Unique genetic and epigenetic mechanisms driving paediatric diffuse high-grade glioma

被引：220

作者：

Jones, Chris ^{[1
,2
]}

Baker, Suzanne J. ^{[3
]}

机构：

[1] Inst Canc Res, Ctr Evolut & Canc, Div Mol Pathol, Sutton SM2 5NG, Surrey, England

[2] Inst Canc Res, Div Canc Therapeut, Sutton SM2 5NG, Surrey, England

[3] St Jude Childrens Res Hosp, Dept Dev Neurobiol, Memphis, TN 38117 USA

来源：

NATURE REVIEWS CANCER | 2014年 / 14卷 / 10期

基金：

美国国家卫生研究院;

关键词：

INTRINSIC PONTINE GLIOMAS; RECEPTOR TYROSINE KINASES; HISTONE H3.3 MUTATIONS; BRAIN-STEM GLIOMA; DRIVER MUTATIONS; GENOMIC LANDSCAPE; CELL; GLIOBLASTOMA; CHILDREN; CANCER;

D O I：

10.1038/nrc3811

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Diffuse high-grade glionnas (HGGs) of childhood are a devastating spectrum of disease with no effective cures. The two-year survival for paediatric HGG ranges from 30%, for tumours arising in the cerebral cortex, to less than 10% for diffuse intrinsic pontine gliomas (DIPGs), which arise in the brainstem. Recent genome-wide studies provided abundant evidence that unique selective pressures drive HGG in children compared to adults, identifying novel oncogenic mutations connecting tunnorigenesis and chromatin regulation, as well as developmental signalling pathways. These new genetic findings give insights into disease pathogenesis and the challenges and opportunities for improving patient survival in these mostly incurable childhood brain tumours.

引用

页码：651 / 661

页数：11

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