已发表论文

MET D1228N突变作为MET Y1003H突变的非小细胞肺癌中克里唑替尼耐药性的获得性潜在机制

 

Authors Zhu J, Chen J, Liu W, Zhang J , Gu Y

Received 6 March 2024

Accepted for publication 14 August 2024

Published 27 August 2024 Volume 2024:15 Pages 123—128

DOI https://doi.org/10.2147/LCTT.S467584

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Fengying Wu

Jinlian Zhu,1 Jie Chen,1 Wei Liu,1 Junling Zhang,2 Yulan Gu1 

1Department of Oncology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu Province, People’s Republic of China; 2Medical Department, 3D Medicines Inc, Shanghai, People’s Republic of China

Correspondence: Yulan Gu, Email 382561683@qq.com

Abstract: Mesenchymal-epithelial transition (MET) gene has been identified as a promising target for treatments. However, different sites of the MET mutation show different effects to MET inhibition. Here, we reported a non-small cell lung cancer (NSCLC) patient harboring MET Y1003H mutation who achieved a durable partial response to crizotinib with a PFS of 22.4 months. Furthermore, we report for the first time the identification of MET D1228N as a possible mechanism of acquired resistance to crizotinib in a patient with MET Y1003H mutation during disease progression.

Keywords: MET Y1003H, MET D1228N, crizotinib, resistance, NSCLC