Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.

@article{OHare2004InhibitionOW,
  title={Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML.},
  author={Thomas O'Hare and Roy Pollock and Eric P. Stoffregen and Jeffrey A. Keats and Omar M. Abdullah and Erika M. Moseson and V. Rivera and Hao Tang and Chester A. Metcalf and Regine S. Bohacek and Yihan Wang and Raji Sundaramoorthi and William Shakespeare and David C Dalgarno and Tim Clackson and Tomi K. Sawyer and Michael Werner Nikolaus Deininger and Brian J. Druker},
  journal={Blood},
  year={2004},
  volume={104 8},
  pages={2532-9}
}
The deregulated, oncogenic tyrosine kinase Bcr-Abl causes chronic myeloid leukemia (CML). Imatinib mesylate (Gleevec, STI571), a Bcr-Abl kinase inhibitor, selectively inhibits proliferation and promotes apoptosis of CML cells. Despite the success of imatinib mesylate in the treatment of CML, resistance is observed, particularly in advanced disease. The most common imatinib mesylate resistance mechanism involves Bcr-Abl kinase domain mutations that impart varying degrees of drug insensitivity… CONTINUE READING
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