| Literature DB >> 33098347 |
David A Dyment1,2, Anne O'Donnell-Luria3,4,5, Pankaj B Agrawal4,5, Zeynep Coban Akdemir6, Kyrieckos A Aleck7, Danny Antaki8,9, Hind Al Sharhan10,11, Ping-Yee B Au12, Hatip Aydin13, Alan H Beggs4,5, Kaya Bilguvar14,15, Eric Boerwinkle16, Harrison Brand3,17,18, Catherine A Brownstein4,5, Steve Buyske19, Bernard Chodirker20, Jungmin Choi14,21, Albert E Chudley20, Carol L Clericuzio22, Gerald F Cox4,5, Cynthia Curry23,24, Elke de Boer25, Bert B A de Vries25,26, Kathryn Dunn5, Cullen M Dutmer27, Eleina M England3, Jill A Fahrner10, Bilgen B Geckinli28, Casie A Genetti4,5, Alper Gezdirici29, William T Gibson30, Joseph G Gleeson8,9, Cheryl R Greenberg20, April Hall31, Ada Hamosh10, Taila Hartley2, Shalini N Jhangiani6, Ender Karaca6, Kristin Kernohan2, Julie L Lauzon12, M E Suzanne Lewis30, R Brian Lowry12, Francesc López-Giráldez14,15, Tara C Matise32, Jennifer McEvoy-Venneri8,9, Brenda McInnes12, Aziz Mhanni20, Sixto Garcia Minaur33, Jukka Moilanen34, An Nguyen8,9, Malgorzata J M Nowaczyk35, Jennifer E Posey6, Katrin Õunap36,37, Davut Pehlivan6,38,39, Sander Pajusalu14,36,37, Lynette S Penney40, Timothy Poterba3,41, Paolo Prontera42, Maria Juliana Rodovalho Doriqui43, Sarah L Sawyer1,2, Nara Sobreira10, Valentina Stanley8,9, Deniz Torun44, David Wargowski45, P Dane Witmer10, Isaac Wong3,17,18, Jinchuan Xing32, Maha S Zaki46, Yeting Zhang32, Kym M Boycott1,2, Michael J Bamshad47,48,49, Deborah A Nickerson49,48, Elizabeth E Blue50, A Micheil Innes12.
Abstract
Dubowitz syndrome (DubS) is considered a recognizable syndrome characterized by a distinctive facial appearance and deficits in growth and development. There have been over 200 individuals reported with Dubowitz or a "Dubowitz-like" condition, although no single gene has been implicated as responsible for its cause. We have performed exome (ES) or genome sequencing (GS) for 31 individuals clinically diagnosed with DubS. After genome-wide sequencing, rare variant filtering and computational and Mendelian genomic analyses, a presumptive molecular diagnosis was made in 13/27 (48%) families. The molecular diagnoses included biallelic variants in SKIV2L, SLC35C1, BRCA1, NSUN2; de novo variants in ARID1B, ARID1A, CREBBP, POGZ, TAF1, HDAC8, and copy-number variation at1p36.11(ARID1A), 8q22.2(VPS13B), Xp22, and Xq13(HDAC8). Variants of unknown significance in known disease genes, and also in genes of uncertain significance, were observed in 7/27 (26%) additional families. Only one gene, HDAC8, could explain the phenotype in more than one family (N = 2). All but two of the genomic diagnoses were for genes discovered, or for conditions recognized, since the introduction of next-generation sequencing. Overall, the DubS-like clinical phenotype is associated with extensive locus heterogeneity and the molecular diagnoses made are for emerging clinical conditions sharing characteristic features that overlap the DubS phenotype.Entities:
Keywords: Dubowitz syndrome; exome sequencing; genetic heterogeneity; genome sequencing; microarray
Year: 2020 PMID: 33098347 DOI: 10.1002/ajmg.a.61926
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.802