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Significance GBM is the most deadly adult brain cancer. The current standard-of-care is surgery followed by RT and temozolomide, which results in a median survival time of only 15 mo. The efficacy of chemotherapies and targeted therapies in GBM is very limited because most of these drugs do not pass the blood−brain barrier (BBB). Ultimately, all patients succumb to the disease. Our study describes radiation-induced cellular plasticity as a resistance mechanism in GBM. We identified a dopamine receptor antagonist as a readily available, FDA-approved drug known to penetrate the BBB, which prevents phenotype conversion of glioma cells into glioma-initiating cells and prolongs survival in mouse models of GBM, thus suggesting that it will improve the efficacy of RT without increasing toxicity.

The dopamine receptor antagonist trifluoperazine prevents phenotype conversion and improves survival in mouse models of glioblastoma