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El receptor del factor de crecimiento epidérmico (EGFR) en el glioblastoma: mecanismo de tumorigénesis y papel como diana terapéutica. [revisión]

Por: Sepúlveda Sánchez, Juan Manuel [Oncología Médica].
Colaborador(es): Servicio de Oncología Médica.
Tipo de material: materialTypeLabelArtículoEditor: Revista de neurología, 2015Descripción: 61(2):85-93.Recursos en línea: Solicitar documento Resumen: A glioblastoma is a primary brain tumour that is very aggressive and resistant to conventional treatment with chemo- or radiotherapy. Given that epidermic growth factor receptor (EGFR) is altered in 50% of glioblastomas, it is currently one of the most promising therapeutic targets in this kind of tumour. Yet, inhibitors of the kinase activity of EGFR have yielded poor results in clinical trials with patients with glioblastomas. In this review we analyse the function of EGFR in glioblastomas and outline the therapeutic approaches aimed against this receptor in this kind of tumour. This sort of analysis could be a starting point for improving the design of future therapies for glioblastomas, based on inhibiting the EGFR function.
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Formato Vancouver:
Zahonero C, Sepúlveda JM, Sánchez Gómez P. El receptor del factor de crecimiento epidérmico (EGFR) en el glioblastoma: mecanismo de tumorigénesis y papel como diana terapéutica. Rev Neurol. 2015 Jul 16;61(2):85-93.

PMID: 26156444

Contiene 81 referencias

A glioblastoma is a primary brain tumour that is very aggressive and resistant to conventional treatment with chemo- or radiotherapy. Given that epidermic growth factor receptor (EGFR) is altered in 50% of glioblastomas, it is currently one of the most promising therapeutic targets in this kind of tumour. Yet, inhibitors of the kinase activity of EGFR have yielded poor results in clinical trials with patients with glioblastomas. In this review we analyse the function of EGFR in glioblastomas and outline the therapeutic approaches aimed against this receptor in this kind of tumour. This sort of analysis could be a starting point for improving the design of future therapies for glioblastomas, based on inhibiting the EGFR function.

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