TO THE EDITOR:

Metabolic re-programming is a hallmark of acute myeloid leukemia (AML) [1]. AML cells co-opt bone marrow niche to utilize fatty acid or amino acids to fuel oxidative phosphorylation (OXPHOS), possibly contributing to resistance [2,3,4,5]. We previously reported leukaemia cells compete over bone marrow micro-environment cells on glucose uptake in a MLL-AF9-driven AML mouse model [6]. Whether glucose uptake by leukaemia cells correlates with response to induction chemotherapy is unknown.

中文翻译：

---

白血病细胞体外葡萄糖摄取能力与急性髓系白血病对诱导治疗的反应相关

 致编辑：

代谢重编程是急性髓系白血病 （AML） 的标志 [1]。AML 细胞利用骨髓生态位利用脂肪酸或氨基酸来促进氧化磷酸化 （OXPHOS），这可能导致耐药性 [2,3,4,5]。我们之前报道了在 MLL-AF9 驱动的 AML 小鼠模型中，白血病细胞在葡萄糖摄取方面与骨髓微环境细胞竞争 [6]。白血病细胞对葡萄糖的摄取是否与对诱导化疗的反应相关尚不清楚。