ArticleESMO open2025
Rare mutations at EGFR L747 position: molecular characteristics and superior response to afatinib in NSCLC patients.
Article in ESMO open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Real-world prevalence of actionable genomic alterations detected by next-generation sequencing in non-small cell lung cancer: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Dynamic therapeutic response to osimertinib and immunotherapy in an EGFR L747S and L858R co-mutant NSCLC.The oncologist · 2026Article
- Lung cancer withTranslational lung cancer research · 2026Review
- Baseline Uncommon EGFR Mutations in Non-Small-Cell Lung Cancer: Structure-Function Classification and Clinical Evidence Interpretation.Cancer control : journal of the Moffitt Cancer CenterReview
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8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundLittle is known about the molecular characteristics and responses to different therapies in missense mutations at epidermal growth factor receptor (EGFR) L747 position (EGFR L747X) due to their low prevalence and frequent misidentification by routine PCR kit. We aimed to investigate the molecular features through next-generation sequencing (NGS) and responses in lung cancer patients with EGFR L747X. PATIENTS AND
methodsThe distribution and molecular characteristics of EGFR L747X mutations were analyzed through NGS tests carried out in 41 369 lung cancer patients. Ba/F3 cells expressing EGFR L747P, L747S and L747V were established to evaluate the sensitivity to different EGFR tyrosine kinase inhibitors (TKIs). Binding affinity was predicted through structural modeling. Data from advanced non-small-cell lung cancer (NSCLC) patients with EGFR L747X were retrospectively collected to evaluate the clinical responses to different therapies in the real world.
resultsEGFR mutations were detected in 17 084 patients (41.3%, 17 084/41 369), including 68 EGFR L747X (0.4%, 68/17 084). Compared with EGFR L747S and L747V, EGFR L747P tended to exist as a single EGFR mutation. In vitro models and structural analysis demonstrated enhanced sensitivity and binding affinity for afatinib compared with other TKIs. Afatinib showed stronger inhibition in EGFR phosphorylation and downstream signaling pathway in three EGFR L747X-mutant models. Clinically, afatinib-treated patients achieved significantly longer median progression-free survival (PFS) (7.0 months) versus first-generation (1G) TKIs (1.4 months, P = 0.0026) and third-generation (3G) TKIs (3.1 months, P = 0.016), with comparable efficacy to chemotherapy (9.3 months). Objective response rates (ORRs) favored afatinib (44.4%) over 1G (20%) and 3G TKIs (16.7%), while chemotherapy showed the highest ORR (63.6%).
conclusionsThis study showed the first NGS-based research on EGFR L747X mutations, which accounted for 0.4% in EGFR-mutated NSCLC patients. EGFR L747P was found to have a different genomic profile than other EGFR L747 variants. Through this largest known treatment cohort analysis, we found that EGFR L747X mutations might exert superior sensitivity to afatinib and chemotherapies.
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