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Updated: May 24, 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

Biomarkers for EGFR-antagonist response: in the genes and on the genes!

Hariharan Easwaran1, Stephen B Baylin

  • 1Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. heaswar2@jhmi.edu

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|February 29, 2012
PubMed

Insights

New research identifies DNA methylation changes linked to epithelial-mesenchymal transition in non-small cell lung carcinoma. These markers may predict response to epidermal growth factor receptor (EGFR) antagonist therapy in patients with wild-type EGFR.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Non-small cell lung carcinoma (NSCLC) patients with activating epidermal growth factor receptor (EGFR) mutations benefit from EGFR-antagonist therapy.
  • EGFR-antagonist sensitivity is associated with epithelial-mesenchymal transition (EMT).

Purpose of the Study:

  • To investigate potential biomarkers for predicting EGFR-antagonist therapy response in NSCLC.
  • To explore the relationship between DNA methylation, EMT, and EGFR-antagonist sensitivity.

Main Methods:

  • Analysis of DNA methylation patterns in NSCLC samples.
  • Correlation of methylation changes with epithelial-mesenchymal transition markers.
  • Assessment of EGFR-antagonist sensitivity in relation to identified methylation profiles.

Main Results:

  • DNA methylation changes are identified as markers of epithelial-mesenchymal transition in NSCLC.
  • These methylation markers show a correlation with EGFR-antagonist sensitivity.

Conclusions:

  • DNA methylation changes associated with EMT could serve as predictive biomarkers for EGFR-antagonist therapy.
  • Further validation may help identify wild-type EGFR NSCLC patients who can benefit from EGFR therapy.

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