Case Report: Sequential Combination Targeted Therapy With Type I and II MET Inhibitors in a Metastatic EGFR-Mutated, MET-Amplified NSCLC Patient With Acquired MET Y1230H Mutation

被引:4
作者
Cai, Boning [1 ]
Li, Xiaomo [2 ]
Huang, Xiang [1 ]
Ma, Tonghui [2 ]
Qu, Baolin [1 ]
Yu, Wei [1 ]
Yang, Wei [1 ]
Zhang, Pei [1 ]
Chen, Jing [1 ]
Liu, Fang [1 ]
机构
[1] Chinese Peoples Liberat Army PLA Gen Hosp, Med Ctr 1, Dept Radiat Oncol, Beijing, Peoples R China
[2] Genetron Hlth Beijing Technol Co Ltd, Dept Translat Med, Beijing, Peoples R China
关键词
non-small cell lung cancer (NSCLC); EGFR mutation; targeted therapy resistance; MET amplification; case report; CELL LUNG-CANCER; TYROSINE KINASE INHIBITORS; RESISTANCE MECHANISM; CRIZOTINIB; CHEMOTHERAPY; AMIVANTAMAB;
D O I
10.3389/fonc.2021.738832
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are the standard of care for advanced non-small-cell lung cancer (NSCLC) patients. However, most patients will eventually develop resistance. For EGFR-TKI resistance mediated by MET amplification, the combination of EGFR and MET TKIs has shown promising results in early clinical trials. However, acquired resistance to MET inhibitors forms a formidable challenge to this dual blockade approach. Here, we presented an NSCLC patient with EGFR exon 19 deletion (ex19del) who was resistant to first-line erlotinib treatment but responded to chemotherapy. Given the finding of MET overexpression/amplification after disease progression, the patient received gefitinib plus crizotinib with a partial response. Her disease progressed again, and molecular testing revealed a novel MET Y1230H mutation and a PD-L1 TPS score of 75%. She received a salvage regime consisting of gefitinib, cabozantinib, and pembrolizumab with a partial response. Since we now know that EGFR ex19del NSCLC patients generally do not respond to PD-1 blockade therapy, this response is more likely the contribution from gefitinib plus cabozantinib. Therefore, sequential use of type I and II MET inhibitors in EGFR/MET dual blockade may be an effective therapeutic option for EGFR-mutant, MET-amplified NSCLC.
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