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dc.contributor.authorZahonero, Cristina 
dc.contributor.authorSánchez-Gómez, Pilar
dc.identifier.citationCell Mol Life Sci . 2014 Sep;71(18):3465-88.es_ES
dc.description.abstractGlioblastoma 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.es_ES
dc.description.sponsorshipThe work in the authors ‘laboratory is funded by Ministerio de Economía y Competitividad (Instituto de Salud Carlos III) (PI12/00775 and RD12/0036/0027). We thank Angel Ayuso-Sacido and Juan Sepúlveda-Sánchez for critical review of the manuscript.es_ES
dc.publisherSpringer es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshCell Hypoxia es_ES
dc.subject.meshDNA Damage es_ES
dc.subject.meshErbB Receptors es_ES
dc.subject.meshGene Expression Regulation, Neoplastic es_ES
dc.subject.meshGlioblastoma es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMice es_ES
dc.subject.meshModels, Biological es_ES
dc.subject.meshSignal Transduction es_ES
dc.titleEGFR-dependent mechanisms in glioblastoma: towards a better therapeutic strategy.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.contributor.funderInstituto de Salud Carlos III 
dc.identifier.journalCellular and molecular life sciences : CMLSes_ES
dc.repisalud.centroISCIII::Instituto de Investigación de Enfermedades Rarases_ES
dc.rights.accessRightsopen accesses_ES

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Atribución-NoComercial-CompartirIgual 4.0 Internacional
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