From signalling pathways to targeted therapies: unravelling glioblastoma's secrets and harnessing two decades of progress.

EGFR amplification/mutation and mTOR mutations may be significant resistance mechanisms associated with BRAF-targeted therapy, as signalling through the EGFR/PI3K/AKT/mTOR cascade overcomes the block on BRAF/MEK to continue cell proliferation. 116 This phenomenon should be explored further to identify the specific subsets of BRAF -mutant glioblastoma patients that may benefit from BRAF/MEK therapy alone and to clarify whether the addition of EGFR or mTOR inhibitors is required for BRAF-resistant tumours.

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