Zeng Yuan, Zeng Qiang, Yang Bin, Hu Yang
Department of Oncology, Hubei Cancer Hospital, TongJi Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Intensive Care Unit, Chengdu Shuangliu Hospital of Traditional Chinese Medicine, Chengdu, China.
Front Oncol. 2024 Nov 1;14:1390523. doi: 10.3389/fonc.2024.1390523. eCollection 2024.
Non-small cell lung cancer (NSCLC) is one of the most common malignancies in the world. tyrosine inhibitors are the preferred first-line treatment for patients with epidermal growth factor-cell receptor mutant ( mutant) advanced NSCLC. Unfortunately, drug resistance inevitably occurs leading to disease progression. Activation of the and bypass signaling pathways is a rare cause of acquired drug resistance for -TKIs.We report two NSCLC-patients with - mutations, in exon 19, and exon 18, correspondingly, who were treated with -TKIs. The first case shows acquired -mutation, and the second case demonstrates acquired -fusion. The overall survival of patients was significantly prolonged by drug-match therapies. As it is well-known that -fusion and -mutations are described forms of acquired resistance. These two case reports contribute to the previous reports that -fusion and -mutation are potential underlying mechanisms of -TKI resistance.
非小细胞肺癌（NSCLC）是世界上最常见的恶性肿瘤之一。酪氨酸激酶抑制剂是表皮生长因子细胞受体突变（EGFR突变）的晚期NSCLC患者的首选一线治疗药物。不幸的是，不可避免地会出现耐药性，导致疾病进展。激活PI3K和旁路信号通路是EGFR-TKIs获得性耐药的罕见原因。我们报告了两名分别在19外显子和18外显子发生EGFR突变的NSCLC患者，他们接受了EGFR-TKIs治疗。第一例显示获得性T790M突变，第二例显示获得性HER2融合。通过药物匹配疗法，患者的总生存期显著延长。众所周知，HER2融合和T790M突变是获得性耐药的已知形式。这两例病例报告为之前关于HER2融合和T790M突变是EGFR-TKI耐药潜在机制的报告提供了补充。
