[Metabolism and therapy in acute myeloid leukemia with isocitrate dehydrogenase 1/2 mutations].

IF 0.6 4区医学 Q4 MEDICINE, RESEARCH & EXPERIMENTAL

M S-medecine Sciences Pub Date : 2025-04-01 Epub Date: 2025-04-28 DOI:10.1051/medsci/2025045

Ludovic Gabellier, Enzo Bosetta, Maël Heiblig, Jean-Emmanuel Sarry

引用次数: 0

Abstract

Isocitrate dehydrogenase IDH1 and IDH2, key enzymes in central and energy metabolism, are frequently mutated in acute myeloid leukemia (AML). They catalyze the production of the oncometabolite R-2-hydroxyglurate, which plays a key role in leukemogenesis and relapse of patients after standard AML treatments. Although the recent introduction of selective inhibitors of IDH1 (ivosidenib) and IDH2 (enasidenib) has improved the prognosis of patients with IDH1- and IDH2-mutant AML, several mechanisms of resistance to these treatments have already been identified, including metabolic reprogramming. The study of these mechanisms has opened up new therapeutic opportunities for the monitoring and treatment of patients with this subtype of AML.

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异柠檬酸脱氢酶1/2突变急性髓系白血病的代谢和治疗。

异柠檬酸脱氢酶IDH1和IDH2是中枢和能量代谢的关键酶，在急性髓性白血病（AML）中经常发生突变。它们催化肿瘤代谢物r -2-羟基谷氨酸盐的产生，这在白血病发生和AML标准治疗后患者复发中起着关键作用。尽管最近引入的IDH1 （ivosidenib）和IDH2 （enasidenib）选择性抑制剂改善了IDH1-和IDH2-突变AML患者的预后，但已经确定了对这些治疗的几种耐药机制，包括代谢重编程。这些机制的研究为监测和治疗该亚型AML患者开辟了新的治疗机会。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

M S-medecine Sciences 医学-医学：研究与实验

CiteScore

0.80

自引率

14.30%

发文量

182

审稿时长

4-8 weeks

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