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In vitro modeling of glioblastoma initiation using PDGF-AA and p53-null neural progenitors.
Neuro-Oncology ( IF 15.9 ) Pub Date : 2020-04-16 , DOI: 10.1093/neuonc/noaa093
Alexandra K Bohm 1, 2 , Jessica DePetro 1, 2 , Carmen E Binding 1, 2 , Amanda Gerber 1, 2 , Nicholas Chahley 1, 2 , N Dan Berger 1, 2 , Mathaeus Ware 1, 2 , Kaitlin Thomas 1, 2 , U Senapathi 1, 2 , Shazreh Bukhari 1, 2 , Cindy Chen 1, 2 , Erin Chahley 1, 2 , Cameron Grisdale 3 , Sam Lawn 1, 2 , Yaping Yu 2 , Raymond Wong 4 , Yaoqing Shen 5 , Hiba Omairi 1, 2 , Reza Mirzaei 1, 3 , Nourah Alshatti 1, 2 , Haley Pedersen 1, 2 , Wee Yong 1, 2, 3 , Samuel Weiss 1, 2, 3 , Jennifer Chan 1, 2, 3 , P J Cimino 6 , John Kelly 1, 2, 3 , Steve Jones 5 , Eric Holland 6 , Michael Blough 1, 2 , Gregory Cairncross 1, 2, 5
Affiliation  

Imagining ways to prevent or treat glioblastoma (GBM) has been hindered by a lack of understanding of its pathogenesis. Although overexpression of platelet derived growth factor with two A-chains (PDGF-AA) may be an early event, critical details of the core biology of GBM are lacking. For example, existing PDGF-driven models replicate its microscopic appearance, but not its genomic architecture. Here we report a model that overcomes this barrier to authenticity.

中文翻译:

使用PDGF-AA和p53-null神经祖细胞对胶质母细胞瘤的体外建模。

缺乏对胶质母细胞瘤发病机理的了解,阻碍了预防或治疗胶质母细胞瘤(GBM)的方法。尽管具有两个A链的血小板衍生生长因子(PDGF-AA)的过表达可能是早期事件,但仍缺乏GBM核心生物学的关键细节。例如,现有的PDGF驱动的模型可以复制其微观外观,但不能复制其基因组架构。在这里,我们报告了一种克服了真实性障碍的模型。
更新日期:2020-04-16
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