Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.

@article{Stella2013SuppressionOS,
  title={Suppression of survivin induced by a BCR-ABL/JAK2/STAT3 pathway sensitizes imatinib-resistant CML cells to different cytotoxic drugs.},
  author={Stefania Stella and Elena Tirr{\`o} and Enrico Conte and Fabio Stagno and Francesco Di Raimondo and Livia Manzella and Paolo Vigneri},
  journal={Molecular cancer therapeutics},
  year={2013},
  volume={12 6},
  pages={
          1085-98
        }
}
The BCR-ABL oncoprotein of chronic myelogenous leukemia (CML) displays exclusive cytoplasmic localization and constitutive tyrosine kinase activity leading to the activation of different pathways that favor cell proliferation and survival. BCR-ABL induces survivin expression at both the mRNA and protein level, thus inhibiting the apoptotic machinery of CML cells and contributing to the expansion of the leukemic clone. We report that, in human CML cell lines, BCR-ABL-mediated upregulation of… CONTINUE READING
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