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Developmentally regulated signaling pathways in glioma invasion

Malignant gliomas are the most common, infiltrative, and lethal primary brain tumors affecting the adult population. The grim prognosis for this disease is due to a combination of the presence of highly invasive tumor cells that escape surgical resection and the presence of a population of therapy-r...

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Detalles Bibliográficos
Autores principales: Mehta, Shwetal, Lo Cascio, Costanza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765207/
https://www.ncbi.nlm.nih.gov/pubmed/28821904
http://dx.doi.org/10.1007/s00018-017-2608-8
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author Mehta, Shwetal
Lo Cascio, Costanza
author_facet Mehta, Shwetal
Lo Cascio, Costanza
author_sort Mehta, Shwetal
collection PubMed
description Malignant gliomas are the most common, infiltrative, and lethal primary brain tumors affecting the adult population. The grim prognosis for this disease is due to a combination of the presence of highly invasive tumor cells that escape surgical resection and the presence of a population of therapy-resistant cancer stem cells found within these tumors. Several studies suggest that glioma cells have cleverly hijacked the normal developmental program of neural progenitor cells, including their transcriptional programs, to enhance gliomagenesis. In this review, we summarize the role of developmentally regulated signaling pathways that have been found to facilitate glioma growth and invasion. Furthermore, we discuss how the microenvironment and treatment-induced perturbations of these highly interconnected signaling networks can trigger a shift in cellular phenotype and tumor subtype.
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spelling pubmed-57652072018-01-25 Developmentally regulated signaling pathways in glioma invasion Mehta, Shwetal Lo Cascio, Costanza Cell Mol Life Sci Review Malignant gliomas are the most common, infiltrative, and lethal primary brain tumors affecting the adult population. The grim prognosis for this disease is due to a combination of the presence of highly invasive tumor cells that escape surgical resection and the presence of a population of therapy-resistant cancer stem cells found within these tumors. Several studies suggest that glioma cells have cleverly hijacked the normal developmental program of neural progenitor cells, including their transcriptional programs, to enhance gliomagenesis. In this review, we summarize the role of developmentally regulated signaling pathways that have been found to facilitate glioma growth and invasion. Furthermore, we discuss how the microenvironment and treatment-induced perturbations of these highly interconnected signaling networks can trigger a shift in cellular phenotype and tumor subtype. Springer International Publishing 2017-08-18 2018 /pmc/articles/PMC5765207/ /pubmed/28821904 http://dx.doi.org/10.1007/s00018-017-2608-8 Text en © The Author(s) 2017 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 Review
Mehta, Shwetal
Lo Cascio, Costanza
Developmentally regulated signaling pathways in glioma invasion
title Developmentally regulated signaling pathways in glioma invasion
title_full Developmentally regulated signaling pathways in glioma invasion
title_fullStr Developmentally regulated signaling pathways in glioma invasion
title_full_unstemmed Developmentally regulated signaling pathways in glioma invasion
title_short Developmentally regulated signaling pathways in glioma invasion
title_sort developmentally regulated signaling pathways in glioma invasion
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5765207/
https://www.ncbi.nlm.nih.gov/pubmed/28821904
http://dx.doi.org/10.1007/s00018-017-2608-8
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