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图像和多omics数据集汇聚在一起,以定义ATRT-SHH子组的不同神经祖先起源

María-Jesús Lobón-Iglesias¹, Mamy Andrianteranagna^1,2, Zhi-Yan Han¹

¹INSERM U830, Laboratory of Translational Research In Pediatric Oncology, PSL Research University, SIREDO Oncology center, Institut Curie Research Center, Paris, France.

Nature communications

|October 20, 2023

概括

非典型的甲状腺形形瘤 (ATRT) 起源于不同的位置. 这项研究揭示了MYC ATRT来自大脑外部,并确定了SHH ATRT子组的特定起源.

科学领域:

神经瘤学神经瘤学
发展生物学发展生物学
基因组学就是基因组学.

背景情况:

非典型的甲状腺狂犬病瘤 (ATRT) 是具有明显分子子组 (MYC,SHH,TYR) 的侵袭性儿科脑瘤.
了解ATRT的精确细胞和解剖起源对于开发向疗法至关重要.
以前的研究表明起源多样化,但确切的解剖位置在很大程度上仍未被描述.

研究的目的:

通过跨物种分析,研究不同ATRT亚组的精确解剖起源.
阐明在SMARCB1损失后推动ATRT发展的分子机制.

主要方法:

用小鼠模型 (Rosa26-CreERT2::Smarcb1flox/flox) 进行诊断时人类ATRT成像的比较分析.
单细胞RNA测序 (scRNA-seq) 的SHH ATRT.
生物信息轨迹和路径分析.

主要成果:

由MYC驱动的ATRT瘤显示出一种脑外来源的证据.
根据它们的起源,可以区分SHH ATRT:小脑前叶 (CAL) 与基底/心室内 (BG/IV) 区域.
CAL SHH ATRT起源于中脑后脑边界,而BG/IV SHH ATRT则起源于质突起.
损失SMARCB1触发了涉及REST,ID和NOTCH通路的脱差过程.

结论:

ATRTs来自特定的解剖位置,MYC瘤起源于中枢神经系统之外.
SHH ATRT亚型在大脑中具有不同的发育起源,为其生物学提供了信息.
SMARCB1损失启动了脱差计划,突出了发展途径中的潜在治疗点.

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