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AKT/GSK3β Signaling in Glioblastoma

Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, su...

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Detalles Bibliográficos
Autores principales: Majewska, Ewelina, Szeliga, Monika
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357492/
https://www.ncbi.nlm.nih.gov/pubmed/27568206
http://dx.doi.org/10.1007/s11064-016-2044-4
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author Majewska, Ewelina
Szeliga, Monika
author_facet Majewska, Ewelina
Szeliga, Monika
author_sort Majewska, Ewelina
collection PubMed
description Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM.
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spelling pubmed-53574922017-03-30 AKT/GSK3β Signaling in Glioblastoma Majewska, Ewelina Szeliga, Monika Neurochem Res Original Paper Glioblastoma (GBM) is the most aggressive of primary brain tumors. Despite the progress in understanding the biology of the pathogenesis of glioma made during the past decade, the clinical outcome of patients with GBM remains still poor. Deregulation of many signaling pathways involved in growth, survival, migration and resistance to treatment has been implicated in pathogenesis of GBM. One of these pathways is phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT)/rapamycin-sensitive mTOR-complex (mTOR) pathway, intensively studied and widely described so far. Much less attention has been paid to the role of glycogen synthase kinase 3 β (GSK3β), a target of AKT. In this review we focus on the function of AKT/GSK3β signaling in GBM. Springer US 2016-08-27 2017 /pmc/articles/PMC5357492/ /pubmed/27568206 http://dx.doi.org/10.1007/s11064-016-2044-4 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original Paper
Majewska, Ewelina
Szeliga, Monika
AKT/GSK3β Signaling in Glioblastoma
title AKT/GSK3β Signaling in Glioblastoma
title_full AKT/GSK3β Signaling in Glioblastoma
title_fullStr AKT/GSK3β Signaling in Glioblastoma
title_full_unstemmed AKT/GSK3β Signaling in Glioblastoma
title_short AKT/GSK3β Signaling in Glioblastoma
title_sort akt/gsk3β signaling in glioblastoma
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357492/
https://www.ncbi.nlm.nih.gov/pubmed/27568206
http://dx.doi.org/10.1007/s11064-016-2044-4
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