EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy

Glioblastoma is a particularly resilient cancer, and while therapies may be able to reach the brain by crossing the blood-brain barrier, they then have to deal with a highly invasive tumor that is very resistant to DNA damage. It seems clear that in order to kill aggressive glioma cells more efficie...

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Detalhes bibliográficos
Autores: Zahonero, Cristina, Sánchez-Gómez, Pilar
Formato: artículo
Fecha de publicación:2014
País:España
Recursos:Instituto de Salud Carlos III (ISCIII)
Repositorio:Repisalud
Idioma:inglés
OAI Identifier:oai:repisalud.isciii.es:20.500.12105/10629
Acesso em linha:http://hdl.handle.net/20.500.12105/10629
Access Level:acceso abierto
Palavra-chave:Animals
Cell Hypoxia
DNA Damage
ErbB Receptors
Gene Expression Regulation, Neoplastic
Glioblastoma
Humans
Mice
Models, Biological
Signal Transduction
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spelling EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategyZahonero, CristinaSánchez-Gómez, PilarAnimalsCell HypoxiaDNA DamageErbB ReceptorsGene Expression Regulation, NeoplasticGlioblastomaHumansMiceModels, BiologicalSignal TransductionGlioblastoma is a particularly resilient cancer, and while therapies may be able to reach the brain by crossing the blood-brain barrier, they then have to deal with a highly invasive tumor that is very resistant to DNA damage. It seems clear that in order to kill aggressive glioma cells more efficiently and with fewer side effects on normal tissue, there must be a shift from classical cytotoxic chemotherapy to more targeted therapies. Since the epidermal growth factor receptor (EGFR) is altered in almost 50% of glioblastomas, it currently represents one of the most promising therapeutic targets. In fact, it has been associated with several distinct steps in tumorigenesis, from tumor initiation to tumor growth and survival, and also with the regulation of cell migration and angiogenesis. However, inhibitors of the EGFR kinase have produced poor results with this type of cancer in clinical trials, with no clear explanation for the tumor resistance observed. Here we will review what we know about the expression and function of EGFR in cancer and in particular in gliomas. We will also evaluate which are the possible molecular and cellular escape mechanisms. As a result, we hope that this review will help improve the design of future EGFR-targeted therapies for glioblastomas.SpringerInstituto de Salud Carlos III20202020-07-0120142014-09-0120142014-09-01research articlehttp://purl.org/coar/resource_type/c_2df8fbb1AMhttp://purl.org/coar/version/c_ab4af688f83e57aainfo:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/20.500.12105/10629reponame:Repisaludinstname:Instituto de Salud Carlos III (ISCIII)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución-NoComercial-CompartirIgual 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-sa/4.0/info:eu-repo/semantics/openAccessoai:repisalud.isciii.es:20.500.12105/106292026-06-12T12:43:37Z
dc.title.none.fl_str_mv EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
title EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
spellingShingle EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
Zahonero, Cristina
Animals
Cell Hypoxia
DNA Damage
ErbB Receptors
Gene Expression Regulation, Neoplastic
Glioblastoma
Humans
Mice
Models, Biological
Signal Transduction
title_short EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
title_full EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
title_fullStr EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
title_full_unstemmed EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
title_sort EGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy
dc.creator.none.fl_str_mv Zahonero, Cristina
Sánchez-Gómez, Pilar
author Zahonero, Cristina
author_facet Zahonero, Cristina
Sánchez-Gómez, Pilar
author_role author
author2 Sánchez-Gómez, Pilar
author2_role author
dc.contributor.none.fl_str_mv Instituto de Salud Carlos III
dc.subject.none.fl_str_mv Animals
Cell Hypoxia
DNA Damage
ErbB Receptors
Gene Expression Regulation, Neoplastic
Glioblastoma
Humans
Mice
Models, Biological
Signal Transduction
topic Animals
Cell Hypoxia
DNA Damage
ErbB Receptors
Gene Expression Regulation, Neoplastic
Glioblastoma
Humans
Mice
Models, Biological
Signal Transduction
description Glioblastoma is a particularly resilient cancer, and while therapies may be able to reach the brain by crossing the blood-brain barrier, they then have to deal with a highly invasive tumor that is very resistant to DNA damage. It seems clear that in order to kill aggressive glioma cells more efficiently and with fewer side effects on normal tissue, there must be a shift from classical cytotoxic chemotherapy to more targeted therapies. Since the epidermal growth factor receptor (EGFR) is altered in almost 50% of glioblastomas, it currently represents one of the most promising therapeutic targets. In fact, it has been associated with several distinct steps in tumorigenesis, from tumor initiation to tumor growth and survival, and also with the regulation of cell migration and angiogenesis. However, inhibitors of the EGFR kinase have produced poor results with this type of cancer in clinical trials, with no clear explanation for the tumor resistance observed. Here we will review what we know about the expression and function of EGFR in cancer and in particular in gliomas. We will also evaluate which are the possible molecular and cellular escape mechanisms. As a result, we hope that this review will help improve the design of future EGFR-targeted therapies for glioblastomas.
publishDate 2014
dc.date.none.fl_str_mv 2014
2014-09-01
2014
2014-09-01
2020
2020-07-01
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
AM
http://purl.org/coar/version/c_ab4af688f83e57aa
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/20.500.12105/10629
url http://hdl.handle.net/20.500.12105/10629
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución-NoComercial-CompartirIgual 4.0 Internacional
http://creativecommons.org/licenses/by-nc-sa/4.0/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución-NoComercial-CompartirIgual 4.0 Internacional
http://creativecommons.org/licenses/by-nc-sa/4.0/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:Repisalud
instname:Instituto de Salud Carlos III (ISCIII)
instname_str Instituto de Salud Carlos III (ISCIII)
reponame_str Repisalud
collection Repisalud
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,812429

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