CELL:组蛋白和PDGFRA双重突变促进胶质瘤发生

2020-12-04 haibei MedSci原创

高级胶质瘤(HGGs)是致命的原发性脑肿瘤,是儿童和青少年死亡的主要原因。这些肿瘤经常携带编码组蛋白3(H3)变异的基因的体性突变或表观遗传修饰物,具有显著的神经解剖学和年龄特异性。

高级胶质瘤(HGGs)是致命的原发性脑肿瘤,是儿童和青少年死亡的主要原因。这些肿瘤经常携带编码组蛋白3(H3)变异的基因的体性突变或表观遗传修饰物,具有显著的神经解剖学和年龄特异性。青少年和年轻成年人(12-35岁)的HGGs主要发生在大脑半球叶,大量的HGGs被认为是表观遗传病。这些HGGs中超过30%的HGGs带有非规范的H3.3变体的杂合突变,导致甘氨酸34转精氨酸或缬氨酸(G34R/V)的氨基酸替换。

G34R/V肿瘤研究不足,很可能被低估,因为其独特的组织病理学异质性,神经元-胶质双区存在程度不一,导致误诊。事实上,近30%的中枢神经系统原始神经外胚层肿瘤(CNS-PNETs),即现在已经过时的混合性高等级神经元肿瘤实体,已被证明是G34R/V突变型HGGs。

另一方面,在分子水平上,G34R/V HGGs表现出统一的特征;它们几乎无一例外地携带α地中海贫血/智力低下综合征X-linked(ATRX)和肿瘤蛋白p53(TP53)的突变,缺乏少突胶质标记OLIG2的免疫反应性,并基于DNA甲基化与其他胶质瘤实体区别开来。

最近,研究人员在CELL杂志发文表明,50%的G34R/V肿瘤(n = 95)具有激活的PDGFRA突变,在复发时显示出强大的选择压力。虽然被认为是胶质瘤,但G34R/V肿瘤实际上产生于GSX2/DLX表达的中间神经元祖细胞中,G34R/V突变损害了神经元的分化。

起源系可能通过连接PDGFRA与GSX2调控元件的染色质环促进PDGFRA的共同选择,促进PDGFRA过度表达和突变。

在单细胞水平上,G34R/V肿瘤具有神经元/星形胶质双重身份,缺乏少突胶质特征,被GSX2/DLX介导的细胞命运规范主动抑制。G34R/V在肿瘤维持中可能成为可有可无的存在,而突变体PDGFRA是强效致癌的。

总的来说,该结果为致命性肿瘤开辟了一条新的研究途径。G34R/V胶质瘤是神经元恶性肿瘤,其中中间神经元前体细胞因G34R/V突变而分化停滞,而恶性胶质的发生是通过共同选择一个潜在的可靶向途径PDGFRA信号来促进的。

 

原始出处:

Carol C.L. Chen et al. Histone H3.3G34-Mutant Interneuron Progenitors Co-opt PDGFRA for Gliomagenesis. CELL (2020). 

 

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    2021-11-05 维他命
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    2021-01-14 tpa

    学习了,谢谢

    0

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    2020-12-06 xqptu
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    2020-12-06 liuyiping
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    2020-12-04 1461f038m76暂无昵称

    努力学习#学习#

    0

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