Related Experiment Video
Updated: Mar 13, 2026

Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
Epidermal growth factor receptor mutation-guided treatment for lung cancers: Where are we now?
1Vanderbilt-Ingram Cancer Center, Department of Medicine/Division of Hematology-Oncology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Abstract:
Epidermal growth factor receptor (EGFR) kinase domain mutations (from exon 18 to 21) alter the efficacy of the EGFR tyrosine kinase inhibitors gefitinib (Iressa) and erlotinib (Tarceva). Lung cancer patients with drug-sensitive EGFR mutations initially respond, but acquire resistance after approximately one year of tyrosine kinase inhibitor treatment. This review summarizes EGFR gene mutation profiles for East Asian non-small-cell lung cancer patients according to recent publications. Strategies for the treatment of acquired resistance mediated by EGFR T790M are also reviewed.
Insights
Epidermal growth factor receptor (EGFR) mutations impact lung cancer drug efficacy. This review covers EGFR mutation profiles in East Asian patients and strategies to overcome acquired resistance, particularly the T790M mutation.
Area of Science:
- Oncology
- Genetics
- Pharmacology
Background:
- Epidermal growth factor receptor (EGFR) kinase domain mutations (exons 18-21) influence the effectiveness of EGFR tyrosine kinase inhibitors (TKIs) like gefitinib and erlotinib.
- Non-small cell lung cancer (NSCLC) patients with sensitive EGFR mutations initially respond to TKIs but often develop acquired resistance within a year.
- Understanding EGFR mutation profiles is crucial for tailoring NSCLC treatment strategies, especially in East Asian populations.
Approach:
- This review synthesizes recent publications on EGFR gene mutation profiles in East Asian NSCLC patients.
- It examines the mechanisms of acquired resistance to EGFR TKIs.
- The review also discusses therapeutic strategies to overcome resistance, focusing on the EGFR T790M mutation.
Key Points:
- EGFR mutations in exons 18-21 are key determinants of TKI response in NSCLC.
- Acquired resistance, often involving the T790M mutation, limits long-term TKI efficacy.
- EGFR mutation profiling in East Asian NSCLC patients reveals specific patterns relevant to treatment.
Conclusions:
- EGFR mutation status is critical for predicting response and resistance to TKIs in NSCLC.
- The T790M mutation represents a significant challenge in NSCLC treatment, necessitating targeted therapeutic approaches.
- Further research into EGFR mutation profiles and resistance mechanisms can guide the development of more effective NSCLC therapies.
More Related Videos
09:38Establishing 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
13:34A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
Related Concept Videos
Mitogens and the Cell Cycle
Targeted Cancer Therapies
There are several types of targeted therapies against...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Treatment for Pulmonary Arterial Hypertension: Receptor Tyrosine Kinase Inhibitors and Calcium Channel Blockers
TKIs, such as imatinib (Gleevec), are particularly effective in tackling the growth and mitogenic factors that become upregulated in PAH patients. These factors contribute to the...
Cancer