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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
Published on: August 11, 2017
A novel point mutation in exon 20 of EGFR showed sensitivity to erlotinib
Kailin Xing1, Xiaoyan Zhou, Xinmin Zhao
1Department of Medical Oncology, Fudan University Shanghai Cancer Center, 270 Dong-An Road, Shanghai, 200032, China.
Abstract:
Mutations of epidermal growth factor receptor (EGFR) gene are good predictors of response to treatment with EGFR tyrosine kinase inhibitors (TKIs) for non-small cell lung cancer (NSCLC). It is well established that classic mutations, such as in-frame deletions in exon 19 and the point mutation L858R in exon 21, are associated with high sensitivity to EGFR TKIs. Though mutations in exon 20 are almost correlated with EGFR-TKIs resistance, the awareness that they might confer sensitivity to TKI treatment should be emphasized. Herein, we describe a novel mutation in exon 20 of EGFR in a Chinese male non-smoker, who was diagnosed with stage IV lung adenocarcinoma and characterized by the codon 769 point mutation GTG>GCG, which translates into alanine instead of valine (p.V769A). In this case, the patient showed a good clinical response to erlotinib after paclitaxel/cisplatin first-line and docetaxel second-line chemotherapies. Therefore, we suggest that this rare mutation (p.V769A) may be a sensitive EGFR mutation in NSCLC. The identification of novel EGFR mutations provides new predictive biomarkers for TKI treatment and is essential to the successful use of targeted therapies.
Insights
A novel EGFR mutation (p.V769A) in exon 20 was identified in a non-small cell lung cancer patient. This rare mutation showed sensitivity to erlotinib, suggesting its potential as a predictive biomarker for targeted therapy.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epidermal Growth Factor Receptor (EGFR) mutations are key predictors of treatment response in non-small cell lung cancer (NSCLC).
- Classic EGFR mutations (exon 19 deletions, L858R in exon 21) confer sensitivity to EGFR tyrosine kinase inhibitors (TKIs).
- Exon 20 mutations are typically associated with EGFR-TKI resistance, but sensitivity is possible.
Observation:
- A novel EGFR mutation, p.V769A (codon 769 GTG>GCG), was identified in exon 20.
- The mutation occurred in a Chinese male non-smoker with stage IV lung adenocarcinoma.
- The patient responded well to erlotinib after prior chemotherapy regimens.
Findings:
- The p.V769A mutation in EGFR exon 20 may confer sensitivity to EGFR TKIs.
- This specific mutation (p.V769A) represents a potential predictive biomarker for targeted therapy in NSCLC.
- The patient's positive response to erlotinib supports the sensitivity of this rare mutation.
Implications:
- Identification of novel EGFR mutations enhances personalized medicine approaches in NSCLC.
- Discovering new predictive biomarkers is crucial for optimizing TKI treatment efficacy.
- This finding expands the understanding of EGFR mutation-driven lung adenocarcinoma and its therapeutic targets.
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