DNA repair contributes to the drug-resistant phenotype of primary acute myeloid leukaemia cells with FLT3 internal tandem duplications and is reversed by the FLT3 inhibitor PKC412

@article{Seedhouse2006DNARC,
  title={DNA repair contributes to the drug-resistant phenotype of primary acute myeloid leukaemia cells with FLT3 internal tandem duplications and is reversed by the FLT3 inhibitor PKC412},
  author={Claire Seedhouse and Hannah Hunter and Bethan Lloyd-Lewis and A-M Massip and Monica Pallis and Geoffrey I Carter and Martin Grundy and Shili Shang and Nigel H. Russell},
  journal={Leukemia},
  year={2006},
  volume={20},
  pages={2130-2136}
}
The presence of internal tandem duplications (ITD) mutations in the FMS-like tyrosine kinase 3 (FLT3) receptor influences the risk of relapse in acute myeloid leukaemia (AML). We have investigated DNA repair in FLT3-ITD and wild-type (WT) cells. Using the comet assay, we have demonstrated that the FLT3 inhibitor PKC412 significantly inhibits repair of DNA damage in the MV4-11-FLT3-ITD cell line and FLT3-ITD patient samples but not in the HL-60-FLT3-WT cell line or FLT3-WT patient samples… CONTINUE READING
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