysis ; Multivariate Analysis ; Mycosis Fungoides - genetics ; Nuclear Proteins - genetics ; Polymorphism, Single Nucleotide ; Sjogren's Syndrome - complications ; Sjogren's Syndrome - genetics ; Skin Neoplasms - genetics ; Tumor Necrosis Factor alpha-Induced Protein 3 ; United Kingdom ; White People - genetics</subject><ispartof>Annals of the rheumatic diseases, 2016-04, Vol.75 (4), p.780-783</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Copyright: 2016 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b450t-aaa13b542e7f70f2859dd111422a18be02376e6801fafa037afc737e43bb4c233</citedby><cites>FETCH-LOGICAL-b450t-aaa13b542e7f70f2859dd111422a18be02376e6801fafa037afc737e43bb4c233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/75/4/780.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/75/4/780.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77343,77374</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26338037$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nocturne, Gaetane</creatorcontrib><creatorcontrib>Tarn, Jessica</creatorcontrib><creatorcontrib>Boudaoud, Saida</creatorcontrib><creatorcontrib>Locke, James</creatorcontrib><creatorcontrib>Miceli-Richard, Corinne</creatorcontrib><creatorcontrib>Hachulla, Eric</creatorcontrib><creatorcontrib>Dubost, Jean-Jacques</creatorcontrib><creatorcontrib>Bowman, Simon</creatorcontrib><creatorcontrib>Gottenberg, Jacques-Eric</creatorcontrib><creatorcontrib>Criswell, Lindsey A</creatorcontrib><creatorcontrib>Lessard, Christopher J</creatorcontrib><creatorcontrib>Sivils, Kathy L</creatorcontrib><creatorcontrib>Carapito, Raphael</creatorcontrib><creatorcontrib>Bahram, Siamak</creatorcontrib><creatorcontrib>Seror, Raphaèle</creatorcontrib><creatorcontrib>Ng, Wan-Fai</creatorcontrib><creatorcontrib>Mariette, Xavier</creatorcontrib><title>Germline variation of TNFAIP3 in primary Sjögren's syndrome-associated lymphoma</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Background and objectiveA germline and coding polymorphism (rs2230926) of TNFAIP3 (A20), a central gatekeeper of nuclear factor-kappa B (NF-kB) activation, was recently found associated with primary Sjögren's syndrome (pSS)-associated lymphoma in a French cohort. We aimed to replicate this association.Patients and methodsThe rs2230926 polymorphism was genotyped in cases and controls of European ancestry from two independent cohorts from UK and France. Case control association tests were performed (Fisher's test) in the two cohorts, followed by a meta-analysis of the two cohorts.ResultsThe UK cohort included 308 controls and 590 patients with pSS including 31 with a history of lymphoma. The French cohort consisted of 448 controls and 589 patients with pSS including 47 with lymphoma. In both cohorts, the rs2230926 missense polymorphism was not associated with pSS. However, in the UK cohort, the rs2230926G variant was significantly associated with pSS-associated lymphoma (OR=2.74, 95% CI (1.07 to 7.03), p=0.0423, compared with patients with pSS without lymphoma, and OR=3.12, 95% CI (1.16 to 8.41), p=0.0314, compared with healthy controls) as observed in the French cohort. The meta-analysis of the two cohorts confirmed these results (OR=2.48, 95% CI (1.87 to 3.28) p=0.0037 and OR=2.60, 95% CI (1.91 to 3.53) p=0.0031, respectively).ConclusionsThis study confirms the role of A20 impairment in pSS-associated lymphoma. Subtle germline abnormalities of genes leading to impaired control of NF-kB activation in B cells continuously stimulated by autoimmunity enhance the risk of lymphoma.