Insertional mutagenesis combined with acquired somatic mutations causes leukemogenesis following gene therapy of SCID-X1 patients.
By S. Howe, M. Mansour, Kerstin Schwarzwaelder, C. Bartholomae, M. Hubank, H. Kempski, M. Brugman, K. Pike-Overzet, S. Chatters, D. de Ridder and 17 more. Journal of Clinical Investigation, 2008
1,241 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/8b948bc90e7121ff8e1306dd4d49abaedb459419
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Citations in the corpus
- Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease (2010, background): “Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia.”
- Clinical use of lentiviral vectors (2018, background): “However, oncogenic potential is likely highly dependent on context, particularly preexisting genetic aberrations in treated patients [49].”
- Gene therapy clinical trials worldwide to 2012 – an update (2013, background): “The preliminary data implicate an insertion upstream of LMO2 and additional chromosomal mutations reminiscent of the genotoxic events occurring in the SCID-X1 trials.”