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Updated: Jul 8, 2026

Ultra-Fast Amplicon-Based Next-Generation Sequencing in Non-Squamous Non-Small Cell Lung Cancer
Published on: September 8, 2023
[Molecular targeted therapy and tailor-made therapy for lung cancer]
Kenji Sugio1, H Uramoto, M Takenoyama
1Second Department of Surgery, University of Occupational and Environmental Health, Kitakyushu, Japan.
Abstract:
Somatically acquired mutations in the epidermal growth factor receptor (EGFR) gene in lung cancer are associated with significant clinical responses to gefitinib, a tyrosine kinase inhibitor (TKI) that targets EGFR. In our previous report, 42.2% of adenocarcinoma patients has EGFR mutations, and these mutations were more frequently found in women than in men, in well differentiated tumors than poorly differentiated tumors, and in patients who were never smokers than in patients who were current/former smokers. Retrospectively, we screened the EGFR gene of tumors in 37 NSCLC patients who had been treated with gefitinib. EGFR mutations were found in 22 patients. Gefitinib was effective (CR/PR) in 15 of 22 (68.2%) patients with mutations compared with none of 15 patients without mutations. Patients with EGFR mutations survived for a longer period than without the mutations after initiation of gefitinib treatment (p = 0.0005). Gefitinib was not effective in 3 patients with K-ras mutations. Three of 4 tumors obtained from patients with acquired resistant to gefitinib, had a secondary T790M mutation. No T790M mutation was detected in pretreatment tumors. Molecular targeted therapy using TKI indicates an effective therapy specifically in lung cancer patients with EGFR mutations, and analyses of mechanisms of resistance to TKI are necessary for establishment of tailor-made therapy.
Insights
Epidermal growth factor receptor (EGFR) mutations in lung cancer predict gefitinib effectiveness. Patients with EGFR mutations showed improved survival and response rates, highlighting targeted therapy benefits. Resistance mechanisms require further study.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Somatic mutations in the epidermal growth factor receptor (EGFR) gene are linked to gefitinib response in lung cancer.
- Previous studies indicated EGFR mutations are more common in specific demographics and tumor types.
Purpose of the Study:
- To investigate the efficacy of gefitinib in non-small cell lung cancer (NSCLC) patients with EGFR mutations.
- To identify molecular mechanisms of resistance to gefitinib.
Main Methods:
- Retrospective analysis of EGFR gene mutations in tumors from 37 NSCLC patients treated with gefitinib.
- Assessment of gefitinib efficacy (CR/PR) and patient survival based on EGFR mutation status.
- Screening for K-ras mutations and acquired T790M mutations in resistant tumors.
Main Results:
- EGFR mutations were identified in 22 out of 37 patients.
- Gefitinib was effective in 68.2% of patients with EGFR mutations versus none without.
- Patients with EGFR mutations had significantly longer survival (p = 0.0005).
- Gefitinib was ineffective in patients with K-ras mutations.
- Three of four tumors from patients with acquired resistance harbored a secondary T790M mutation.
Conclusions:
- Molecular targeted therapy with tyrosine kinase inhibitors (TKIs) like gefitinib is effective in lung cancer patients with EGFR mutations.
- Analysis of resistance mechanisms, such as the T790M mutation, is crucial for developing personalized therapies.
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