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New Cellular Dimensions on Glioblastoma Progression
Gliomas are brain tumors originated from glial cells. The most frequent form of glioma is the glioblastoma (GB). This lethal tumor is frequently originated from genetic alterations in epidermal growth factor receptor (EGFR) and PI3K pathways. Recent results suggest that signaling pathways, other tha...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7249559/ https://www.ncbi.nlm.nih.gov/pubmed/32548582 http://dx.doi.org/10.1177/2633105520923076 |
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author | Portela, Marta Casas-Tintó, Sergio |
author_facet | Portela, Marta Casas-Tintó, Sergio |
author_sort | Portela, Marta |
collection | PubMed |
description | Gliomas are brain tumors originated from glial cells. The most frequent form of glioma is the glioblastoma (GB). This lethal tumor is frequently originated from genetic alterations in epidermal growth factor receptor (EGFR) and PI3K pathways. Recent results suggest that signaling pathways, other than primary founder mutations, play a central role in GB progression. Some of these signals are depleted by GB cells from healthy neurons via specialized filopodia known as tumor microtubes (TMs). Here, we discuss the contribution of TMs to vampirize wingless/WNT ligand from neurons. In consequence, wingless/WNT pathway is upregulated in GB to promote tumor progression, and the reduction of these signals in neurons causes the reduction of synapse number and neurodegeneration. These processes contribute to neurological defects and premature death. |
format | Online Article Text |
id | pubmed-7249559 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-72495592020-06-15 New Cellular Dimensions on Glioblastoma Progression Portela, Marta Casas-Tintó, Sergio Neurosci Insights Commentary Gliomas are brain tumors originated from glial cells. The most frequent form of glioma is the glioblastoma (GB). This lethal tumor is frequently originated from genetic alterations in epidermal growth factor receptor (EGFR) and PI3K pathways. Recent results suggest that signaling pathways, other than primary founder mutations, play a central role in GB progression. Some of these signals are depleted by GB cells from healthy neurons via specialized filopodia known as tumor microtubes (TMs). Here, we discuss the contribution of TMs to vampirize wingless/WNT ligand from neurons. In consequence, wingless/WNT pathway is upregulated in GB to promote tumor progression, and the reduction of these signals in neurons causes the reduction of synapse number and neurodegeneration. These processes contribute to neurological defects and premature death. SAGE Publications 2020-05-22 /pmc/articles/PMC7249559/ /pubmed/32548582 http://dx.doi.org/10.1177/2633105520923076 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Commentary Portela, Marta Casas-Tintó, Sergio New Cellular Dimensions on Glioblastoma Progression |
title | New Cellular Dimensions on Glioblastoma Progression |
title_full | New Cellular Dimensions on Glioblastoma Progression |
title_fullStr | New Cellular Dimensions on Glioblastoma Progression |
title_full_unstemmed | New Cellular Dimensions on Glioblastoma Progression |
title_short | New Cellular Dimensions on Glioblastoma Progression |
title_sort | new cellular dimensions on glioblastoma progression |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7249559/ https://www.ncbi.nlm.nih.gov/pubmed/32548582 http://dx.doi.org/10.1177/2633105520923076 |
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