TITLE

CD117 (c-kit) Expression on CD34+ Cells Participates in the Cytogenetic Response to Imatinib in Patients with Chronic Myeloid Leukemia in the First Chronic Phase

AUTHOR(S)
Dybko, Jaroslaw; Haus, Olga; Jaźwiec, Bożena; Urbaniak, Joanna; Woźniak, Mieczysław; Kaczmar-Dybko, agnieszka; Urbaniak-Kujda, Donata; Kapelko-Slowik, Katarzyna; Kuliczkowski, Kazimierz
PUB. DATE
August 2014
SOURCE
Acta Haematologica;Aug2014, Vol. 132 Issue 2, p166
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Background: Chronic 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. Methods: Cytogenetic analysis, real-time quantitative reverse-transcriptase polymerase chain reaction, flow-cytometric analysis and imatinib serum level quantification were applied. Results: The 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. Conclusion: To achieve optimal treatment response in CML patients, the elimination of CD34+CD117+ may be necessary through an apoptotic pathway. © 2014 S. Karger AG, Basel
ACCESSION #
97552691

 

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