Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls
Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 ( CCL3L1 ) and its contribution to rheumatoid arthritis (RA) susceptibility. In order...
Gespeichert in:
| Veröffentlicht in: | Genes and immunity 2012-10, Vol.13 (7), p.579-582 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 582 |
|---|---|
| container_issue | 7 |
| container_start_page | 579 |
| container_title | Genes and immunity |
| container_volume | 13 |
| creator | Nordang, G B N Carpenter, D Viken, M K Kvien, T K Armour, J A L Lie, B A |
| description | Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 (
CCL3L1
) and its contribution to rheumatoid arthritis (RA) susceptibility. In order to draw robust conclusions about
CCL3L1
involvement in RA, we have performed association analysis (CNVtools) using genotyping by the paralogue ratio test of a Norwegian RA case–control material (
N
=1877). We also analyzed the associations after stratification for anti-citrullinated peptide antibody (ACPA) status. Clear clusters representing specific copy number classes were evident, but significant differential bias was observed resulting in a systematic trend toward slightly higher apparent copy number for cases relative to controls. Controlling for bias revealed no significant differences in copy number distribution either between all patients and controls, or after ACPA stratification. Our results do not support involvement of the
CCL3L1
CNV in RA susceptibility. |
| doi_str_mv | 10.1038/gene.2012.30 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1125237067</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A306972470</galeid><sourcerecordid>A306972470</sourcerecordid><originalsourceid>FETCH-LOGICAL-c557t-ab3f68e4ac71527318e334e1524dbf50db8dcd3ae9d85c633cd59f574b5875ba3</originalsourceid><addsrcrecordid>eNqNkluL1DAUx4so7rr65rMEfFGwYy7NpY_D4GVhUPDyHNL0tJOlbcYkRec77IfelFkvI4tIHnJIfud_ck7-RfGU4BXBTL3uYYIVxYSuGL5XnJNKipJXEt9fYiHKSsn6rHgU4xXGRBBRPyzOKJWKC0LPi-t1jN46k5yfkJnMcIguIt-htAO02WzZliDr9wc0zWMDAQ3ezhE1B7Q3wQy-nwGFJRkliAm5CX3w4Tv0zkwo7GAeTfKuRSakXXApK-8zDFOKuVaLdmCGtDvkAlMKfoiPiwedGSI8ud0viq9v33zZvC-3H99dbtbb0nIuU2ka1gkFlbGScCoZUcBYBTmu2qbjuG1Ua1tmoG4Vt4Ix2_K647JquJK8MeyieHHU3Qf_bc4P16OLFobBTODnqAmhnDKJhfwPlLBaYYEX9Plf6JWfQx5p1FRURFJV4_pfVNaiinJS4d9UbwbQbup8CsYupfWaYVFLmn84U6s7qLxaGF0eKnQun58kvDxJWAYPP1Jv5hj15edPp-yrI2uDjzFAp_fBjSYcNMF6cZ5enKcX52m24M9u-5qbEdpf8E-rZaA8AjFfTT2EPxq_S_AGJpnhHQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1112825140</pqid></control><display><type>article</type><title>Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Nordang, G B N ; Carpenter, D ; Viken, M K ; Kvien, T K ; Armour, J A L ; Lie, B A</creator><creatorcontrib>Nordang, G B N ; Carpenter, D ; Viken, M K ; Kvien, T K ; Armour, J A L ; Lie, B A</creatorcontrib><description>Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 (
CCL3L1
) and its contribution to rheumatoid arthritis (RA) susceptibility. In order to draw robust conclusions about
CCL3L1
involvement in RA, we have performed association analysis (CNVtools) using genotyping by the paralogue ratio test of a Norwegian RA case–control material (
N
=1877). We also analyzed the associations after stratification for anti-citrullinated peptide antibody (ACPA) status. Clear clusters representing specific copy number classes were evident, but significant differential bias was observed resulting in a systematic trend toward slightly higher apparent copy number for cases relative to controls. Controlling for bias revealed no significant differences in copy number distribution either between all patients and controls, or after ACPA stratification. Our results do not support involvement of the
CCL3L1
CNV in RA susceptibility.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/gene.2012.30</identifier><identifier>PMID: 22785612</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/208/205 ; 631/208/737/1505 ; 692/699/1670/498 ; 692/700/478/174 ; Antibodies ; Arthritis, Rheumatoid - genetics ; Association analysis ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Case-Control Studies ; CC chemokines ; Chemokines ; Chemokines, CC - genetics ; Citrulline ; Consortia ; Copy number ; Copy number variations ; Disease ; Disease susceptibility ; DNA Copy Number Variations ; Gene Expression ; Genes ; Genetic aspects ; Genetic Association Studies ; Genetic Loci ; Genomes ; Genotyping ; Health risk assessment ; Hospitals ; Human Genetics ; Humans ; Immunology ; Ligands ; Norway - epidemiology ; Peptides ; Rheumatoid arthritis ; Risk factors ; short-communication</subject><ispartof>Genes and immunity, 2012-10, Vol.13 (7), p.579-582</ispartof><rights>Macmillan Publishers Limited 2012</rights><rights>COPYRIGHT 2012 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Oct 2012</rights><rights>Macmillan Publishers Limited 2012.