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K27M in canonical and noncanonical H3 variants occurs in distinct oligodendroglial cell lineages in brain midline gliomas.K27M 在经典和非经典 H3 变体中发生在脑中线胶质瘤中不同的少突胶质细胞谱系中。
Nat Genet. 2022 Dec;54(12):1865-1880. doi: 10.1038/s41588-022-01205-w. Epub 2022 Dec 5.
2
Defining the cell of origin for diffuse midline gliomas.确定弥漫性中线胶质瘤的起源细胞。
Nat Genet. 2022 Dec;54(12):1770-1771. doi: 10.1038/s41588-022-01231-8.
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The landscape of tumor cell states and spatial organization in H3-K27M mutant diffuse midline glioma across age and location.H3-K27M 突变弥漫性中线胶质瘤在年龄和位置上的肿瘤细胞状态和空间组织景观。
Nat Genet. 2022 Dec;54(12):1881-1894. doi: 10.1038/s41588-022-01236-3. Epub 2022 Dec 5.
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Synergistic anti-tumor efficacy of mutant isocitrate dehydrogenase 1 inhibitor SYC-435 with standard therapy in patient-derived xenograft mouse models of glioma.突变型异柠檬酸脱氢酶1抑制剂SYC-435与标准疗法在人源胶质瘤异种移植小鼠模型中的协同抗肿瘤疗效
Transl Oncol. 2022 Apr;18:101368. doi: 10.1016/j.tranon.2022.101368. Epub 2022 Feb 16.
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Evaluation of an EZH2 inhibitor in patient-derived orthotopic xenograft models of pediatric brain tumors alone and in combination with chemo- and radiation therapies.评估 EZH2 抑制剂在小儿脑肿瘤患者来源的原位异种移植模型中的作用，以及与化疗和放疗联合应用的效果。
Lab Invest. 2022 Feb;102(2):185-193. doi: 10.1038/s41374-021-00700-8. Epub 2021 Nov 20.
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Spatial Dissection of Invasive Front from Tumor Mass Enables Discovery of Novel microRNA Drivers of Glioblastoma Invasion.肿瘤块中侵袭前沿的空间解析使新型胶质母细胞瘤侵袭 microRNA 驱动子的发现成为可能。
Adv Sci (Weinh). 2021 Dec;8(23):e2101923. doi: 10.1002/advs.202101923. Epub 2021 Nov 1.
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The 2021 WHO Classification of Tumors of the Central Nervous System: a summary.2021 年世卫组织中枢神经系统肿瘤分类：概述。
Neuro Oncol. 2021 Aug 2;23(8):1231-1251. doi: 10.1093/neuonc/noab106.
8
Maximizing the potential of aggressive mouse tumor models in preclinical drug testing.最大限度地发挥侵袭性小鼠肿瘤模型在临床前药物测试中的潜力。
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Impact of SCID mouse gender on tumorigenicity, xenograft growth and drug-response in a large panel of orthotopic PDX models of pediatric brain tumors.SCID 小鼠性别对一大组儿童脑肿瘤原位 PDX 模型的致瘤性、异种移植物生长和药物反应的影响。
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10
A phase I trial of surgical resection with Gliadel Wafer placement followed by vaccination with dendritic cells pulsed with tumor lysate for patients with malignant glioma.一项针对恶性胶质瘤患者的I期试验，先进行手术切除并植入Gliadel晶片，然后用肿瘤裂解物脉冲处理的树突状细胞进行疫苗接种。
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CD57 定义了一种新型的癌症干细胞，可驱动弥漫性小儿型高级别神经胶质瘤的侵袭。

CD57 defines a novel cancer stem cell that drive invasion of diffuse pediatric-type high grade gliomas.

机构信息

Shenzhen Key Laboratory for Systems Medicine in Inflammatory Diseases, School of Medicine, Sun Yat-sen University, Shenzhen, Guangdong, 510080, China.

Program of Precision Medicine PDOX Modeling of Pediatric Tumors, Ann & Robert H. Lurie Children's Hospital of Chicago, Department of Pediatrics, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.

出版信息

Br J Cancer. 2024 Jul;131(2):258-270. doi: 10.1038/s41416-024-02724-5. Epub 2024 Jun 4.

DOI:10.1038/s41416-024-02724-5
PMID:38834745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11263392/
Abstract

BACKGROUND

Diffuse invasion remains a primary cause of treatment failure in pediatric high-grade glioma (pHGG). Identifying cellular driver(s) of pHGG invasion is needed for anti-invasion therapies.

METHODS

Ten highly invasive patient-derived orthotopic xenograft (PDOX) models of pHGG were subjected to isolation of matching pairs of invasive (HGG) and tumor core (HGG) cells.

RESULTS

pHGG cells were intrinsically more invasive than their matching pHGG cells. CSC profiling revealed co-positivity of CD133 and CD57 and identified CD57CD133 cells as the most abundant CSCs in the invasive front. In addition to discovering a new order of self-renewal capacities, i.e., CD57CD133 > CD57CD133 > CD57CD133 > CD57CD133 cells, we showed that CSC hierarchy was impacted by their spatial locations, and the highest self-renewal capacities were found in CD57CD133 cells in the HGG front (HGG/CD57CD133 cells) mediated by NANOG and SHH over-expression. Direct implantation of CD57 (CD57/CD133 and CD57/CD133) cells into mouse brains reconstituted diffusely invasion, while depleting CD57 cells (i.e., CD57CD133) abrogated pHGG invasion.

CONCLUSION

We revealed significantly increased invasive capacities in HGG cells, confirmed CD57 as a novel glioma stem cell marker, identified CD57CD133 and CD57CD133 cells as a new cellular driver of pHGG invasion and suggested a new dual-mode hierarchy of HGG stem cells.

摘要

背景

弥漫性浸润仍然是小儿高级别神经胶质瘤（pHGG）治疗失败的主要原因。需要鉴定 pHGG 浸润的细胞驱动因素，以进行抗浸润治疗。

方法

对 10 种高度侵袭性的 pHGG 患者来源的原位异种移植（PDOX）模型进行了侵袭性（HGG）和肿瘤核心（HGG）细胞的配对分离。

结果

pHGG 细胞天生比其匹配的 pHGG 细胞更具侵袭性。CSC 特征分析显示 CD133 和 CD57 的共阳性，并鉴定 CD57CD133 细胞为侵袭前沿中最丰富的 CSCs。除了发现新的自我更新能力顺序，即 CD57CD133 > CD57CD133 > CD57CD133 > CD57CD133 细胞外，我们还表明 CSC 层次结构受到其空间位置的影响，并且在 HGG 前沿（HGG/CD57CD133 细胞）中发现了最高的自我更新能力 CD57CD133 细胞，由 NANOG 和 SHH 的过度表达介导。直接将 CD57（CD57/CD133 和 CD57/CD133）细胞植入小鼠大脑中，重新构建了弥漫性浸润，而耗尽 CD57 细胞（即 CD57CD133）则消除了 pHGG 的浸润。

结论

我们揭示了 HGG 细胞中侵袭能力显著增加，证实 CD57 是一种新的神经胶质瘤干细胞标志物，鉴定 CD57CD133 和 CD57CD133 细胞是 pHGG 浸润的新细胞驱动因素，并提出了一种新的 HGG 干细胞双重模式层次结构。