Absence of ABL1 exon 2-encoded SH3 residues in BCR::ABL1 destabilizes the autoinhibited kinase conformation and confers resistance to asciminib

Leukemia. 2024 Sep;38(9):2046-2050. doi: 10.1038/s41375-024-02353-0. Epub 2024 Jul 31.
No abstract available

Publication types

  • Letter

MeSH terms

  • Drug Resistance, Neoplasm* / genetics
  • Exons* / genetics
  • Fusion Proteins, bcr-abl* / genetics
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Niacinamide / analogs & derivatives
  • Protein Conformation
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • Proto-Oncogene Proteins c-abl / genetics
  • Pyrazoles / pharmacology
  • Pyrazoles / therapeutic use
  • src Homology Domains

Substances

  • Fusion Proteins, bcr-abl
  • asciminib
  • Protein Kinase Inhibitors
  • Proto-Oncogene Proteins c-abl
  • ABL1 protein, human
  • Pyrazoles
  • BCR-ABL1 fusion protein, human
  • Niacinamide