A novel recombinant immunotoxin-based therapy targeting wild-type and mutant EGFR improves survival in murine models of glioblastoma.

Both the amplification of the gene coding for wild-type (wt) epidermal growth factor receptor (EGFR) and the overexpression of the EGFR deletion mutant, commonly known as EGFRvIII, are hallmarks of glioblastoma. We have recently reported a novel, recombinant immunotoxin, D2C7-(scdsFv)-PE38KDEL, that targets both wt EGFR and EGFRvIII, exhibiting potent antineoplastic effects against established murine gliomas.

Duke Scholars

Author Vidyalakshmi Chandramohan Neurosurgery, Neuro-Oncology

Author Darell Doty Bigner Neurosurgery