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在小鼠中,MYC过度表达和SMARCA4损失合作驱动脑髓母细胞瘤的形成

Carolin Göbel^1,2, Shweta Godbole³, Melanie Schoof^1,2

¹Department of Pediatric Hematology and Oncology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, Hamburg, 20251, Germany.

Acta neuropathologica communications

|November 3, 2023

概括

第三组脑髓母细胞瘤是一种侵袭性的儿童大脑瘤,可能涉及MYC和SMARCA4基因. 失去了SMARCA4,与MYC过度表达相结合,成功诱导了小鼠的侵略性瘤,这表明SMARCA4缺乏促进了脑髓母细胞瘤.

科学领域:

神经瘤学神经瘤学
儿科瘤学儿科瘤学
癌症遗传学癌症遗传学

背景情况:

第三组髓母细胞瘤是一种高度攻击性的儿科脑瘤.
大约30%的这些瘤中发现了MYC和SMARCA4的遗传变化.
在脑髓母细胞瘤的发展和治疗潜力中SMARCA4突变的作用在很大程度上是未知的.

研究的目的:

研究SMARCA4损失与MYC过度表达在脑髓母细胞瘤发展中的功能意义.
为研究SMARCA4/MYC驱动的脑髓母细胞瘤建立一个临床前模型.
为了确定参与SMARCA4缺陷脑髓母细胞瘤的分子途径.

主要方法:

结合MYC过度表达和小鼠颗粒细胞前体中的SMARCA4损失.
将基因工程细胞移植到接受者小鼠体内.
瘤组织学,基因表达特征 (RNA测序) 和DNA甲基化分析.
将小鼠数据与人类第3组脑髓母细胞瘤样本进行整合.

主要成果:

结合MYC过度表达和SMARCA4损失,诱导了活体中的侵略性,形髓母细胞瘤.
瘤仅由SMARCA4阴性细胞组成,这表明具有强大的选择性优势.
转录组分析揭示了特定于SMARCA4/MYC驱动的瘤发生的潜在基因表达变化.
在分子层面上,小鼠瘤与人类的第三组髓母细胞瘤非常相似.

结论:

在3组脑髓母细胞瘤的发展中,SMARCA4缺乏症起着促进瘤的作用.
开发的小鼠模型对研究SMARCA4/MYC驱动的脑髓母细胞瘤有价值.
这些发现为探索针对SMARCA4改变的脑髓母细胞瘤的向治疗策略提供了基础.

关键词:

在BAF复杂的 BAF复杂.这就是BRG1的原因.染色体重塑染色体重塑的方法第3组脑髓母细胞瘤我的世界 MYC

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