Combining bulk and single-cell genomics, this study finds tumor heterogeneity impacts MEK inhibition in glioblastomas, suggesting new therapeutic strategies.
Key Points
Tumor heterogeneity affects the response to MEK inhibitors in NF1-mutant glioblastomas, indicating the need for personalized treatments.
CDKN2A/B homozygous deletion serves as a poor prognostic marker specifically in NF1-mutant glioblastomas.
Single-cell RNA sequencing revealed enriched MEK activation signatures in MES-like tumor cells, driving heterogeneous responses to treatment.
Targeting the Ras/RAF/MEK pathway enhances the efficacy of MEK inhibitors like selumetinib in NF1-mutant glioblastomas.