CCAAT增强子结合蛋白α与急性髓细胞白血病的发生  

Roles of CCAAT enhancer binding protein α in acute myeloblastic leukemia

作　　者：史庭 叶琇锦[1] SHI Ting;YE Xiujin(Department of Hematology,the First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China)

机构地区：[1]浙江大学医学院附属第一医院血液科,浙江杭州310003

出　　处：《浙江大学学报（医学版）》2018年第5期552-557,共6页Journal of Zhejiang University(Medical Sciences)

基　　金：浙江省科技计划(2016C33137);浙江省医药卫生科技计划(2017KY059)

摘　　要：CCAAT增强子结合蛋白α(C/EBPα)在髓系造血过程中起着重要的调控作用,其基因表达失调是急性髓细胞白血病(AML)发生的重要机制。C/EBPα基因表达失控的结局是p30过表达和p42不完全丧失,两者均促使AML的发生。因此,恢复C/EBPα表达比例,过表达p42或阻断p30致癌通路是治疗此类原因所致AML的重要途径。本文回顾了近年来关于C/EBPα表达失调及其两种蛋白体在AML发病机制中的研究进展。The CCAAT enhancer binding protein α(C/EBP α:p42 and p30),which encoded by CCAAT enhancer binding protein α(C/EBPα) gene,plays a pretty crucial role in the regulation of myeloid hematopoiesis.The disorder of CEBPA gene expression is an pivotal mechanism of acute myeloid leukemia(AML).The result of uncontrolled expression of C/EBP α gene is the over-expression of p30 and the incomplete loss of p42,both of which contribute to the occurrence of AML.Restoring the expression ratio of C/EBP α such as over-expression of p42 or blocking the carcinogenic pathway of p30 seems to be important for the treatment of AML caused by such causes.In order to better guide medical decision-making,this article reviews research progress on C/EBPα in the pathogenesis of AML.

关 键 词：CCAAT增强子结合蛋白α 白血病 髓样 急性 基因表达 突变 综述 

分 类 号：R733.71[医药卫生—肿瘤]