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Related Experiment Video

Updated: Jun 16, 2026

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

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

EGFR mutations and the terminal respiratory unit.

Yasushi Yatabe¹

¹Department of Pathology and Molecular Diagnostics, Aichi Cancer Center, Kanokoden, Chikusa-ku, Nagoya, 464-8681, Japan. yyatabe@aichi-cc.jp

Cancer Metastasis Reviews

|February 6, 2010

Summary

Epidermal growth factor receptor (EGFR) mutations are key in lung adenocarcinoma, driving responses to targeted therapies. Research now focuses on understanding and overcoming treatment resistance in these specific non-small cell lung cancer cases.

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

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Published on: August 11, 2017

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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Epidermal growth factor receptor (EGFR) mutations were identified in 2004.
EGFR mutations are prevalent in lung adenocarcinoma, particularly in never-smokers and females.
EGFR-tyrosine kinase inhibitors (TKIs) have shown significant clinical efficacy in patients with EGFR-mutated non-small cell lung cancer (NSCLC).

Purpose of the Study:

To review the clinicopathological characteristics of EGFR mutations in lung cancer.
To provide an overview of EGFR-mutated lung adenocarcinoma, including its molecular classification.
To discuss the role of EGFR mutations in tumorigenesis and resistance mechanisms.

Main Methods:

Literature review of studies on EGFR mutations in lung cancer.
Analysis of clinical trial data for EGFR-TKI efficacy.
Examination of molecular and pathological aspects of EGFR-mutated lung adenocarcinoma.

Main Results:

EGFR mutations lead to dramatic responses to EGFR-TKIs in NSCLC patients.
Mechanisms of resistance to EGFR-TKIs have been largely elucidated.
EGFR amplification plays a role in the progression of lung adenocarcinoma.

Conclusions:

Understanding EGFR mutations provides insights into lung adenocarcinoma biology and classification.
Targeted therapies and strategies to overcome resistance are advancing treatment for EGFR-mutated NSCLC.
EGFR mutations are crucial in early lung adenocarcinoma development, while amplification is linked to progression.