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The epidermal growth factor receptor (EGFR) is receptor tyrosine kinase (RTK) dysregulated in glioblastoma (GBM) through overexpression, mutation or inappropriate expression of ligand. Activation of the EGFR by these mechanisms contributes to the development and progression of GBM by engaging downstream targets, such as the PI3K pathway. The de2-7 EGFR (or EGFRvIII), a naturally occurring mutation of the EGFR frequently expressed in GBM, preferentially activates this pathway. Clinical trials with EGFR-specific tyrosine kinase inhibitors (TKIs) have been disappointing with very little antitumor activity observed. The outcome of controlled clinical trials with EGFR-specific antibodies is yet to be reported. Encouraging preclinical and preliminary clinical data suggests that the combination of EGFR therapeutics and compounds that target molecules downstream of EGFR might have increased efficacy. Finally, the identification of biomarkers that predict those patients most likely to respond to EGFR inhibition is desperately needed.

Advances in the Development of EGFR Targeted Therapies for the Treatment of Glioblastoma