Lessons learned from rindopepimut treatment in patients with EGFRvIII-expressing glioblastoma

David C. Binder, Erik Ladomersky, Alicia Lenzen, Lijie Zhai, Kristen L. Lauing, Sebastian D. Otto-Meyer, Rimas V. Lukas, Derek A. Wainwright


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.