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Epidermal growth factor receptor and EGFRvIII in glioblastoma: signaling pathways and targeted therapies

Abstract

Amplification of epidermal growth factor receptor (EGFR) and its active mutant EGFRvIII occurs frequently in glioblastoma (GBM). While EGFR and EGFRvIII play critical roles in pathogenesis, targeted therapy with EGFR-tyrosine kinase inhibitors (TKIs) or antibodies has only shown limited efficacy in patients. Here we discuss signaling pathways mediated by EGFR/EGFRvIII, current therapeutics, and novel strategies to target EGFR/EGFRvIII-amplified GBM.

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Acknowledgements

ZA is supported by the Alex’s Lemonade Stand Foundation and by Program for Breakthrough Biomedical Research, which is partially funded by the Sandler Foundation. The Weiss lab is supported by NIH grants CA148699, NS091620, NS0883555, NS089868, CA183692, CA176287, and CA82103; the Alex’s Lemonade Stand, Children’s Tumor, Katie Dougherty, Pediatric Brain Tumor, Ross K. MacNeill, St. Baldrick, and Samuel G. Waxman Foundations; and the Evelyn and Mattie Anderson Chair.

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An, Z., Aksoy, O., Zheng, T. et al. Epidermal growth factor receptor and EGFRvIII in glioblastoma: signaling pathways and targeted therapies. Oncogene 37, 1561–1575 (2018). https://doi.org/10.1038/s41388-017-0045-7

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