MET D1228N突变是伴有MET Y1003H突变的NSCLC患者克唑替尼耐药的后天潜在机制

IF 5.1 Q1 ONCOLOGY

Lung Cancer: Targets and Therapy Pub Date : 2024-08-27 eCollection Date: 2024-01-01 DOI:10.2147/LCTT.S467584

Jinlian Zhu, Jie Chen, Wei Liu, Junling Zhang, Yulan Gu

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引用次数: 0

摘要

间充质-上皮转化（MET）基因已被确定为有希望的治疗靶点。然而，不同位点的MET突变对MET抑制的效果不同。在此，我们报告了一名携带MET Y1003H突变的非小细胞肺癌（NSCLC）患者，该患者对克唑替尼获得了持久的部分应答，PFS达22.4个月。此外，我们还首次报道了在一名MET Y1003H突变患者的疾病进展过程中发现MET D1228N可能是克唑替尼获得性耐药的机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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

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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来源期刊

Lung Cancer: Targets and Therapy Medicine-Oncology

CiteScore

8.10

自引率

0.00%

发文量

审稿时长

16 weeks