Targeting of GSK3β promotes imatinib-mediated apoptosis in quiescent CD34+ chronic myeloid leukemia progenitors, preserving normal stem cells.

@article{Reddiconto2012TargetingOG,
  title={Targeting of GSK3β promotes imatinib-mediated apoptosis in quiescent CD34+ chronic myeloid leukemia progenitors, preserving normal stem cells.},
  author={Giovanni Reddiconto and Claudia Toto and Ilaria Elena Palam{\`a} and Simone De Leo and Emanuela de Luca and Serena De Matteis and Luciana Dini and Carlo Gambacorti Passerini and Nicola di Renzo and Michele Maffia and Addolorata Maria Luce Coluccia},
  journal={Blood},
  year={2012},
  volume={119 10},
  pages={2335-45}
}
The targeting of BCR-ABL, a hybrid oncogenic tyrosine (Y) kinase, does not eradicate chronic myeloid leukemia (CML)-initiating cells. Activation of β-catenin was linked to CML leukemogenesis and drug resistance through its BCR-ABL-dependent Y phosphorylation and impaired binding to GSK3β (glycogen synthase kinase 3β). Herein, we show that GSK3β is constitutively Y(216) phospho-activated and predominantly relocated to the cytoplasm in primary CML stem/progenitor cells compared with its balanced… CONTINUE READING
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Insights into the stem cells of chronic myeloid leukemia

  • AC Eaves, MJ Barnett, L Ponchio, JD Cashman, AL Petzer, CJ Eaves
  • 2010

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