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在非小细胞肺癌中，使用 T790M 特异性第三代 EGFR 抑制剂（HM61713）治疗后获得 C797S 突变。

Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non-Small Cell Lung Cancer.

机构信息

Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; Department of Internal Medicine, Gyeongsang National University School of Medicine, Jinju, Republic of Korea.

Division of Hematology and Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.

出版信息

J Thorac Oncol. 2016 Apr;11(4):e45-7. doi: 10.1016/j.jtho.2015.12.093. Epub 2015 Dec 31.

DOI:10.1016/j.jtho.2015.12.093
PMID:26749488
Abstract

T790M mutation is most common resistant mechanism to epidermal growth factor receptor gene (EGFR) tyrosin kinase inhibitor (TKI). Several third-generation EGFR-mutant selective TKI, such as AZD9291 (AstraZeneca), Rociletinib (Clovis), or HM61713 (Hanmi) have been developed. Acquired resistant C797S mutation was known to be one of the resistance mechanisms of AZD9291, which has not been reported for HM61713 yet. This is the first case report of C797S mutation as resistance mechanism of HM61713.

摘要

T790M 突变是表皮生长因子受体基因（EGFR）酪氨酸激酶抑制剂（TKI）最常见的耐药机制。已经开发了几种第三代 EGFR 突变选择性 TKI，如 AZD9291（阿斯利康）、rociletinib（Clovis）或 HM61713（韩美）。已发现获得性耐药 C797S 突变是 AZD9291 的耐药机制之一，但尚未有 HM61713 的报道。这是首例 C797S 突变作为 HM61713 耐药机制的病例报告。

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