ASXL1 mutations predict inferior molecular response to nilotinib treatment in chronic myeloid leukemia View Full Text


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Article Info

DATE

2022-07-28

AUTHORS

Lioba Schönfeld, Jenny Rinke, Anna Hinze, Saskia N. Nagel, Vivien Schäfer, Thomas Schenk, Christian Fabisch, Tim H. Brümmendorf, Andreas Burchert, Philipp le Coutre, Stefan W. Krause, Susanne Saussele, Fatemeh Safizadeh, Markus Pfirrmann, Andreas Hochhaus, Thomas Ernst

ABSTRACT

Gene mutations independent of BCR::ABL1 have been identified in newly diagnosed patients with chronic myeloid leukemia (CML) in chronic phase, whereby mutations in epigenetic modifier genes were most common. These findings prompted the systematic analysis of prevalence, dynamics, and prognostic significance of such mutations, in a clinically well-characterized patient population of 222 CML patients from the TIGER study (CML-V) by targeted next-generation sequencing covering 54 myeloid leukemia-associated genes. In total, 53/222 CML patients (24%) carried 60 mutations at diagnosis with ASXL1 being most commonly affected (n = 20). To study mutation dynamics, longitudinal deep sequencing analysis of serial samples was performed in 100 patients after 12, 24, and 36 months of therapy. Typical patterns of clonal evolution included eradication, persistence, and emergence of mutated clones. Patients carrying an ASXL1 mutation at diagnosis showed a less favorable molecular response to nilotinib treatment, as a major molecular response (MMR) was achieved less frequently at month 12, 18, and 24 compared to all other patients. Patients with ASXL1 mutations were also younger and more frequently found in the high risk category, suggesting a central role of clonal evolution associated with ASXL1 mutations in CML pathogenesis. More... »

PAGES

2242-2249

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41375-022-01648-4

    DOI

    http://dx.doi.org/10.1038/s41375-022-01648-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1149818389

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35902731


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