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c557t-ab3f68e4ac71527318e334e1524dbf50db8dcd3ae9d85c633cd59f574b5875ba3</citedby><cites>FETCH-LOGICAL-c557t-ab3f68e4ac71527318e334e1524dbf50db8dcd3ae9d85c633cd59f574b5875ba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27933,27934</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22785612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nordang, G B N</creatorcontrib><creatorcontrib>Carpenter, D</creatorcontrib><creatorcontrib>Viken, M K</creatorcontrib><creatorcontrib>Kvien, T K</creatorcontrib><creatorcontrib>Armour, J A L</creatorcontrib><creatorcontrib>Lie, B A</creatorcontrib><title>Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 (
CCL3L1
) and its contribution to rheumatoid arthritis (RA) susceptibility. In order to draw robust conclusions about
CCL3L1
involvement in RA, we have performed association analysis (CNVtools) using genotyping by the paralogue ratio test of a Norwegian RA case–control material (
N
=1877). We also analyzed the associations after stratification for anti-citrullinated peptide antibody (ACPA) status. Clear clusters representing specific copy number classes were evident, but significant differential bias was observed resulting in a systematic trend toward slightly higher apparent copy number for cases relative to controls. Controlling for bias revealed no significant differences in copy number distribution either between all patients and controls, or after ACPA stratification. Our results do not support involvement of the
CCL3L1
CNV in RA susceptibility.</description><subject>631/208/205</subject><subject>631/208/737/1505</subject><subject>692/699/1670/498</subject><subject>692/700/478/174</subject><subject>Antibodies</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Association analysis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>CC chemokines</subject><subject>Chemokines</subject><subject>Chemokines, CC - genetics</subject><subject>Citrulline</subject><subject>Consortia</subject><subject>Copy number</subject><subject>Copy number variations</subject><subject>Disease</subject><subject>Disease susceptibility</subject><subject>DNA Copy Number Variations</subject><subject>Gene Expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic Association Studies</subject><subject>Genetic Loci</subject><subject>Genomes</subject><subject>Genotyping</subject><subject>Health risk assessment</subject><subject>Hospitals</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunology</subject><subject>Ligands</subject><subject>Norway - epidemiology</subject><subject>Peptides</subject><subject>Rheumatoid arthritis</subject><subject>Risk factors</subject><subject>short-communication</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkluL1DAUx4so7rr65rMEfFGwYy7NpY_D4GVhUPDyHNL0tJOlbcYkRec77IfelFkvI4tIHnJIfud_ck7-RfGU4BXBTL3uYYIVxYSuGL5XnJNKipJXEt9fYiHKSsn6rHgU4xXGRBBRPyzOKJWKC0LPi-t1jN46k5yfkJnMcIguIt-htAO02WzZliDr9wc0zWMDAQ3ezhE1B7Q3wQy-nwGFJRkliAm5CX3w4Tv0zkwo7GAeTfKuRSakXXApK-8zDFOKuVaLdmCGtDvkAlMKfoiPiwedGSI8ud0viq9v33zZvC-3H99dbtbb0nIuU2ka1gkFlbGScCoZUcBYBTmu2qbjuG1Ua1tmoG4Vt4Ix2_K647JquJK8MeyieHHU3Qf_bc4P16OLFobBTODnqAmhnDKJhfwPlLBaYYEX9Plf6JWfQx5p1FRURFJV4_pfVNaiinJS4d9UbwbQbup8CsYupfWaYVFLmn84U6s7qLxaGF0eKnQun58kvDxJWAYPP1Jv5hj15edPp-yrI2uDjzFAp_fBjSYcNMF6cZ5enKcX52m24M9u-5qbEdpf8E-rZaA8AjFfTT2EPxq_S_AGJpnhHQ</recordid><startdate>20121001</startdate><enddate>20121001</enddate><creator>Nordang, G B N</creator><creator>Carpenter, D</creator><creator>Viken, M K</creator><creator>Kvien, T K</creator><creator>Armour, J A L</creator><creator>Lie, B A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20121001</creationdate><title>Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls</title><author>Nordang, G B N ; Carpenter, D ; Viken, M K ; Kvien, T K ; Armour, J A L ; Lie, B A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c557t-ab3f68e4ac71527318e334e1524dbf50db8dcd3ae9d85c633cd59f574b5875ba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>631/208/205</topic><topic>631/208/737/1505</topic><topic>692/699/1670/498</topic><topic>692/700/478/174</topic><topic>Antibodies</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Association