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.
Acta Haematol
; 132(2): 166-71, 2014.
Article
in En
| MEDLINE
| ID: mdl-24577437
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.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Piperazines
/
Pyrimidines
/
Neoplastic Stem Cells
/
Benzamides
/
Bone Marrow
/
Leukemia, Myeloid, Chronic-Phase
/
Proto-Oncogene Proteins c-kit
/
Protein Kinase Inhibitors
/
Neoplasm Proteins
/
Antineoplastic Agents
Limits:
Adult
/
Aged
/
Female
/
Humans
/
Male
/
Middle aged
Language:
En
Journal:
Acta Haematol
Year:
2014
Document type:
Article