{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T00:45:49Z","timestamp":1789865149782,"version":"4.0.1"},"reference-count":43,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2019,3,13]],"date-time":"2019-03-13T00:00:00Z","timestamp":1552435200000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2019,3,13]],"date-time":"2019-03-13T00:00:00Z","timestamp":1552435200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100004440","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["084730"],"award-info":[{"award-number":["084730"]}],"id":[{"id":"10.13039\/100004440","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000001","name":"National Science Foundation","doi-asserted-by":"publisher","award":["32EP30_136042\/1"],"award-info":[{"award-number":["32EP30_136042\/1"]}],"id":[{"id":"10.13039\/100000001","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007660","name":"Universiteit Antwerpen","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100007660","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001655","name":"Deutscher Akademischer Austauschdienst","doi-asserted-by":"publisher","award":["57073880"],"award-info":[{"award-number":["57073880"]}],"id":[{"id":"10.13039\/501100001655","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2019,4]]},"abstract":"Summary<\/jats:title>\n \n Objective<\/jats:title>\n \n Copy number variations (\n CNV<\/jats:styled-content>\n s) represent a significant genetic risk for several neurodevelopmental disorders including epilepsy. As knowledge increases, reanalysis of existing data is essential. Reliable estimates of the contribution of\n CNV<\/jats:styled-content>\n s to epilepsies from sizeable populations are not available.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We assembled a cohort of 1255 patients with preexisting array comparative genomic hybridization or single nucleotide polymorphism array based\n CNV<\/jats:styled-content>\n data. All patients had \u201cepilepsy plus,\u201d defined as epilepsy with comorbid features, including intellectual disability, psychiatric symptoms, and other neurological and nonneurological features.\n CNV<\/jats:styled-content>\n classification was conducted using a systematic filtering workflow adapted to epilepsy.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Of 1097 patients remaining after genetic data quality control, 120 individuals (10.9%) carried at least one autosomal\n CNV<\/jats:styled-content>\n classified as pathogenic; 19 individuals (1.7%) carried at least one autosomal\n CNV<\/jats:styled-content>\n classified as possibly pathogenic. Eleven patients (1%) carried more than one (possibly) pathogenic\n CNV<\/jats:styled-content>\n . We identified\n CNV<\/jats:styled-content>\n s covering recently reported (\n \n HNRNPU<\/jats:styled-content>\n )\n <\/jats:italic>\n or emerging (\n \n RORB<\/jats:styled-content>\n <\/jats:italic>\n ) epilepsy genes, and further delineated the phenotype associated with mutations of these genes. Additional novel epilepsy candidate genes emerge from our study. Comparing phenotypic features of pathogenic\n CNV<\/jats:styled-content>\n carriers to those of noncarriers of pathogenic\n CNV<\/jats:styled-content>\n s, we show that patients with nonneurological comorbidities, especially dysmorphism, were more likely to carry pathogenic\n CNV<\/jats:styled-content>\n s (odds ratio\u00a0=\u00a04.09, confidence interval\u00a0=\u00a02.51\u20106.68;\n P<\/jats:italic>\n \u00a0=\u00a02.34\u00a0\u00d7\u00a010\n \u22129<\/jats:sup>\n ). Meta\u2010analysis including data from published control groups showed that the presence or absence of epilepsy did not affect the detected frequency of\n CNV<\/jats:styled-content>\n s.\n <\/jats:p>\n <\/jats:sec>\n \n Significance<\/jats:title>\n \n The use of a specifically adapted workflow enabled identification of pathogenic autosomal\n CNV<\/jats:styled-content>\n s in 10.9% of patients with epilepsy plus, which rose to 12.7% when we also considered possibly pathogenic\n CNV<\/jats:styled-content>\n s. Our data indicate that epilepsy with comorbid features should be considered an indication for patients to be selected for a diagnostic algorithm including\n CNV<\/jats:styled-content>\n detection. Collaborative large\u2010scale\n CNV<\/jats:styled-content>\n reanalysis leads to novel declaration of pathogenicity in unexplained cases and can promote discovery of promising candidate epilepsy genes.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/epi.14683","type":"journal-article","created":{"date-parts":[[2019,3,13]],"date-time":"2019-03-13T18:27:43Z","timestamp":1552501663000},"page":"689-706","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":74,"title":["Diagnostic implications of genetic copy number variation in epilepsy plus"],"prefix":"10.1111","volume":"60","author":[{"given":"Antonietta","family":"Coppola","sequence":"first","affiliation":[{"name":"Department of Clinical and Experimental Epilepsy UCL Queen Square Institute of Neurology WC1N3BG UK"},{"name":"The Chalfont Centre for Epilepsy Chesham Lane, Chalfont St Peter Bucks UK"},{"name":"Epilepsy Centre Department of Neuroscience, Reproductive and Odontostomatological Sciences Federico II University Naples Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Cellini","sequence":"additional","affiliation":[{"name":"Pediatric Neurology, Neurogenetics and Neurobiology Unit and Laboratories Neuroscience Department A Meyer Children\u2018s Hospital University of Florence Florence Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"Stamberger","sequence":"additional","affiliation":[{"name":"Neurogenetics Group Center for Molecular Neurology VIB 2650 Antwerp Belgium"},{"name":"Laboratory of Neurogenetics Institute Born\u2010Bunge University of Antwerp Antwerp Belgium"},{"name":"Department of Neurology Antwerp University Hospital Antwerp Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elmo","family":"Saarentaus","sequence":"additional","affiliation":[{"name":"Analytic and Translational Genetics Unit Massachusetts General Hospital Harvard Medical School Boston Massachusetts USA"},{"name":"Stanley Center for Psychiatric Research Broad Institute of MIT and Harvard Cambridge Massachusetts USA"},{"name":"Institute of Molecular Medicine Finland FIMM University of Helsinki Helsinki Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valentina","family":"Cetica","sequence":"additional","affiliation":[{"name":"Pediatric Neurology, Neurogenetics and Neurobiology Unit and Laboratories Neuroscience Department A Meyer Children\u2018s Hospital University of Florence Florence Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dennis","family":"Lal","sequence":"additional","affiliation":[{"name":"Analytic and Translational Genetics Unit Massachusetts General Hospital Harvard Medical School Boston Massachusetts USA"},{"name":"Stanley Center for Psychiatric Research Broad Institute of MIT and Harvard Cambridge Massachusetts USA"},{"name":"Epilepsy Center Neurological Institute Cleveland Clinic 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