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Open AccessFeature PaperPerspective

Finding the Right Way to Target EGFR in Glioblastomas; Lessons from Lung Adenocarcinomas

Department of Neurology, Erasmus MC Cancer Institute; 3015 CD Rotterdam, The Netherlands
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Author to whom correspondence should be addressed.
Cancers 2018, 10(12), 489; https://doi.org/10.3390/cancers10120489
Received: 9 November 2018 / Revised: 29 November 2018 / Accepted: 30 November 2018 / Published: 4 December 2018
(This article belongs to the Special Issue Glioblastoma: State of the Art and Future Perspectives)
The EGFR gene is one of the most frequently mutated and/or amplified gene both in lung adenocarcinomas (LUAD) and in glioblastomas (GBMs). Although both tumor types depend on the mutation for growth, clinical benefit of EGFR tyrosine kinase inhibitors (TKIs) has only been observed in LUAD patients and, thus-far, not in GBM patients. Also in LUAD patients however, responses are restricted to specific EGFR mutations only and these ‘TKI-sensitive’ mutations hardly occur in GBMs. This argues for mutation-specific (as opposed to tumor-type specific) responses to EGFR-TKIs. We here discuss potential reasons for the differences in mutation spectrum and highlight recent evidence for specific functions of different EGFR mutations. These mutation-specific effects likely underlie the differential treatment response between LUAD and GBMs and provide new insights into how to target EGFR in GBM patients. View Full-Text
Keywords: EGFR; glioblastoma; glioma; pulmonary adenocarcinoma; lung cancer; erlotinib; gefitinib; lapatinib EGFR; glioblastoma; glioma; pulmonary adenocarcinoma; lung cancer; erlotinib; gefitinib; lapatinib
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Gao, Y.; Vallentgoed, W.R.; French, P.J. Finding the Right Way to Target EGFR in Glioblastomas; Lessons from Lung Adenocarcinomas. Cancers 2018, 10, 489.

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