Editorial
Lessons learned from rindopepimut treatment in patients with EGFRvIII-expressing glioblastoma
Abstract
EGFRvIII is the most common mutation of EGFR and results in the creation of a tumor-specific antigen that is detectable in 23–33% of human glioblastoma (GBM) (1). EGFRvIII arises due to the deletion of EGFR exons 2–7, which generates a truncated extracellular domain capable of constitutive EGFR activation.
