Durable Response of Dabrafenib, Trametinib, and Capmatinib in an NSCLC Patient With Co-Existing BRAF-KIAA1549 Fusion and MET Amplification: A Case Report

fusions are rare driver oncogenes in non-small cell lung cancer (NSCLC). Similar with V600E mutation, it could also activate the MAPK signaling pathway. There are a few case reports which had indicated the potential response to BRAF inhibitors and its important role as driver mutation. In addition, the co-occurring amplification has been defined as a poor prognostic factor in patients with epidermal growth factor receptor ( ) mutant NSCLC. Currently, there are ongoing clinical trials which investigate the amplification as a therapeutic target in patients with mutant NSCLC and acquired resistance to osimertinib, which imply that the amplification also had a therapeutic significance. However, the co-occurring amplification had not been studied in patients with fusion before. A 67-year-old man was diagnosed with metastatic poorly-differentiated adenocarcinoma. He received first-line therapy with the combination of pembrolizumab and chemotherapy because the genomic test revealed wild-type , and negativity of ALK and ROS1 by immunohistochemical stain. Upon disease progression, the next-generation sequencing revealed co-occurring fusion and amplification. Subsequent dabrafenib, trametinib, and capmatinib combination therapy showed a remarkable treatment effect. The combination therapy targeting the co-occurring driver mutations is a potential effective treatment for NSCLC patients. Further prospective study is still warranted to investigate the role of co-occurring driver mutations and the relevant treatment strategy.