融合蛋白AML1-ETO的生物学功能及致癌机制探讨  

Biological function and cancerogenic mechanism of AML1-ETO fusion protein

作　　者：刘晓晓[1,2] 张波[1] 赵倩[1] 

机构地区：[1]上海交通大学医学院病理生理教研室 [2]中国科学院上海生命科学研究院/上海交通大学医学院健康科学研究所,上海200025

出　　处：《中国病理生理杂志》2011年第3期603-606,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30870979);上海科委基础研究重点资助项目(No.08JC1413500)

摘　　要：AML1-ETO融合蛋白是染色体易位t（8;21）（q22;q22）的产物,见于15%的急性髓细胞性白血病（acute myelocytic leukemia,AML）,在FAB（French-American-British,FAB）分型M2型白血病中的阳性率为40%-50%,其中M2b亚型中的阳性率为90%,少见于M0、M1和M4型白血病,极少见于骨髓增生异常综合征（myelodysplastic syndrome,MDS）。AML1-ETO fusion protein is the product of（8;21） translocation in M2 type acute myelocytic leukemia（AML）.As a transcription repressor,AML1-ETO can block the differentiation of hematopoietic cells by repressing the expression of some important hematopoiesis-related transcription factors.Recent results indicate that the fusion protein also induces the epigenetic silencing of some target genes,resulting in the delay of hematopoietic maturation.Moreover,AML1-ETO promotes the proliferation of hematopoietic stem cells through up-regulating the expression of Jagged1 and miR-24.Meanwhile,a panel of results in the pathogenesis of AML1-ETO show that the expression of AML1-ETO alone can not induce AML.The secondary events or hits like c-kit gene mutation and the AML1-ETO9a truncation play an important role in leukemogenesis of AML1-ETO-positive cells.

关 键 词：AML1-ETO融合蛋白 转录阻遏 造血干细胞 二次打击事件 

分 类 号：R363[医药卫生—病理学]