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Updated: Jun 23, 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

[Overcoming resistance to EGFR-TKI in lung cancer]

Koji Takeda1

  • 1Department of Clinical Oncology, Osaka City General Hospital, Osaka, Japan.

Gan to Kagaku Ryoho. Cancer & Chemotherapy
|April 22, 2009
PubMed

Insights

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) effectively treat advanced non-small cell lung cancer (NSCLC) with EGFR mutations. However, acquired resistance mechanisms like T790M and MET amplification necessitate personalized treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represent a targeted therapy for advanced non-small cell lung cancer (NSCLC).
  • Patients with activating EGFR mutations show significant initial response to EGFR-TKIs.
  • HER3 signaling is crucial for enhancing EGFR pathways, including PI3K/Akt.

Purpose of the Study:

  • To review the mechanisms of acquired resistance to EGFR-TKIs in NSCLC.
  • To highlight the role of HER3 in EGFR signaling and resistance.
  • To emphasize the need for individualized medicine strategies in NSCLC treatment.

Main Methods:

  • Literature review of studies on EGFR-TKI resistance in NSCLC.
  • Analysis of molecular mechanisms underlying acquired resistance.
  • Discussion of emerging resistance pathways and therapeutic implications.

Main Results:

  • Activating EGFR mutations predict good response to EGFR-TKIs.
  • Acquired resistance to EGFR-TKIs is a significant clinical challenge.
  • Key resistance mechanisms include T790M mutations, MET amplification, and increased HGF ligand for MET.

Conclusions:

  • Understanding resistance mechanisms is vital for effective NSCLC treatment.
  • HER3 plays a critical role in EGFR signaling and resistance development.
  • Personalized medicine approaches are essential for managing advanced NSCLC.

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