Acquired MET-DSTN Fusion Mediated Resistance to EGFR-TKIs in Lung Adenocarcinoma and Responded to Crizotinib Plus Gefitinib: A Case Report

医学 吉非替尼 肺癌 表皮生长因子受体 肿瘤科 克里唑蒂尼 腺癌 内科学 癌症研究 融合基因 奥西默替尼 埃罗替尼 癌症 基因 生物 遗传学 恶性胸腔积液
作者
Yalun Li,Ke Wang,Panwen Tian,Weimin Li
出处
期刊:Clinical Lung Cancer [Elsevier BV]
卷期号:23 (1): e83-e86 被引量:9
标识
DOI:10.1016/j.cllc.2021.10.006
摘要

•Mesenchymal-epithelial transition factor receptor (MET) is a potential therapeutic target in non-small cell lung cancer (NSCLC). However, MET gene fusions in NSCLC have rarely been found. •A novel gene fusion, MET-DSTN, and EGFR-L858R were detected by next-generation sequencing after the occurrence of resistance to osimertinib therapy. The patient obtained a dramatic clinical benefit upon treatment with crizotinib plus gefitinib, achieving a complete response one month later. •MET-DSTN fusion could be explored as one kind of mechanism of acquired resistance to EGFR-TKIs. Combined treatment with MET inhibitors and EGFR-TKIs is a potential therapeutic strategy. •Mesenchymal-epithelial transition factor receptor (MET) is a potential therapeutic target in non-small cell lung cancer (NSCLC). However, MET gene fusions in NSCLC have rarely been found. •A novel gene fusion, MET-DSTN, and EGFR-L858R were detected by next-generation sequencing after the occurrence of resistance to osimertinib therapy. The patient obtained a dramatic clinical benefit upon treatment with crizotinib plus gefitinib, achieving a complete response one month later. •MET-DSTN fusion could be explored as one kind of mechanism of acquired resistance to EGFR-TKIs. Combined treatment with MET inhibitors and EGFR-TKIs is a potential therapeutic strategy.
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