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Cancers 2011, 3(1), 1129-1140; doi:10.3390/cancers3011129
Review

Genetic Alterations in Glioma

 and *
Received: 4 January 2011; in revised form: 28 February 2011 / Accepted: 1 March 2011 / Published: 7 March 2011
(This article belongs to the Special Issue Cancer Diagnosis and Targeted Therapy)
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Abstract: 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.
Keywords: glioma; EGFR; PTEN; CDKN2A; RB; TP53; LOH 1p19q; IDH1; pathway glioma; EGFR; PTEN; CDKN2A; RB; TP53; LOH 1p19q; IDH1; pathway
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Bralten, L.B.C.; French, P.J. Genetic Alterations in Glioma. Cancers 2011, 3, 1129-1140.

AMA Style

Bralten LBC, French PJ. Genetic Alterations in Glioma. Cancers. 2011; 3(1):1129-1140.

Chicago/Turabian Style

Bralten, Linda B. C.; French, Pim J. 2011. "Genetic Alterations in Glioma." Cancers 3, no. 1: 1129-1140.



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