Introduction
- BRAF Class I and fusion alterations are two common oncogenic drivers in glioma 1
- The FDA has approved two regimens for the treatment of BRAF-altered glioma: a BRAF-V600E monomer inhibitor (dabrafenib) in combination with a MEK inhibitor (trametinib) or a pan-RAF inhibitor (tovorafenib)
- However, the efficacy of BRAF inhibitors (BRAFi) is limited by intrinsic and acquired resistance • In other solid tumors, MAPK/ERK-dependence signatures have been identified that predict overall survival and response to BRAFi 2,3,4
- The tumor immune microenvironment (TME) also mediates response to BRAFi and predicts survival in melanoma 5,6,7, 8, 9
- However, it is unknown whether MAPK/ERK-dependence and TME signatures can predict survival and resistance to BRAFi in glioma