Abstract
Recurrent glioblastoma (rGBM) remains vastly understudied with few biological targets for therapeutic development. Using a highly specific antibody panel for all Eph receptor tyrosine kinases, we identify that EphA2 and EphA3 co-expression marks a highly tumorigenic cell population in rGBM that is enriched in cancer stem cell marker expression. Knockdown of EphA2 and EphA3 together blocks this tumorigenicity, and is marked by an increase in the expression of differentiation marker GFAP. Treatment with a bispecific antibody (BsAb) that co-targets EphA2 and EphA3 reduces the tumorigenic potential of rGBM by down regulating Akt and Erk signaling pathways and increasing differentiation. For the first time, we show that strategic co-targeting of both EphA2 and EphA3 in GBM CSCs presents a novel and rational therapeutic approach for recurrent GBM.
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