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Newborn screening of duchenne muscular dystrophy specifically targeting deletions amenable to exon-skipping therapy.
Beckers, Pablo; Caberg, Jean-Hubert; Dideberg, Vinciane; Dangouloff, Tamara; den Dunnen, Johan T; Bours, Vincent; Servais, Laurent; Boemer, François.
Afiliación
  • Beckers P; Biochemical Genetics Laboratory, Human Genetic Department, CHU de Liège, Université de Liège, CHU Sart-Tilman, Domaine Universitaire du Sart-Tilman, Avenue de l'Hôpital, 1, 4000, Liège, Belgium.
  • Caberg JH; Molecular Genetics Laboratory, Human Genetic Department, CHU Sart-Tilman, University of Liege, Liège, Belgium.
  • Dideberg V; Molecular Genetics Laboratory, Human Genetic Department, CHU Sart-Tilman, University of Liege, Liège, Belgium.
  • Dangouloff T; Division of Child Neurology, Neuromuscular Reference Center Disease, Department of Pediatrics, University Hospital Liège & University of Liège, Liège, Belgium.
  • den Dunnen JT; Department of Human Genetics and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands.
  • Bours V; Head of Human Genetics Department, CHU Sart-Tilman, University of Liege, Liège, Belgium.
  • Servais L; Division of Child Neurology, Neuromuscular Reference Center Disease, Department of Pediatrics, University Hospital Liège & University of Liège, Liège, Belgium.
  • Boemer F; Department of Paediatrics, MDUK Neuromuscular Center, University of Oxford, Oxford, UK.
Sci Rep ; 11(1): 3011, 2021 02 04.
Article en En | MEDLINE | ID: mdl-33542429
Duchenne Muscular Dystrophy (DMD) is a lethal progressive muscle-wasting disease. New treatment strategies relying on DMD gene exon-skipping therapy have recently been approved and about 30% of patients could be amenable to exon 51, 53 or 45 skipping. We evaluated the spectrum of deletions reported in DMD registries, and designed a method to screen newborns and identify DMD deletions amenable to exon 51, 53 and 45 skipping. We developed a multiplex qPCR assay identifying hemi(homo)-zygotic deletions of the flanking exons of these therapeutic targets in DMD exons (i.e. exons 44, 46, 50, 52 and 54). We conducted an evaluation of our new method in 51 male patients with a DMD phenotype, 50 female carriers of a DMD deletion and 19 controls. Studies were performed on dried blood spots with patient's consent. We analyzed qPCR amplification curves of controls, carriers, and DMD patients to discern the presence or the absence of the target exons. Analysis of the exons flanking the exon-skipping targets permitted the identification of patients that could benefit from exon-skipping. All samples were correctly genotyped, with either presence or absence of amplification of the target exon. This proof-of-concept study demonstrates that this new assay is a highly sensitive method to identify DMD patients carrying deletions that are rescuable by exon-skipping treatment. The method is easily scalable to population-based screening. This targeted screening approach could address the new management paradigm in DMD, and could help to optimize the beneficial therapeutic effect of DMD therapies by permitting pre-symptomatic care.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Terapia Genética / Distrofina / Tamizaje Neonatal / Distrofia Muscular de Duchenne Tipo de estudio: Diagnostic_studies / Screening_studies Límite: Female / Humans / Male / Newborn Idioma: En Revista: Sci Rep Año: 2021 Tipo del documento: Article País de afiliación: Bélgica

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Terapia Genética / Distrofina / Tamizaje Neonatal / Distrofia Muscular de Duchenne Tipo de estudio: Diagnostic_studies / Screening_studies Límite: Female / Humans / Male / Newborn Idioma: En Revista: Sci Rep Año: 2021 Tipo del documento: Article País de afiliación: Bélgica
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