Related Experiment Video

Updated: Mar 3, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

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[Progress of c-MET Signaling Pathway and TKIs in Non-small Cell Lung Cancer]

Xiaoqing Yu1, Yanjun Xu2, Yun Fan2

  • 1Zhejiang Chinese Medical University, Hangzhou 310053, China.

Zhongguo Fei AI Za Zhi = Chinese Journal of Lung Cancer
|April 27, 2017
PubMed

Insights

MET activation is a key driver in non-small cell lung cancer (NSCLC), emerging after EGFR and ALK discoveries. Targeting MET offers new therapeutic strategies for NSCLC patients, especially those resistant to other treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • c-MET is an oncogenic driver in non-small cell lung cancer (NSCLC).
  • MET activation (mutation, amplification, overexpression) is linked to poor prognosis.
  • MET is implicated as a primary driver and a resistance mechanism to EGFR-TKIs.

Purpose of the Study:

  • To review MET activation in NSCLC.
  • To discuss the latest clinical trials for MET-targeted therapies in NSCLC.

Main Methods:

  • Literature review of scientific publications.
  • Analysis of clinical trial data on MET inhibitors.

Main Results:

  • MET activation is a significant factor in NSCLC pathogenesis.
  • Emerging therapies targeting MET show promise.
  • MET-targeted treatments are being investigated for various NSCLC subtypes.

Conclusions:

  • MET pathway alterations are crucial therapeutic targets in NSCLC.
  • Targeting MET presents a viable strategy for overcoming resistance and improving patient outcomes.

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