Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy.
Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy.
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DOI：
10.1016/j.rmcr.2017.02.009
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发表时间：
2017
影响因子：
1.1
通讯作者：
Suda T
中科院分区：
文献类型：
--
作者：
Yoshimura K;Inui N;Karayama M;Inoue Y;Enomoto N;Fujisawa T;Nakamura Y;Takeuchi K;Sugimura H;Suda T
MET是非小细胞肺癌（NSCLC）中的驱动癌基因，其扩增与对表皮生长因子受体（EGFR）-酪氨酸激酶抑制剂的获得性耐药相关。1例携带EGFR 21号外显子L 858 R突变的56岁日本男性肺腺癌患者接受厄洛替尼治疗，治疗12个月后缓解。疾病进展后，重新活检分析显示新出现的MET扩增。未检测到EGFR 20号外显子T790 M突变或MET 14号外显子突变。MET抑制剂克唑替尼显示出显著的反应。这是第一份成功的克唑替尼单药治疗在厄洛替尼治疗期间获得MET扩增的EGFR突变型NSCLC的报告。
MET is a driver oncogene in non-small-cell lung cancer (NSCLC), and its amplification is associated with acquired resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors. A 56-year-old Japanese male with lung adenocarcinoma harboring an EGFR exon 21 L858R mutation received erlotinib to which he responded for 12 months. After disease progression, re-biopsy analyses revealed newly developed MET amplification. Neither EGFR exon 20 T790M mutation nor MET exon 14 mutations were detected. The MET inhibitor, crizotinib, showed a dramatic response. This is the first report of successful crizotinib single-agent therapy in EGFR-mutant NSCLC that acquired MET amplification during erlotinib therapy.