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Mutation of MET D1228N as an Acquired Potential Mechanism of Crizotinib Resistance in NSCLC with MET Y1003H Mutation.
Zhu, Jinlian; Chen, Jie; Liu, Wei; Zhang, Junling; Gu, Yulan.
Afiliação
  • Zhu J; Department of Oncology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu Province, People's Republic of China.
  • Chen J; Department of Oncology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu Province, People's Republic of China.
  • Liu W; Department of Oncology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu Province, People's Republic of China.
  • Zhang J; Medical Department, 3D Medicines Inc, Shanghai, People's Republic of China.
  • Gu Y; Department of Oncology, Affiliated Changshu Hospital of Nantong University, Changshu, Jiangsu Province, People's Republic of China.
Lung Cancer (Auckl) ; 15: 123-128, 2024.
Article em En | MEDLINE | ID: mdl-39221108
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.
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Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article