Alternative genomic diagnoses for individuals with a clinical diagnosis of Dubowitz syndrome.
David A DymentAnne H O'Donnell-LuriaPankaj B AgrawalZeynep Coban AkdemirKyrieckos A AleckDanny AntakiHind Al SharhanPing-Yee B AuHatip AydinAlan H BeggsKaya BilguvarEric BoerwinkleHarrison BrandCatherine A BrownsteinSteve BuyskeBernard ChodirkerJungmin ChoiAlbert E ChudleyCarol L ClericuzioGerald F CoxCynthia CurryElke de BoerBert B A de VriesKathryn DunnCullen M DutmerEleina M EnglandJill A FahrnerBilgen Bilge GeckinliCasie A GenettiAlper GezdiriciWilliam T GibsonJoseph G GleesonCheryl R GreenbergApril HallAda HamoshTaila HartleyShalini N JhangianiEnder KaracaKristin KernohanJulie L LauzonM E Suzanne LewisR Brian LowryFrancesc López-GiráldezTara C MatiseJennifer McEvoy-VenneriBrenda McInnesAziz MhanniSixto Garcia MinaurJukka MoilanenAn NguyenMalgorzata J M NowaczykJennifer E PoseyKatrin ÕunapDavut PehlivanSander PajusaluLynette S PenneyTimothy PoterbaPaolo PronteraMaria Juliana Rodovalho DoriquiSarah L SawyerNara SobreiraValentina StanleyDeniz TorunDavid WargowskiP Dane WitmerIsaac WongJinchuan XingMaha Saad ZakiYeting Zhangnull nullnull nullKym M BoycottMichael J BamshadDeborah A NickersonElizabeth E BlueA Micheil InnesPublished in: American journal of medical genetics. Part A (2020)
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.