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STAT3 as a mediator of BCR-ABL1-independent resistance in chronic myeloid leukemia

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Acknowledgements

PG and MWD received grant support from LLS Screen-to-Lead and MWD received research funding from Bristol-Myers Squibb, Novartis, Celgene, Genzyme and Gilead. The symposium and publication of this supplement were sponsored by the Division of Hematology/Oncology at the Warren Alpert Medical School of Brown University and NIH Center of Biomedical Research Excellence (COBRE) for Stem Cell Biology at Rhode Island Hospital.

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Correspondence to M W Deininger.

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MWD served as a paid advisory board member and consultant for Bristol-Myers Squibb, ARIAD Pharmaceuticals Inc., Novartis, Incyte Corporation and Pfizer. The remaining authors declare no conflict of interest.

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Eiring, A., Kraft, I., Page, B. et al. STAT3 as a mediator of BCR-ABL1-independent resistance in chronic myeloid leukemia. Leukemia Suppl 3, S5–S6 (2014). https://doi.org/10.1038/leusup.2014.3

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Keywords

  • TKI resistance
  • BCR-ABL1-independent resistance
  • BCR-ABL1-dependent resistance
  • CML stem cell
  • STAT3
  • pSTAT3Y705
  • BP-5-087

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