自噬在慢性髓细胞白血病中的研究进展  

Research progress of autophagy in chronic myeloid leukemia

作　　者：徐玲珑[1] 王云玲[2] 陈建霖[2] 董丽华 叶东宝 

机构地区：[1]浙江中医药大学第一临床医学院,杭州310053 [2]台州市中心医院血液科 [3]郑州大学附属肿瘤医院血液科河南省血液病研究所 [4]浙江省中医院血液科

出　　处：《临床血液学杂志》2017年第1期76-79,共4页Journal of Clinical Hematology

基　　金：台州市科技局资助项目(No:131KY14-03)

摘　　要：一线酪氨酸激酶抑制剂（TKI）给慢性髓细胞白血病（CML）的治疗带来了革命性进步。但长期应用TKI所带来的毒副作用、经济负担、CML干细胞的残留等问题,给TKI的临床应用带来了挑战。TKI的耐药问题也成为了目前CML研究中的热点。自噬是一种细胞面临营养缺乏或者应激状态时的自我保护机制。近年来越来越多的研究提示,自噬在CML细胞增殖、TKI耐药等过程中发挥重要作用。Despite of taking a revolutionary progress to the treatment of chronic myeloid leukemia（CML）,tyrosine kinase inhibitor（TKI）has raised a series of issues,such as relapse,drug-resistance,adverse effects and unbearable financial burden.It＇s recently been the highlight of CML research to prolong the overall survival of patients by regaining the sensitivity of TKI,as well as eliminating CML stem cells.It＇s been recently elucidated that autophagy,as a self-protected process against nutrients insufficiency or stress,participates in various pathophysiological activities.Autophagy plays both a pro-survival and pro-death role in tumorigenesis.Specific mechanism by which autophagy regulates CML cells needs to be explored in order to further improve the outcome of CML.Here,we make a comprehensive review on the molecular biologics of autophagy and its relations with CML.

关 键 词：自噬 白血病 髓系 慢性 BCR-ABL 酪氨酸激酶抑制剂 

分 类 号：R733.72[医药卫生—肿瘤]