analysis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>CC chemokines</topic><topic>Chemokines</topic><topic>Chemokines, CC - genetics</topic><topic>Citrulline</topic><topic>Consortia</topic><topic>Copy number</topic><topic>Copy number variations</topic><topic>Disease</topic><topic>Disease susceptibility</topic><topic>DNA Copy Number Variations</topic><topic>Gene Expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic Association Studies</topic><topic>Genetic Loci</topic><topic>Genomes</topic><topic>Genotyping</topic><topic>Health risk assessment</topic><topic>Hospitals</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunology</topic><topic>Ligands</topic><topic>Norway - epidemiology</topic><topic>Peptides</topic><topic>Rheumatoid arthritis</topic><topic>Risk factors</topic><topic>short-communication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nordang, G B N</creatorcontrib><creatorcontrib>Carpenter, D</creatorcontrib><creatorcontrib>Viken, M K</creatorcontrib><creatorcontrib>Kvien, T K</creatorcontrib><creatorcontrib>Armour, J A L</creatorcontrib><creatorcontrib>Lie, B A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research 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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nordang, G B N</au><au>Carpenter, D</au><au>Viken, M K</au><au>Kvien, T K</au><au>Armour, J A L</au><au>Lie, B A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2012-10-01</date><risdate>2012</risdate><volume>13</volume><issue>7</issue><spage>579</spage><epage>582</epage><pages>579-582</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Genotyping of multiallelic copy number variants (CNVs) is technically difficult and can lead to inaccurate conclusions. This is reflected by inconsistent results published for the CNV C-C chemokine ligand 3-like 1 (
CCL3L1
) and its contribution to rheumatoid arthritis (RA) susceptibility. In order to draw robust conclusions about
CCL3L1
involvement in RA, we have performed association analysis (CNVtools) using genotyping by the paralogue ratio test of a Norwegian RA case–control material (
N
=1877). We also analyzed the associations after stratification for anti-citrullinated peptide antibody (ACPA) status. Clear clusters representing specific copy number classes were evident, but significant differential bias was observed resulting in a systematic trend toward slightly higher apparent copy number for cases relative to controls. Controlling for bias revealed no significant differences in copy number distribution either between all patients and controls, or after ACPA stratification. Our results do not support involvement of the
CCL3L1
CNV in RA susceptibility.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>22785612</pmid><doi>10.1038/gene.2012.30</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1466-4879 |
| ispartof | Genes and immunity, 2012-10, Vol.13 (7), p.579-582 |
| issn | 1466-4879 1476-5470 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1125237067 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 631/208/205 631/208/737/1505 692/699/1670/498 692/700/478/174 Antibodies Arthritis, Rheumatoid - genetics Association analysis Biomedical and Life Sciences Biomedicine Cancer Research Case-Control Studies CC chemokines Chemokines Chemokines, CC - genetics Citrulline Consortia Copy number Copy number variations Disease Disease susceptibility DNA Copy Number Variations Gene Expression Genes Genetic aspects Genetic Association Studies Genetic Loci Genomes Genotyping Health risk assessment Hospitals Human Genetics Humans Immunology Ligands Norway - epidemiology Peptides Rheumatoid arthritis Risk factors short-communication |
| title | Association analysis of the CCL3L1 copy number locus by paralogue ratio test in Norwegian rheumatoid arthritis patients and healthy controls |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-03T12%3A54%3A50IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Association%20analysis%20of%20the%20CCL3L1%20copy%20number%20locus%20by%20paralogue%20ratio%20test%20in%20Norwegian%20rheumatoid%20arthritis%20patients%20and%20healthy%20controls&rft.jtitle=Genes%20and%20immunity&rft.au=Nordang,%20G%20B%20N&rft.date=2012-10-01&rft.volume=13&rft.issue=7&rft.spage=579&rft.epage=582&rft.pages=579-582&rft.issn=1466-4879&rft.eissn=1476-5470&rft_id=info:doi/10.1038/gene.2012.30&rft_dat=%3Cgale_proqu%3EA306972470%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1112825140&rft_id=info:pmid/22785612&rft_galeid=A306972470&rfr_iscdi=true |