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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

Resistance mechanisms of tumour cells to EGFR inhibitors

F Morgillo1, F Cantile, M Fasano

  • 1Dipartimento di Internistica clinica e sperimentale, "F. Magrassi A. Lanzara", Seconda Università degli studi di Napoli, Naples, Italy. florianamorgillo@yahoo.com

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|May 20, 2009
PubMed

Insights

Resistance to epidermal growth factor receptor (EGFR) inhibitors can occur despite effective treatment. Understanding molecular mechanisms of EGFR inhibitor sensitivity and resistance is crucial for cancer treatment decisions and translational research.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Epidermal growth factor receptor (EGFR) is a key target in cancer therapy.
  • Despite overexpression and inhibition, resistance to EGFR inhibitors (monoclonal antibodies, tyrosine kinase inhibitors) is a clinical challenge.

Purpose of the Study:

  • To review the primary molecular mechanisms underlying acquired sensitivity and resistance to EGFR inhibitors in cancer cells.
  • To provide insights for optimizing cancer treatment strategies and guiding future translational studies.

Main Methods:

  • Literature review of relevant studies on EGFR inhibitor resistance.
  • Analysis of molecular pathways and genetic alterations affecting cancer cell response to EGFR-targeted therapies.

Main Results:

  • Multiple mechanisms contribute to EGFR inhibitor resistance, including secondary mutations in EGFR, activation of bypass signaling pathways, and alterations in downstream effectors.
  • Understanding these mechanisms can predict treatment response and identify potential therapeutic vulnerabilities.

Conclusions:

  • Acquired resistance to EGFR inhibitors is a complex, multifactorial process.
  • Targeting these resistance mechanisms holds promise for improving patient outcomes in EGFR-driven cancers.

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