</description><subject>Blood & organ donations</subject><subject>Case-Control Studies</subject><subject>Cohort Studies</subject><subject>DNA-Binding Proteins - genetics</subject><subject>France</subject><subject>Germ-Line Mutation - genetics</subject><subject>Hodgkin Disease - genetics</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Logistic Models</subject><subject>Lymphoma</subject><subject>Lymphoma - complications</subject><subject>Lymphoma - genetics</subject><subject>Lymphoma, B-Cell - genetics</subject><subject>Meta-analysis</subject><subject>Multivariate Analysis</subject><subject>Mycosis Fungoides - genetics</subject><subject>Nuclear Proteins - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Sjogren's Syndrome - complications</subject><subject>Sjogren's Syndrome - genetics</subject><subject>Skin Neoplasms - genetics</subject><subject>Tumor Necrosis Factor alpha-Induced Protein 3</subject><subject>United Kingdom</subject><subject>White People - genetics</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkN1KwzAYhoMobv7cggY80JNqftomPRzDzcHQgfO4pG3iWppkJquwG_MGvDEzOkU88iThg-d9-b4HgEuMbjGm6Z0wxq1kp6vaRwThJDyMUXwAhjhOeZhSdAiGCCEaxVnKBuDE-yaMiGN-DAYkpZQjyoZgMZVOt7WR8F24Wmxqa6BVcPk4Gc0WFNYGrl2thdvC5-bz49VJc-2h35rKWS0j4b0tQ0pWsN3q9cpqcQaOlGi9PN__p-Blcr8cP0Tzp-lsPJpHRZygTSSEwLRIYiKZYkgRnmRVhTGOCRGYFxIRylKZcoSVUCKsKlTJKJMxLYq4JJSegpu-d-3sWyf9Jte1L2XbCiNt53PMGOEk44QH9OoP2tjOmbDdjuKIxTjJAsV6qnTWeydVvr88xyjfSc9_Sc930vNeekhe7Pu7QsvqJ_dtOQCkBwrd_Lv1CwDakPA</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Nocturne, Gaetane</creator><creator>Tarn, Jessica</creator><creator>Boudaoud, Saida</creator><creator>Locke, James</creator><creator>Miceli-Richard, Corinne</creator><creator>Hachulla, Eric</creator><creator>Dubost, Jean-Jacques</creator><creator>Bowman, Simon</creator><creator>Gottenberg, Jacques-Eric</creator><creator>Criswell, Lindsey A</creator><creator>Lessard, Christopher J</creator><creator>Sivils, Kathy L</creator><creator>Carapito, Raphael</creator><creator>Bahram, Siamak</creator><creator>Seror, Raphaèle</creator><creator>Ng, Wan-Fai</creator><creator>Mariette, Xavier</creator><general>Elsevier Limited</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20160401</creationdate><title>Germline variation of TNFAIP3 in primary Sjögren's syndrome-associated lymphoma</title><author>Nocturne, Gaetane ; Tarn, Jessica ; Boudaoud, Saida ; Locke, James ; Miceli-Richard, Corinne ; Hachulla, Eric ; Dubost, Jean-Jacques ; Bowman, Simon ; Gottenberg, Jacques-Eric ; Criswell, Lindsey A ; Lessard, Christopher J ; Sivils, Kathy L ; Carapito, Raphael ; Bahram, Siamak ; Seror, Raphaèle ; Ng, Wan-Fai ; Mariette, Xavier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b450t-aaa13b542e7f70f2859dd111422a18be02376e6801fafa037afc737e43bb4c233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Blood & organ donations</topic><topic>Case-Control Studies</topic><topic>Cohort Studies</topic><topic>DNA-Binding Proteins - genetics</topic><topic>France</topic><topic>Germ-Line Mutation - genetics</topic><topic>Hodgkin Disease - genetics</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Logistic Models</topic><topic>Lymphoma</topic><topic>Lymphoma - complications</topic><topic>Lymphoma - genetics</topic><topic>Lymphoma, B-Cell - genetics</topic><topic>Meta-analysis</topic><topic>Multivariate Analysis</topic><topic>Mycosis Fungoides - genetics</topic><topic>Nuclear Proteins - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Sjogren's Syndrome - complications</topic><topic>Sjogren's Syndrome - genetics</topic><topic>Skin Neoplasms - genetics</topic><topic>Tumor Necrosis Factor alpha-Induced Protein 3</topic><topic>United Kingdom</topic><topic>White People - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nocturne, Gaetane</creatorcontrib><creatorcontrib>Tarn, Jessica</creatorcontrib><creatorcontrib>Boudaoud, Saida</creatorcontrib><creatorcontrib>Locke, James</creatorcontrib><creatorcontrib>Miceli-Richard, Corinne</creatorcontrib><creatorcontrib>Hachulla, Eric</creatorcontrib><creatorcontrib>Dubost, Jean-Jacques</creatorcontrib><creatorcontrib>Bowman, Simon</creatorcontrib><creatorcontrib>Gottenberg, Jacques-Eric</creatorcontrib><creatorcontrib>Criswell, Lindsey A</creatorcontrib><creatorcontrib>Lessard, Christopher