Contact information
corinne.betts@paediatrics.ox.ac.uk
01865 618799
https://orcid.org/0000-0003-0579-8843
Room 3A26, Level 3, Academic Centre, John Radcliffe Hospital, Headington, OX3 9DU
Corinne Betts
Clinical Trial Coordinator and Operations Manager
Corinne Betts is the Clinical Trial Co-ordinator and Operations Manager for the STRONG Team, led by Prof. Laurent Servais and Dr Sithara Ramdas at the MDUK Oxford Neuromuscular Centre. She manages a portfolio of academic and industry led studies in the paediatric neuromuscular field.
Corinne obtained her BMedSci degree from the University of Kwa-Zulu Natal, and her DPhil/PhD from the University of Oxford, where she worked with Prof. Matthew Wood in the field of antisense therapy for the treatment of Duchenne Muscular Dystrophy. She continued in Prof. Wood’s laboratory working as a postdoctoral researcher for a further 5 years.
Corinne has worked as a Project Manager within the STRONG Team, where she assisted with regulatory approvals and the initiation of multiple clinical studies. She has 12 years’ experience in the biomedical field focussed on drug discovery and pre-clinical screening for rare neuromuscular diseases, and spent 4 years working in quality management for a successful immunodiagnostics biotech company. She has extensive experience managing independent research, leading teams, and successfully collaborating with experts in multiple fields.
Recent publications
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Dystrophin involvement in peripheral circadian SRF signalling.
Journal article
Betts CA. et al, (2021), Life Sci Alliance, 4
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Uniform sarcolemmal dystrophin expression is required to prevent extracellular microRNA release and improve dystrophic pathology.
Journal article
van Westering TLE. et al, (2020), J Cachexia Sarcopenia Muscle, 11, 578 - 593
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A fusion peptide directs enhanced systemic dystrophin exon skipping and functional restoration in dystrophin-deficient mdx mice.
Journal article
Yin H. et al, (2019), Hum Mol Genet, 28
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Cell-Penetrating Peptide Conjugates of Steric Blocking Oligonucleotides as Therapeutics for Neuromuscular Diseases from a Historical Perspective to Current Prospects of Treatment.
Journal article
Gait MJ. et al, (2019), Nucleic Acid Ther, 29, 1 - 12
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Cmah-dystrophin deficient mdx mice display an accelerated cardiac phenotype that is improved following peptide-PMO exon skipping treatment.
Journal article
Betts CA. et al, (2019), Hum Mol Genet, 28, 396 - 406