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首页> 外文期刊>Cancer Cell >Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.
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Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.

机译：突变型p53蛋白的表达暗示了鼠模型中神经干细胞与恶性星形胶质细胞瘤之间的谱系关系。

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Recent studies have identified genes and core pathways that are altered in human glioblastoma. However, the mechanisms by which alterations of these glioblastoma genes singly and cooperatively transform brain cells remain poorly understood. Further, the cell of origin of glioblastoma is largely elusive. By targeting a p53 in-frame deletion mutation to the brain, we show that p53 deficiency provides no significant growth advantage to adult brain cells, but appears to induce pleiotropic accumulation of cooperative oncogenic alterations driving gliomagenesis. Our data show that accumulation of a detectable level of mutant p53 proteins occurs first in neural stem cells in the subventricular zone (SVZ) and that subsequent expansion of mutant p53-expressing Olig2(+) transit-amplifying progenitor-like cells in the SVZ-associated areas initiates glioma formation.
机译：最近的研究已经鉴定出人类胶质母细胞瘤中改变的基因和核心途径。但是，这些胶质母细胞瘤基因的改变单独和协同转化脑细胞的机制仍然知之甚少。此外，胶质母细胞瘤的起源细胞在很大程度上难以捉摸。通过针对大脑的p53框内缺失突变，我们表明p53缺乏对成年脑细胞没有明显的生长优势，但似乎诱导了驱动胶质瘤发生的协同致癌性改变的多效性积累。我们的数据表明，可检测水平的突变型p53蛋白的积累首先发生在脑室下区域（SVZ）的神经干细胞中，随后在SVZ-中表达突变型p53的Olig2（+）转运放大祖细胞样细胞的扩增。相关区域启动神经胶质瘤的形成。

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