威尼斯人
阿扎胞苷
医学
髓系白血病
癸他滨
靶向治疗
表观遗传学
联合疗法
精密医学
养生
肿瘤科
癌症研究
白血病
内科学
癌症
生物
基因
DNA甲基化
遗传学
慢性淋巴细胞白血病
基因表达
病理
作者
Sangeetha Venugopal,Justin M. Watts
出处
期刊:Hematology
[American Society of Hematology]
日期:2023-12-08
卷期号:2023 (1): 192-197
被引量:1
标识
DOI:10.1182/hematology.2023000429
摘要
Abstract The routine use of next-generation sequencing methods has underscored the genetic and clonal heterogeneity of acute myeloid leukemia (AML), subsequently ushering in an era of precision medicine–based targeted therapies exemplified by the small-molecule inhibitors of FLT3, IDH1/IDH2, and BCL2. This advent of targeted drugs in AML has broadened the spectrum of antileukemic therapies, and the approval of venetoclax in combination with a hypomethylating agent has been a welcome addition to our AML patients unable to tolerate intensive chemotherapy. Mounting evidence demonstrates that molecularly targeted agents combined with epigenetic therapies exhibit synergistic augmented leukemic cell kill compared to single-agent therapy. With such great power comes greater responsibility in determining the appropriate frontline AML treatment regimen in a molecularly defined subset and identifying safe and effective combination therapies with different mechanisms of action to outmaneuver primary and secondary resistance mechanisms in AML.
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