医学
奥佐美星
阿糖胞苷
威尼斯人
髓系白血病
癸他滨
阿扎胞苷
米多司他林
卡奇霉素
药理学
氟达拉滨
肿瘤科
低甲基化剂
移植
柔红霉素
内科学
白血病
化疗
环磷酰胺
CD33
干细胞
慢性淋巴细胞白血病
生物化学
基因表达
遗传学
化学
川地34
基因
DNA甲基化
生物
出处
期刊:PubMed
日期:2018-10-12
卷期号:59 (10): 1988-1996
被引量:2
标识
DOI:10.11406/rinketsu.59.1988
摘要
The mainstay of therapeutic modalities of acute myeloid leukemia (AML) includes intensive chemotherapies and allogeneic hematopoietic cell transplantation. The gold standard of the induction treatment is a regular dose of cytarabine plus anthracycline, and several courses of consolidation therapy are administered. Allogeneic hematopoietic cell transplantation is employed in patients with intermediate-poor risks. No new drugs have been introduced to the treatment of AML for nearly 30 years. However, in 2017, the US Food and Drug Administration approved four novel drugs for treating AML: FLT3 inhibitor midostaurin, IDH2 inhibitor enasidenib, liposomal cytarabine-daunorubicin CPX-351, and revived antibody-drug conjugate gemtuzumab ozogamicin. In Japan, several new agents are also undergoing clinical trials, including Bcl-2 inhibitor venetoclax, CDK9 inhibitor alvocidib, smoothened (SMO) inhibitor glasdegib, hypomethylating agents guadecitabine and azacitidine, NEDD8 inhibitor pevonedistat, and FLT3 inhibitors quizartinib and gilteritinib. These agents will be incorporated into the conventional 7+3 regimen or combined with hypomethylating agents or low-dose cytarabine to improve the therapeutic outcomes of AML.
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