Lung Cancer: Targets and Therapy (Aug 2024)

Mutation of MET D1228N as an Acquired Potential Mechanism of Crizotinib Resistance in NSCLC with MET Y1003H Mutation

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

Journal volume & issue
Vol. Volume 15
pp. 123 – 128

Abstract

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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 ChinaCorrespondence: Yulan Gu, Email [email protected]: 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

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