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对KMT2A::AFF1-融合的本体基因特异性诱导促使一个独特的CD24阳性白血病前状态的发展

Ariana S Calderón¹, Roshanak Ghazanfari¹, Zahra Masoumi¹

¹Division of Molecular Hematology, Lund Stem Cell Center, Lund University, Lund, Sweden.

|July 11, 2025

概括

婴儿急性淋巴细胞白血病 (ALL) 是由KMT2A::AFF1驱动的,起源于子宫内. 一种新的小鼠模型揭示了一个独特的胚胎白血病前细胞群,这对于了解疾病发病和潜在的治疗点至关重要.

科学领域:

血液学血液学血液学
在瘤学瘤学.
发展生物学发展生物学

背景情况:

婴儿急性淋巴细胞白血病 (ALL) 是由KMT2A::AFF1合驱动的,是一种预后不佳的严重疾病.
对于KMT2A::AFF1 ALL的胚胎起源和早期发育阶段的了解仍然很少.

研究的目的:

开发和利用一种新的小鼠模型来研究KMT2A::AFF1驱动的婴儿ALL的胚胎起源.
识别和描述白血病前细胞群及其在疾病发病中的作用.

主要方法:

开发一种新的可诱导的KMT2A::AFF1小鼠模型.
针对不同发育阶段的造血干细胞和原生细胞 (HSPCs).
单细胞转录组学用于分析白血病前细胞特征.
鉴定细胞群的谱系可塑性和植入能力的评估.

主要成果:

一个独特的CD24+PreProB细胞子集在胚胎KMT2A::AFF1环境中专门扩展,而不是针对后来的祖先.
这种CD24+PreProB亚组表现出白血病前干细胞特征,包括血统可塑性和异常移植.
单细胞转录组学发现了一个干细胞特征,包括Hmga2上调,可转移到人类KMT2A::AFF1 ALL患者.

结论:

原始细胞对KMT2A::AFF1白血病发生至关重要,鉴定出明显的胚胎白血病前状态.
CD24+ PreProB子集代表了与人类婴儿ALL相关的潜在的白血病前干细胞群.
这些发现强调CD24作为KMT2A::AFF1驱动的婴儿ALL的潜在治疗点.

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