Anti-leukemic activity of axitinib against cells harboring the BCR-ABL T315I point mutation

J Hematol Oncol. 2015 Aug 4:8:97. doi: 10.1186/s13045-015-0190-9.

Abstract

The BCR-ABL; breakpoint cluster region-Abelson point mutation T315I is resistant to ABL tyrosine kinase inhibitors. However, axitinib, a vascular endothelial growth factor receptor inhibitor, is effective against this mutation. In this study, we investigated axitinib activity against ponatinib-resistant cells and found that axitinib inhibited cellular growth and apoptosis in Ba/F3 T315I-mutant cells and T315I-mutant primary samples, but not in ponatinib-resistant Ba/F3 cells and primary samples. Thus, an alternative strategy may be required to improve the prognosis of Philadelphia-chromosome-positive leukemia patients harboring BCR-ABL point mutations.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Axitinib
  • Fusion Proteins, bcr-abl / genetics*
  • Humans
  • Imidazoles / pharmacology
  • Imidazoles / therapeutic use*
  • Indazoles / pharmacology
  • Indazoles / therapeutic use*
  • Point Mutation / genetics*
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use*

Substances

  • Imidazoles
  • Indazoles
  • Protein Kinase Inhibitors
  • Axitinib
  • Fusion Proteins, bcr-abl