mTOR signaling in glioblastoma: lessons learned from bench to bedside

Phosphatidyl-inositol-3 kinases (PI3Ks) constitute a family of intracellular lipid kinases that are frequently hyperactivated in glioblastoma. The PI3K complex links growth factor signaling with cellular proliferation, differentiation, metabolism, and survival. Mammalian target of rapamycin (mTOR) a...

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Detalles Bibliográficos
Autores principales: Akhavan, David, Cloughesy, Timothy F., Mischel, Paul S.
Formato: Texto
Lenguaje:English
Publicado: Oxford University Press 2010
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940679/
https://www.ncbi.nlm.nih.gov/pubmed/20472883
http://dx.doi.org/10.1093/neuonc/noq052
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author Akhavan, David
Cloughesy, Timothy F.
Mischel, Paul S.
author_facet Akhavan, David
Cloughesy, Timothy F.
Mischel, Paul S.
author_sort Akhavan, David
collection PubMed
description Phosphatidyl-inositol-3 kinases (PI3Ks) constitute a family of intracellular lipid kinases that are frequently hyperactivated in glioblastoma. The PI3K complex links growth factor signaling with cellular proliferation, differentiation, metabolism, and survival. Mammalian target of rapamycin (mTOR) acts both as a downstream effector and upstream regulator of PI3K, thus highlighting its importance in glioblastoma. This review highlights laboratory and clinical evidence of mTOR's role in glioblastoma. Mechanisms of escape from mTOR inhibition are also discussed, as well as future clinical strategies of mTOR inhibition.
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spelling pubmed-29406792011-08-01 mTOR signaling in glioblastoma: lessons learned from bench to bedside Akhavan, David Cloughesy, Timothy F. Mischel, Paul S. Neuro Oncol Review Phosphatidyl-inositol-3 kinases (PI3Ks) constitute a family of intracellular lipid kinases that are frequently hyperactivated in glioblastoma. The PI3K complex links growth factor signaling with cellular proliferation, differentiation, metabolism, and survival. Mammalian target of rapamycin (mTOR) acts both as a downstream effector and upstream regulator of PI3K, thus highlighting its importance in glioblastoma. This review highlights laboratory and clinical evidence of mTOR's role in glioblastoma. Mechanisms of escape from mTOR inhibition are also discussed, as well as future clinical strategies of mTOR inhibition. Oxford University Press 2010-08 2010-05-14 /pmc/articles/PMC2940679/ /pubmed/20472883 http://dx.doi.org/10.1093/neuonc/noq052 Text en © The Author(s) 2010. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. http://creativecommons.org/licenses/by-nc/2.5/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Akhavan, David
Cloughesy, Timothy F.
Mischel, Paul S.
mTOR signaling in glioblastoma: lessons learned from bench to bedside
title mTOR signaling in glioblastoma: lessons learned from bench to bedside
title_full mTOR signaling in glioblastoma: lessons learned from bench to bedside
title_fullStr mTOR signaling in glioblastoma: lessons learned from bench to bedside
title_full_unstemmed mTOR signaling in glioblastoma: lessons learned from bench to bedside
title_short mTOR signaling in glioblastoma: lessons learned from bench to bedside
title_sort mtor signaling in glioblastoma: lessons learned from bench to bedside
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940679/
https://www.ncbi.nlm.nih.gov/pubmed/20472883
http://dx.doi.org/10.1093/neuonc/noq052
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