期刊
LUNG CANCER
卷 146, 期 -, 页码 355-357出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.lungcan.2020.06.004
关键词
BRAF N581S; Gefitinib; Dabrafenib; Trametinib
资金
- National Key Development Plan for Precision Medicine Research of China [2017YFC0910004]
- National Major Sci-Tech Project of China [2017ZX10103004-012]
- National Science Foundation of China [81871890, 91859203]
Objectives: BRAFG469A and V600E were reported as the mechanisms of acquired resistance to first-generation EGFR tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer patients. Here, we described a rare case of BRAF N581S after gefitinib resistance and response to BRAF inhibitor plus MEK inhibitor. Materials and methods: Next-generation sequencing (NGS) was performed on the tumor tissue and plasma samples of a patient with metastatic lung adenocarcinoma harboring EGFR exon 19 deletion (EGFR 19del). Results: EGFR 19del and MET amplification was detected after resistance to the initial gefitinib therapy. After 9 months of treatment with gefitinib plus crizotinib, the disease progressed again. NGS revealed the known EGFR 19del and a BRAF N581S missense mutation after progression. The patient obtained durable clinical benefit upon treatment with dabrafenib plus trametinib, achieving a progression-free survival (PFS) of more than 33 months. Conclusion: BRAF N581S mutation could be explored as one kind of mechanism of acquired resistance to EGFRTKIs. Combined inhibition of BRAF and MEK is a potential therapeutic strategy.
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