Elsevier

The Lancet

Volume 353, Issue 9154, 27 February 1999, Pages 727-728
The Lancet

Research Letters
New possibilities for prenatal diagnosis of muscular dystrophies: forced myogenesis with an adenoviral MyoD-vector

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Cited by (13)

  • Transcription factor rational design improves directed differentiation of human mesenchymal stem cells into skeletal myocytes

    2011, Molecular Therapy
    Citation Excerpt :

    These findings complement studies on the enhanced contribution of fibroblasts14,15 and mesoangioblasts of patients affected by inclusion-body myositis8 to skeletal muscle cell formation upon ectopic MyoD expression. MyoD-mediated myogenic conversion of nonmuscle cells is also used for the molecular diagnosis of muscular dystrophies, in particular DMD, as a way of bypassing the constraints associated with limited human muscle availability.16,17,18,19,20 For the same reason, MyoD-forced myogenesis is applied in the testing of exon skipping therapy for DMD.21

  • Dystrophinopathy carrier determination and detection of protein deficiencies in muscular dystrophy using lentiviral MyoD-forced myogenesis

    2007, Neuromuscular Disorders
    Citation Excerpt :

    Overexpression of MyoD in non-muscle cells produces fused multi-nucleated myotubes with well-defined sarcomeric structure, morphologically indistinguishable from their muscle-derived counterparts. Studies by Sancho and Roest have highlighted the potential of MyoD-forced myogenesis for prenatal diagnosis of Duchenne muscular dystrophy (DMD) by either direct immunohistochemical detection of dystrophin [8], or as a source of muscle-specific cDNA for use in a protein truncation test [9,10]. In the latter case, identification of a nonsense mutation resulting in a premature stop codon was then used for prenatal diagnosis of Duchenne muscular dystrophy in a subsequent pregnancy.

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