Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

@article{Heidel2006ClinicalRT,
  title={Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.},
  author={Florian H Heidel and Fian K. Solem and Frank Breitenbuecher and Daniel B. Lipka and Stefan Kasper and Melanie Thiede and Christian Brandts and Hubert Serve and Johannes L Roesel and F. R. Giles and Eric M. Feldman and Gerhard Ehninger and Gary J. Schiller and Stephen Nimer and Richard M Stone and Yanfeng Wang and Thomas Kindler and Pamela S Cohen and Christoph Huber and Thomas Fischer},
  journal={Blood},
  year={2006},
  volume={107 1},
  pages={293-300}
}
Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is… CONTINUE READING

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