Liu Hailong, Zhang Jing, Wang Ziwei, Wang Wei, Han Dongming, Chen Xuan, Su Yu, Zhang Jiao, Daniels Craig, Saulnier Olivier, Wang Zeyuan John, Gu Chunyu, Liu Fei, Deng Kaiwen, Wang Dongyang, Feng Zhaoyang, Zhao Yahui, Jiang Yifei, Gao Yu, Liu Zijia, Ma Mingxu, Li Yanong, Zhao Zitong, Yuan Hongyu, Sun Youliang, Shi Yanfeng, Yang Tao, Li Wenxing, Qi Xueling, Duan Zejun, Zhang Junping, Zhang Mingshan, Yu Chunjiang, Jin Wei, Yu Xinguang, Tian Yu, Li Shuaicheng, Li Chunde, Taylor Michael D, Li Jiankang, Liu Yong-Qiang, Qiu Xiaoguang, Jiang Tao
Department of Radiotherapy, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Beijing Neurosurgical Institute, Beijing 100070, China; China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China; Chinese Institute for Medical Research, Beijing 100069, China.
Department of Radiotherapy, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China.
Cell Rep Med. 2025 Jan 21;6(1):101914. doi: 10.1016/j.xcrm.2024.101914. Epub 2025 Jan 13.
Medulloblastoma (MB), a heterogeneous pediatric brain tumor, poses challenges in the treatment of tumor recurrence and dissemination. To characterize cellular diversity and genetic features, we comprehensively analyzed single-cell/nucleus RNA sequencing (sc/snRNA-seq), single-nucleus assay for transposase-accessible chromatin sequencing (snATAC-seq), and spatial transcriptomics profiles and identified distinct cellular populations in SHH (sonic hedgehog) and Group_3 subgroups, with varying proportions in local recurrence or dissemination. Local recurrence showed higher cycling tumor cell enrichment, whereas disseminated lesions had a relatively notable presence of differentiated subsets. Chromosomal alteration evaluation revealed distinct genetic subclones during MB progression, such as chr7q gain and chr11 loss in Group_3 disseminations. A subpopulation termed "high cellular plasticity (HCP)" emerged during MB progression and was associated with increased dividing potential and chromatin accessibility, contributing to recurrence. Inhibiting HCP-associated markers, like protein tyrosine phosphatase receptor type Z1 (PTPRZ1), efficiently suppressed MB progression in preclinical models. These findings address critical gaps in understanding the cellular diversity, chromosomal alterations, and biological dynamics of recurrent MB, offering potential therapeutic insights.
髓母细胞瘤(MB)是一种异质性儿童脑肿瘤,在肿瘤复发和播散的治疗方面存在挑战。为了表征细胞多样性和基因特征,我们全面分析了单细胞/细胞核RNA测序(sc/snRNA-seq)、转座酶可及染色质测序的单核分析(snATAC-seq)以及空间转录组学图谱,并在SHH(音猬因子)和3组亚组中鉴定出不同的细胞群,它们在局部复发或播散中的比例各不相同。局部复发显示出更高的循环肿瘤细胞富集,而播散性病变中分化亚群的存在相对显著。染色体改变评估揭示了MB进展过程中不同的基因亚克隆,例如3组播散中7号染色体长臂增益和11号染色体缺失。在MB进展过程中出现了一个被称为“高细胞可塑性(HCP)”的亚群,它与增加的分裂潜能和染色质可及性相关,促进复发。抑制与HCP相关的标志物,如蛋白酪氨酸磷酸酶受体Z1型(PTPRZ1),在临床前模型中有效抑制了MB进展。这些发现填补了在理解复发性MB的细胞多样性、染色体改变和生物学动态方面的关键空白,提供了潜在的治疗见解。