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  • Original Paper
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Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2

Abstract

The chimeric gene, AML1/ETO (MTG8), generated in t(8;21) acute myeloid leukemia enhances the expression of Bcl-2. To evaluate whether this enhancement is the primary role of AML1/ETO in leukemogenesis, effects of over-expression of Bcl-2 in the murine myeloid precursor cell line, 32Dcl3, were examined. When 32Dcl3 cells expressing exogenous Bcl-2 were induced to differentiate, the onset of morphological differentiation was delayed. However, even the cells expressing very high levels of exogenous Bcl-2 eventually underwent differentiation without a significant decrease in the synthesis of Bcl-2. On the contrary, 32Dcl3 cells stably expressing AML1/ETO were completely resistant to differentiation and continued to grow in the presence of G-CSF. These results are consistent with the interpretation that stimulation of Bcl-2 expression is not the primary target of AML1/ETO.

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Acknowledgements

We thank M Tsujimoto (Osaka University), H Yamauchi and S Fujita (Ehime University), A Friedman (Johns Hopkins University) and T Era (Osaka University) for Bcl-2 cDNA (pSKMBKR), ME-1 cells, 32Dcl3 cells and AML1/ETO cDNA, respectively. This work was supported by Grant-in-Aid 0925322 for Priority Area on Cancer Research from the Ministry of Education, Science and Culture, Japan.

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Kohzaki, H., Ito, K., Huang, G. et al. Block of granulocytic differentiation of 32Dcl3 cells by AML1/ETO(MTG8) but not by highly expressed Bcl-2. Oncogene 18, 4055–4062 (1999). https://doi.org/10.1038/sj.onc.1202735

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