The TREAT-NMD DMD Global Database: Analysis of More than 7,000 Duchenne Muscular Dystrophy Mutations

Catherine L. Bladen(Muscular Dystrophy UK), David Salgado(Inserm), Soledad Monges(Garrahan Hospital), María Eugenia Foncuberta(Garrahan Hospital), Kyriaki Kekou(National and Kapodistrian University of Athens), Konstantina Kosma(National and Kapodistrian University of Athens), Hugh Dawkins(Government of Western Australia Department of Health), Leanne Lamont(Government of Western Australia Department of Health), Anna J. Roy(Institut Scientifique de Santé Publique), Teodora Chamova(Medical University of Sofia), Velina Guergueltcheva(Medical University of Sofia), H.S. Chan(Queen Mary Hospital), Lawrence Korngut(University of Calgary), Craig Campbell(Western University), Yi Dai(Chinese Academy of Medical Sciences & Peking Union Medical College), Jen Wang(Chinese People's Armed Police General Hospital), Nina Barišić(University Hospital Centre Zagreb), Petr Brabec(Masaryk University), Jaana Lähdetie(Turku University Hospital), Maggie C. Walter(Ludwig-Maximilians-Universität München), Olivia Schreiber‐Katz(Ludwig-Maximilians-Universität München), Veronika Karcagi, Marta Garami, Venkatarman Viswanathan, Farhad Bayat(Pasteur Institute of Iran), Filippo Buccella(Parent Project Onlus), En Kimura, Zaïda Koeks(Leiden University Medical Center), J.C. van den Bergen(Leiden University Medical Center), Miriam Rodrigues(Auckland District Health Board), Richard Roxburgh(Auckland District Health Board), Anna Łusakowska(Medical University of Warsaw), Anna Kostera‐Pruszczyk(Medical University of Warsaw), Janusz Zimowski(Institute of Psychiatry and Neurology), Rosário Santos(Centro de Genética Clínica), Elena Neagu, Svetlana Artemieva(Scientific Center of Children's Health), Vedrana Milić Rašić(University of Belgrade), Dina Vojinović(University of Belgrade), Manuel Posada de la Paz(Instituto de Salud Carlos III), Clemens Bloetzer(University of Lausanne), P.Y. Jeannet(University of Lausanne), Franziska Joncourt(University Hospital of Bern), Jordi Díaz‐Manera(Hospital de Sant Pau), Eduard Gallardo(Hospital de Sant Pau), Ayşen Karaduman(Hacettepe University), Haluk Topaloğlu(Hacettepe University Hospital), Rasha El Sherif(Ain Shams University Hospital), Angela Stringer, Andriy Shatillo(Institute of Neurology, Psychiatry and Narcology), Ann Martin, Holly L. Peay, M. Bellgard(Murdoch University), Janbernd Kirschner(University Medical Center Freiburg), Kevin M. Flanigan(Nationwide Children's Hospital), Volker Straub(Muscular Dystrophy UK), Kate Bushby(Muscular Dystrophy UK), Jan J.G.M. Verschuuren(Leiden University Medical Center), Annemieke Aartsma‐Rus(Leiden University Medical Center), Christophe Béroud(Inserm), Hanns Lochmüller(Muscular Dystrophy UK)
Human Mutation
January 21, 2015
Cited by 742Open Access
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Abstract

Analyzing the type and frequency of patient-specific mutations that give rise to Duchenne muscular dystrophy (DMD) is an invaluable tool for diagnostics, basic scientific research, trial planning, and improved clinical care. Locus-specific databases allow for the collection, organization, storage, and analysis of genetic variants of disease. Here, we describe the development and analysis of the TREAT-NMD DMD Global database (http://umd.be/TREAT_DMD/). We analyzed genetic data for 7,149 DMD mutations held within the database. A total of 5,682 large mutations were observed (80% of total mutations), of which 4,894 (86%) were deletions (1 exon or larger) and 784 (14%) were duplications (1 exon or larger). There were 1,445 small mutations (smaller than 1 exon, 20% of all mutations), of which 358 (25%) were small deletions and 132 (9%) small insertions and 199 (14%) affected the splice sites. Point mutations totalled 756 (52% of small mutations) with 726 (50%) nonsense mutations and 30 (2%) missense mutations. Finally, 22 (0.3%) mid-intronic mutations were observed. In addition, mutations were identified within the database that would potentially benefit from novel genetic therapies for DMD including stop codon read-through therapies (10% of total mutations) and exon skipping therapy (80% of deletions and 55% of total mutations).


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