Related Experiment Video
Updated: Aug 7, 2026
A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
Epidermal growth factor receptor activating mutations in Spanish gefitinib-treated non-small-cell lung cancer
H Cortes-Funes1, C Gomez, R Rosell
1Hospital Doce de Octubre, Madrid, Spain.
Background:
North American and Japanese non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) activation via tyrosine kinase (TK) mutations respond dramatically to gefitinib treatment. To date, however, the frequency and effect of EGFR TK mutations have not been examined in European patients.
Patients And Methods:
Eighty-three Spanish advanced NSCLC patients who had progressed after chemotherapy, were treated with compassionate use of gefitinib. Patients were selected on the basis of available tumor tissue. Tumor genomic DNA was retrieved from paraffin-embedded tissue obtained by laser capture microdissection. EGFR mutations in exons 19 and 21 were examined by direct sequencing.
Results:
EGFR mutations were found in 10 of 83 (12%) of patients. All mutations were found in adenocarcinomas, more frequently in females (P=0.007) and non-smokers (P=0.01). Response was observed in 60% of patients with mutations and 8.8% of patients with wild-type EGFR (P=0.001). Time to progression for patients with mutations was 12.3 months, compared with 3.6 months for patients with wild-type EGFR (P=0.002). Median survival was 13 months for patients with mutations and 4.9 months for those with wild-type EGFR (P=0.02).
Conclusions:
EGFR TK mutational analysis is a novel predictive test for selecting lung adenocarcinoma patients for targeted therapy with EGFR TK inhibitors.
Insights
EGFR TK mutations in lung adenocarcinoma predict gefitinib response in European patients. This analysis identifies patients likely to benefit from targeted therapy, improving treatment outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epidermal growth factor receptor (EGFR) tyrosine kinase (TK) mutations are linked to gefitinib response in North American and Japanese non-small-cell lung cancer (NSCLC) patients.
- The prevalence and impact of these EGFR TK mutations in European NSCLC populations remained unexamined.
Purpose of the Study:
- To investigate the frequency and clinical significance of EGFR TK mutations in Spanish advanced NSCLC patients.
- To determine if EGFR mutational status predicts response to gefitinib treatment.
Main Methods:
- Eighty-three Spanish advanced NSCLC patients received gefitinib via compassionate use after chemotherapy progression.
- Tumor DNA was isolated from paraffin-embedded tissues using laser capture microdissection.
- EGFR mutations in exons 19 and 21 were analyzed via direct sequencing.
Main Results:
- EGFR mutations were identified in 12% (10/83) of patients, exclusively in adenocarcinomas.
- Mutations were more common in females and non-smokers.
- Patients with EGFR mutations showed significantly higher response rates (60% vs. 8.8%), longer time to progression (12.3 vs. 3.6 months), and improved median survival (13 vs. 4.9 months) compared to wild-type EGFR patients.
Conclusions:
- EGFR TK mutational analysis serves as a predictive biomarker for selecting lung adenocarcinoma patients for EGFR TK inhibitor therapy.
- This finding supports the use of EGFR mutational testing to personalize lung cancer treatment strategies.
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
09:38Establishment and Characterization of Three Afatinib-resistant Lung Adenocarcinoma PC-9 Cell Lines Developed with Increasing Doses of Afatinib
Published on: June 26, 2019
Related Concept Videos
02:38Mitogens and the Cell Cycle
02:57Targeted Cancer Therapies
There are several types of targeted therapies against specific...
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase