奎扎替尼治疗急性髓系白血病及其耐药机制研究进展  

Progress of quizartinib in treatment of acute myeloid leukemia and its mechanism of drug resistance

作　　者：马蓉艳 李莉娟[1] 郭晓嘉[1] 郝正栋[1] 刘敏杰 李婷[1] 张连生[1] MA Rongyan;LI Lijuan;GUO Xiaojia

机构地区：[1]兰州大学第二医院血液科,兰州730030

出　　处：《临床血液学杂志》2020年第3期359-364,共6页Journal of Clinical Hematology

基　　金：国家自然科学基金(No:31660112)。

摘　　要：急性髓细胞白血病(acute myeloid leukemia,AML)是一组以髓系造血干祖细胞增殖失控、分化障碍、凋亡受阻为特点的高度异质性疾病,多种基因突变是其主要的发病基础[1]。近年来,随着二代测序技术的发展和应用,越来越多的AML相关基因突变被发现,FMS样酪氨酸激酶-3(FMS-like tyrosine kinase 3,FLT3)突变是AML患者最常见的基因突变之一,与AML的高风险复发和不良预后相关[2],尤其是FLT3-内部串联重复(internal tandem duplications,ITD)阳性患者,其抑制剂的相关研究始终是众多学者期望改善高危AML患者的突破点。In recent years,FMS-like tyrosine kinase-3(FLT3) inhibitors,midostaurin and gilteritinib have been approved by the US FDA for the treatment of acute myeloid leukemia(AML),making FLT3 inhibitors stand out from the numerous molecular targeted drugs of AML.This has spurred researchers’ interest in the development and exploration of novel FLT3 inhibitors.Quizartinib is a new generation of oral FLT3 inhibitors that highly specifically target FLT3-ITD mutations and sustainably inhibit the proliferation of mutant AML cells,clinically showing effective anti-tumor activity and good tolerance.In particular,it improves the response rate and overall survival of patients with relapsed/refractory AML,bringing new hope to these patients.This article reviews the research progress of quizartinib in the treatment of AML and its resistance mechanism.

关 键 词：急性髓系白血病 FLT3基因突变 FLT3抑制剂 奎扎替尼 

分 类 号：R733.31[医药卫生—肿瘤]