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作 者:徐娜娜 吴涛[1] 白海[1] Xu Nana;Wu Tao;Bai Hai(Department of Hematology,Lanzhou General Hospital,Lanzhou Command,Lanzhou 730050,China)
机构地区:[1]兰州军区兰州总医院全军血液病中心,730050
出 处:《国际遗传学杂志》2019年第5期359-364,共6页International Journal of Genetics
摘 要:亲嗜性病毒整合位点1(ecotropic viral integration site 1,EVI1)基因高表达与急性髓系白血病(acute myeloid leukemia,AML)的发生、治疗及预后密切相关.已证实EVI1能够引起髓系分化和凋亡受阻,且在治疗过程中对化疗药物不敏感,其诱导缓解率和长期生存率低,是AML预后不良的分子生物学标记.但其中许多机制仍在探索中,且临床治疗效果欠佳.因此进一步阐明EVI1基因介导白血病发生的重要机制以及和AML的关系,将为开发新的靶向治疗提供依据.本文就EVI1基因表达在急性髓系白血病中的研究进展作一综述.The high expression of ecotropic viral integration site 1(EVI1)gene is closely related to the occurrence,treatment and prognosis of acute myeloid leukemia(AML).EVI1 is known to cause myeloid differentiation and apoptosis blockade,and is insensitive to chemotherapeutic drugs in the course of treatment.Its induction remission rate and long-term survival rate are low.EVI1 is a molecular biological marker for poor prognosis of AML.However,many of these mechanisms are still being explored,and the clinical treatment is not effective.Therefore,further elucidation of the important mechanism of EVI1 gene-mediated leukemia and its relationship with AML will provide a basis for the development of new targeted therapies.This article reviews the progress of EVI1 gene expression in acute myeloid leukemia.
关 键 词:EVI1 急性髓系白血病 3q26 重排 GATA2 H2AFY 三氧化二砷 线粒体肌酸激酶 吡咯-咪唑聚酰胺
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