Department of Pulmonary, Shanghai Chest Hospital, Shanghai Jiao Tong University , Shanghai , China.
Cancer Biol Ther. 2019;20(9):1183-1186. doi: 10.1080/15384047.2019.1617568. Epub 2019 May 27.
First-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) could induce dramatic tumor responses in non-small-cell lung cancer patients with EGFR-activating mutations. However, a small proportion of patients have no tumor response on initial EGFR TKI treatment with an activating EGFR mutation and the primary resistance mechanism is not well understood. Here, we report the patient with primary dual MET/EGFR mutation treated with icotinib shows a disease progression, but the chest computed tomography shows the mass has significantly shrunk after 3 weeks of single-agent crizotinib. These suggest that de novo MET amplification could be a potential mechanism of intrinsic resistance to first-generation EGFR TKI.
第一代表皮生长因子受体（EGFR）酪氨酸激酶抑制剂（TKI）可诱导具有 EGFR 激活突变的非小细胞肺癌患者产生显著的肿瘤反应。然而，一小部分患者在初始 EGFR TKI 治疗时对激活的 EGFR 突变没有肿瘤反应，其主要耐药机制尚不清楚。在这里，我们报告了一例原发性双重 MET/EGFR 突变患者，该患者接受伊可替尼治疗后出现疾病进展，但胸部 CT 显示在单独使用克唑替尼治疗 3 周后肿块明显缩小。这些提示，MET 扩增可能是对第一代 EGFR TKI 产生内在耐药的潜在机制。
