• Jaroslaw Dybko, Olga Haus, Bozena Jazwiec, Joanna Urbaniak, Mieczysław Wozniak, Agnieszka Kaczmar-Dybko, Donata Urbaniak-Kujda, Katarzyna Kapelko-Slowik, and Kazimierz Kuliczkowski.
• Acta Haematol. 2014 Jan 1;132(2):166-71.

BackgroundChronic myeloid leukemia (CML) biology seemed to be perfectly explored especially at the beginning of the tyrosine kinase inhibitors era. Later years with imatinib and second-generation tyrosine kinase inhibitors showed a variety of resistance mechanisms and it became obvious that the bcr-abl chimeric gene is not the only enemy to fight. Some studies assumed the decreased rate of programmed cell death (apoptotic) to be the primary mechanism by which BCR-ABL affects expansion of the leukemic clone in CML. Therefore, the aim of this study was to investigate the role of c-kit inhibition in treatment response.MethodsCytogenetic analysis, real-time quantitative reverse-transcriptase polymerase chain reaction, flow-cytometric analysis and imatinib serum level quantification were applied.ResultsThe percentage of CD34+ cells expressing c-kit (CD117) isolated from bone marrow samples of 54 CML patients treated with standard-dose imatinib was significantly lower among imatinib responders. The fraction of apoptotic CD34+CD117+ cells in this patient group was significantly higher than in nonresponders.ConclusionTo achieve optimal treatment response in CML patients, the elimination of CD34+CD117+ may be necessary through an apoptotic pathway.© 2014 S. Karger AG, Basel

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