KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.

@article{Corbin2013KITSG,
  title={KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.},
  author={Amie S. Corbin and Thomas O'Hare and Zhimin Gu and Ira L. Kraft and Anna M. Eiring and Jamshid S Khorashad and Anthony D. Pomicter and Tian Yi Zhang and Christopher A. Eide and Paul William Manley and Jorge E. Cortes and Brian J. Druker and Michael Werner Nikolaus Deininger},
  journal={Cancer research},
  year={2013},
  volume={73 18},
  pages={5775-86}
}
Imatinib and other BCR-ABL1 inhibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors target additional kinases including KIT, raising the question of whether off-target effects contribute to clinical efficacy. On the basis of its involvement in CML pathogenesis, we hypothesized that KIT may govern responses of CML cells to imatinib. To test this, we assessed the growth of primary CML progenitor cells under conditions of sole BCR-ABL1, sole KIT, and dual… CONTINUE READING
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