We present 8-year follow-up on the first patient with stage 4 ameloblastoma carrying a BRAF V600E mutation treated with dual BRAF/MEK inhibition (BRAF/MEKi). He experienced a durable clinical response while on dabrafenib (BRAFi) and trametinib (MEKi) without toxicity nor evidence for drug-resistant tumor progression. He was asymptomatic when he self-discontinued therapy after 4 years of sustained clinical response.
View Article and Find Full Text PDFProgrammed cell death protein-1 (PD-1) and programmed cell death-ligand 1 (PD-L1) checkpoint inhibitors induce tumor response by activating the patient's own immune system to fight cancer. Tumors with high tumor mutational burden or those that express high levels of PD-1/PD-L1 are more responsive to PD1/PDL1 inhibitors. There is much interest in determining how to improve response to PD-1/PD-L1 inhibitors.
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