Department of Medicine, the Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, China.
Department of Medicine, the Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, China.
Lung Cancer. 2019 Mar;129:72-74. doi: 10.1016/j.lungcan.2019.01.009. Epub 2019 Jan 23.
De novo mesenchymal-epithelial transition (MET) amplification is believed to promote primary resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in the non-squamous non-small cell lung cancer (NSCLC). We sought to seek the treatment of a patient with EGFR-mutant NSCLC harboring de novo MET amplification.
After clinical diagnosis, tissue and plasma samples were obtained from the patient and subjected to next-generation sequencing to identify and dynamic monitor the mutations.
The patient was treated with gefitinib monotherapy in the beginning and experienced primary resistance to gefitinib but achieved a good response to the combination therapy of gefitinib and crizotinib. He achieved a 16.8-month progress free survival with the combination therapy. NGS of plasma circulating cell-free tumor DNA shown that L858R mutation was no longer detectable and the copy number of MET dropped when the patient got remission.
The combination of EGFR- and MET- tyrosine kinase inhibitors may be an effective treatment for the rare mutations.
新出现的间质-上皮转化（MET）扩增被认为可促进非鳞状非小细胞肺癌（NSCLC）中表皮生长因子受体（EGFR）酪氨酸激酶抑制剂的原发性耐药。我们试图寻求一种针对 EGFR 突变型 NSCLC 伴新出现 MET 扩增的治疗方法。
在临床诊断后，从患者获得组织和血浆样本，并进行下一代测序以鉴定和动态监测突变。
患者最初接受吉非替尼单药治疗，对吉非替尼产生原发性耐药，但对吉非替尼和克唑替尼联合治疗有良好反应。联合治疗使他的无进展生存期达到 16.8 个月。对血浆循环无细胞肿瘤 DNA 的 NGS 显示，当患者缓解时，L858R 突变不再可检测到，MET 的拷贝数下降。
EGFR 和 MET 酪氨酸激酶抑制剂的联合治疗可能是针对罕见突变的有效治疗方法。
