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Updated: Dec 20, 2025
Author Spotlight: Advancements in Molecular Biomarker Testing for Non-Squamous Non-Small Cell Lung Cancer
Published on: September 8, 2023
Progress on treatment of MET signaling pathway in non-small cell lung cancer
Xiaoqing Yu1,2,3, Sizhe Yu2,3, Yun Fan4,5,6
1Institute of Cancer and Basic Medicine (ICBM), Chinese Academy of Sciences, Hangzhou, China.
Abstract:
MET activation includes gene mutation, amplification, and protein overexpression. Clinical evidence suggests that MET activation is both a primary oncogenic driver in lung cancer, and a secondary driver after acquired resistance to EGFR tyrosine kinase inhibitors (TKIs). Several small molecule TKIs have already shown to be effective in the MET pathway. However, the activation form and the diagnostic criteria of MET oncogene are still controversial, especially in patients resistant to EGFR TKIs or ALK TKIs. With the development of new MET inhibitors, a quantity of emerging trials has focused on the mechanism of acquired resistance to MET TKIs and therapeutic strategies after resistance.
Insights
MET activation drives lung cancer and resistance to targeted therapies. Ongoing research explores MET inhibitors and resistance mechanisms for improved treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MET activation, through mutation, amplification, or overexpression, is a key driver in lung cancer.
- MET activation can be a primary oncogenic driver or emerge as a secondary driver following resistance to therapies like EGFR tyrosine kinase inhibitors (TKIs).
- The precise diagnostic criteria and activation forms of the MET oncogene remain subjects of debate, particularly in cases of resistance to EGFR or ALK TKIs.
Purpose of the Study:
- To review the role of MET activation in lung cancer.
- To discuss the controversies surrounding MET oncogene diagnostics in resistant populations.
- To highlight emerging therapeutic strategies and resistance mechanisms related to MET inhibitors.
Main Methods:
- Literature review of clinical evidence and ongoing trials.
- Analysis of MET pathway activation mechanisms.
- Examination of diagnostic criteria for MET oncogene.
Main Results:
- MET activation is implicated as both a primary and secondary oncogenic driver.
- Several small molecule MET TKIs demonstrate efficacy.
- Controversies persist regarding MET activation forms and diagnostic criteria, especially in resistant lung cancer.
Conclusions:
- Understanding MET activation is crucial for lung cancer treatment.
- Further research is needed to clarify diagnostic standards and overcome resistance to MET inhibitors.
- Development of novel MET inhibitors and combination therapies holds promise for overcoming acquired resistance.
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