만성 골수성 백혈병 세포주에서 As2O3에 의한 Bcr-Abl 융합유전자 발현의 변화
Arsenic Trioxide-Induced Bcr-Abl Fusion Oncogene Expression in the Chronic Myelogenous Leukemia Cell Line
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Abstract
Human chronic myelogenous leukemia(CML) is a malignacy of pluripotent hematopoietic cells caused by a dysregulated activity of the tyrosine kinase encoded by the chimeric bcr-abl oncogene. Arsenic trioxide(As2O3) has recently been demonstrated to be an effective inducer of apoptosis in patients with relapsed acute promyelocytic leukemia(APL) and in patients with APL in whom all-trans-retinoic acid and conventional chemotherapy has failed. As2O3 induced apoptosis in NB4 cells, cloned from a relapsed patient with APL, by inducing loss of the PML/RAR α protein and by suppressing expression of the Bcl-2 protein. We have focused our studies on the effects of As2O3 on the CML K562 cells and examined morphological changes of the cellsundergoing apoptosis with electron microscopy. Next the bcr-abl rearrangement was not detected after treatment with concentrations more than 50μ M/L As2O3 for 24 h. This result shows that As2O3 is a new promising antileukemic drug for treatment of CML and we needs to be investigated further.