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Review
. 2022 Aug 20;25(8):615-621.
doi: 10.3779/j.issn.1009-3419.2022.102.23.

[Research Progress of Acquired Resistance Mediated by MET Amplification in Advanced Non-small Cell Lung Cancer]

[Article in Chinese]
Sisi Pan  1 , Na Wang  1 , Xia Song  2
Affiliations
Review

[Research Progress of Acquired Resistance Mediated by MET Amplification in Advanced Non-small Cell Lung Cancer]

[Article in Chinese]
Sisi Pan et al. Zhongguo Fei Ai Za Zhi. .

Abstract
in English, Chinese

Mesenchymal-epithelial transition factor (MET) amplification is an important driver of resistance in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC), and the combination of MET proto-oncogene (MET) and EGFR-tyrosine kinase inhibitors (TKIs) has shown promise in overcoming this molecularly defined acquired resistance. Emerging data also demonstrate MET amplification as a resistance driver to TKIs-treated anaplastic lymphoma kinase (ALK)-, RET-, and ROS1-fusion NSCLC. Here, we review the literature on recent research progress of MET amplification as a resistance driver to targeted therapy in oncogene-driven NSCLC and summarize the progress of clinical strategies to overcome the resistance mechanism. .

【中文题目：晚期非小细胞肺癌MET扩增介导 获得性耐药的研究进展】 【中文摘要：间质-上皮细胞转化因子（mesenchymal-epithelial transition factor, MET）扩增是表皮生长因子受体（epidermal growth factor receptor, EGFR）阳性非小细胞肺癌（non-small cell lung cancer, NSCLC）耐药的重要驱动因素，MET-酪氨酸激酶抑制剂（tyrosine kinase inhibitors, TKIs）联合EGFR-TKIs的治疗策略可以克服MET介导的获得性耐药。研究表明，MET扩增也是间变性淋巴瘤激酶（anaplastic lymphoma kinase, ALK）、RET、ROS1等驱动基因阳性NSCLC患者接受TKIs类药物治疗后耐药的驱动因素。本文综述了近年来关于MET扩增作为驱动基因阳性NSCLC靶向治疗耐药驱动因素的研究进展，并总结了克服这种耐药机制的治疗策略。 】 【中文关键词：肺肿瘤；靶向治疗；MET扩增；获得性耐药】.

Keywords: Acquired resistance; Lung neoplasms; MET amplification; Targeted therapy.

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References

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