Genetic Alterations in Glioma

Cancers

Linda B. C. Bralten¹ 

[1] Department of Neurology, Erasmus University Medical Center, Erasmus University Rotterdam, Dr Molewaterplein 50, 3000 CA, Rotterdam, the Netherlands; E-Mail

关键词: glioma;    EGFR;    PTEN;    CDKN2A;    RB;    TP53;    LOH 1p19q;    IDH1;    pathway;   

DOI  :  10.3390/cancers3011129

来源: mdpi

【 摘 要 】

Gliomas are the most common type of primary brain tumor and have a dismal prognosis. Understanding the genetic alterations that drive glioma formation and progression may help improve patient prognosis by identification of novel treatment targets. Recently, two major studies have performed in-depth mutation analysis of glioblastomas (the most common and aggressive subtype of glioma). This systematic approach revealed three major pathways that are affected in glioblastomas: The receptor tyrosine kinase signaling pathway, the TP53 pathway and the pRB pathway. Apart from frequent mutations in the IDH1/2 gene, much less is known about the causal genetic changes of grade II and III (anaplastic) gliomas. Exceptions include TP53 mutations and fusion genes involving the BRAF gene in astrocytic and pilocytic glioma subtypes, respectively. In this review, we provide an update on all common events involved in the initiation and/or progression across the different subtypes of glioma and provide future directions for research into the genetic changes.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.