J</creatorcontrib><creatorcontrib>Sivils, Kathy L</creatorcontrib><creatorcontrib>Carapito, Raphael</creatorcontrib><creatorcontrib>Bahram, Siamak</creatorcontrib><creatorcontrib>Seror, Raphaèle</creatorcontrib><creatorcontrib>Ng, Wan-Fai</creatorcontrib><creatorcontrib>Mariette, Xavier</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nocturne, Gaetane</au><au>Tarn, Jessica</au><au>Boudaoud, Saida</au><au>Locke, James</au><au>Miceli-Richard, Corinne</au><au>Hachulla, Eric</au><au>Dubost, Jean-Jacques</au><au>Bowman, Simon</au><au>Gottenberg, Jacques-Eric</au><au>Criswell, Lindsey A</au><au>Lessard, Christopher J</au><au>Sivils, Kathy L</au><au>Carapito, Raphael</au><au>Bahram, Siamak</au><au>Seror, Raphaèle</au><au>Ng, Wan-Fai</au><au>Mariette, Xavier</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Germline variation of TNFAIP3 in primary Sjögren's syndrome-associated lymphoma</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>75</volume><issue>4</issue><spage>780</spage><epage>783</epage><pages>780-783</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Background and objectiveA germline and coding polymorphism (rs2230926) of TNFAIP3 (A20), a central gatekeeper of nuclear factor-kappa B (NF-kB) activation, was recently found associated with primary Sjögren's syndrome (pSS)-associated lymphoma in a French cohort. We aimed to replicate this association.Patients and methodsThe rs2230926 polymorphism was genotyped in cases and controls of European ancestry from two independent cohorts from UK and France. Case control association tests were performed (Fisher's test) in the two cohorts, followed by a meta-analysis of the two cohorts.ResultsThe UK cohort included 308 controls and 590 patients with pSS including 31 with a history of lymphoma. The French cohort consisted of 448 controls and 589 patients with pSS including 47 with lymphoma. In both cohorts, the rs2230926 missense polymorphism was not associated with pSS. However, in the UK cohort, the rs2230926G variant was significantly associated with pSS-associated lymphoma (OR=2.74, 95% CI (1.07 to 7.03), p=0.0423, compared with patients with pSS without lymphoma, and OR=3.12, 95% CI (1.16 to 8.41), p=0.0314, compared with healthy controls) as observed in the French cohort. The meta-analysis of the two cohorts confirmed these results (OR=2.48, 95% CI (1.87 to 3.28) p=0.0037 and OR=2.60, 95% CI (1.91 to 3.53) p=0.0031, respectively).ConclusionsThis study confirms the role of A20 impairment in pSS-associated lymphoma. Subtle germline abnormalities of genes leading to impaired control of NF-kB activation in B cells continuously stimulated by autoimmunity enhance the risk of lymphoma.</abstract><cop>England</cop><pub>Elsevier Limited</pub><pmid>26338037</pmid><doi>10.1136/annrheumdis-2015-207731</doi><tpages>4</tpages></addata></record> |
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| ispartof | Annals of the rheumatic diseases, 2016-04, Vol.75 (4), p.780-783 |
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| language | eng |
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| source | MEDLINE; BMJ Journals - NESLi2 |
| subjects | Blood & organ donations Case-Control Studies Cohort Studies DNA-Binding Proteins - genetics France Germ-Line Mutation - genetics Hodgkin Disease - genetics Humans Hypotheses Intracellular Signaling Peptides and Proteins - genetics Logistic Models Lymphoma Lymphoma - complications Lymphoma - genetics Lymphoma, B-Cell - genetics Meta-analysis Multivariate Analysis Mycosis Fungoides - genetics Nuclear Proteins - genetics Polymorphism, Single Nucleotide Sjogren's Syndrome - complications Sjogren's Syndrome - genetics Skin Neoplasms - genetics Tumor Necrosis Factor alpha-Induced Protein 3 United Kingdom White People - genetics |
| title | Germline variation of TNFAIP3 in primary Sjögren's syndrome-associated lymphoma |
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