克拉屈滨
癸他滨
阿糖胞苷
髓系白血病
医学
养生
耐火材料(行星科学)
肿瘤科
药品
诱导化疗
内科学
药理学
化疗
白血病
髓样
免疫学
化学
生物
生物化学
基因表达
天体生物学
DNA甲基化
基因
作者
Matteo Molica,Massimo Breccia,Saveria Capria,Silvia Maria Trisolini,Roberto Foá,Elias Jabbour,Tapan M. Kadia
标识
DOI:10.1080/10428194.2019.1672060
摘要
Despite advances in understanding the pathogenesis of acute myeloid leukemia (AML), the standard therapy remained nearly unchanged for several decades. There have been many efforts to improve the response and survival by either increasing the cytarabine (ARA-C) dose or adding a third agent to the standard chemotherapy regimen. Several studies have evaluated the addition of cladribine (CdA) to standard induction, exploiting its property to potentiate ARA-C uptake. Response rates for combination regimens including CdA in relapsed/refractory (R/R) adults are approximately 50% and approximately 70% in de novo AML. Recently, a low intensity combination of CdA and ARA‐C alternating with decitabine has shown promising results in older patients with AML. In this review, we will discuss the role of CdA in the treatment of AML, summarizing the recent clinical data regarding its incorporation into the induction therapy for adult AML.
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