Abstract
The t(8; 21) (q22; q22) results in fusion of acute myeloid leukemia (AML)1 gene on chromosome 21 and ETO gene on chromosome 8, and produces AML1-ETO fusion gene, which plays a critical role in leukemogenesis by recruiting mSin3/N-CoR/SMART/HDACs corepressor complex to promoter of AML1 target genes including interluekin (IL)-3 and granulocyte macrophage-colony stimulating factor (GM-CSF) related to differentiation of hematopoietic stem cells and inactivating tumor suppressor genes. Histon deacetylase inhibitors (HDACI) reexpress silenced suppressor genes through regulation of histone acetylation and chromatin remodeling. Moreover, some of HDACI are able to degrade AML1-ETO fusion and play a selective role in AML1-ETO positive AML. The combinations of HDACI with DNA hypomethylated medicine, glucocorticoid, heat shock protein (HSP)-90 inhibitor and arsenic trioxide (ATO) are explored for the therapy of AML1-ETO positive AML. Herein, we discuss the effect and mechanism of HDACI on fusion protein of the AML1-ETO, and its target genes, as well as the mechanism in treatment of AML1-ETO positive AML with HDACI. Key words: Histone deacetylase inhibitors; Core binding factors; Leukemia, myeloid, acute
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