ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
EGFR exon 19 insertions: a new family of sensitizing EGFR mutations in lung adenocarcinoma.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.
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72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 149 citations in OpenAlex.
- Molecular testing guideline for selection of lung cancer patients for EGFR and ALK tyrosine kinase inhibitors: guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for Molecular Pathology.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2013Guideline
- Molecular testing guideline for selection of lung cancer patients for EGFR and ALK tyrosine kinase inhibitors: guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for Molecular Pathology.Archives of pathology & laboratory medicine · 2013Guideline
- EGFR Mutations and Tyrosine Kinase Inhibitors: Structural Insights and Therapeutic Advances.ACS omega · 2026Review
- Efficacy of TKIs in non-small cell lung cancer with atypical EGFR p.L747P and p.L747S mutations.Frontiers in oncology · 2026Article
- Molecular characteristics and responses to EGFR tyrosine kinase inhibitors in non-small cell lung cancer patients with EGFR exon 19 insertions.BMC medicine · 2025Article
- Efficacy of EGFR tyrosine kinase inhibitors in patients with non-small cell lung cancer with EGFR exon 19 insertions: clinical-genomic, preclinical analysis through LC-SCRUM-Asia (multi-institutional genomic screening registry).Lung cancer (Amsterdam, Netherlands) · 2025Article
- The changing treatment landscape of EGFR-mutant non-small-cell lung cancer.Nature reviews. Clinical oncology · 2025Review
- Lung adenocarcinoma with EGFR exon 19 insertion identified using a compact panel and its response to osimertinib: a case report.Respiratory medicine case reports · 2025Article
- Patients with Advanced Non-Small Cell Lung Cancer and the EGFR Exon 19 Deletion p.L747 Benefit from Chemotherapy and First-Generation Tyrosine Kinase Inhibitors Compared with Patients with p.E746.OncoTargets and therapy · 2025Article
- Long-term survival with pemetrexed-based chemotherapy in a patient with metastatic lung adenocarcinoma of unclear primary origin harboring MTHFR C677T(T/T) mutation: a case report.Frontiers in oncology · 2024Article
- Review
- EGFR exon 19 insertion EGFR-K745_E746insIPVAIK and others with rare XPVAIK amino-acid insertions: Preclinical and clinical characterization of the favorable therapeutic window to all classes of approved EGFR kinase inhibitors.Lung cancer (Amsterdam, Netherlands) · 2023Article
- Overview on Therapeutic Options in Uncommon EGFR Mutant Non-Small Cell Lung Cancer (NSCLC): New Lights for an Unmet Medical Need.International journal of molecular sciences · 2023Review
- Article
- Structure-Guided Strategies of Targeted Therapies for Patients withBiomolecules · 2023Review
- Real-world study of PD-1/L1 immune checkpoint inhibitors for advanced non-small cell lung cancer after resistance to EGFR-TKIs.Frontiers in oncology · 2023Article
- Allele-specific activation, enzyme kinetics, and inhibitor sensitivities of EGFR exon 19 deletion mutations in lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- MicroRNAs as the critical regulators of tyrosine kinase inhibitors resistance in lung tumor cells.Cell communication and signaling : CCS · 2022Review
- Efficacy of EGFR-TKI sequential therapy in patients withWorld journal of clinical cases · 2022Article
- Identification of a novel gene signature of lung adenocarcinoma based on epidermal growth factor receptor-tyrosine kinase inhibitor resistance.Frontiers in oncology · 2022Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
purposeEpidermal growth factor receptor (EGFR) genotyping is now standard in the management of advanced lung adenocarcinoma, as this biomarker predicts marked benefit from treatment with EGFR tyrosine kinase inhibitors (TKI). EGFR exon 19 insertions are a poorly described family of EGFR mutations, and their association with EGFR-TKI sensitivity in lung adenocarcinoma is uncertain. EXPERIMENTAL
designPatients with lung cancers harboring EGFR exon 19 insertions were studied. The predicted effects of the insertions on the structure of the EGFR protein were examined, and EGFR exon 19 insertions were introduced into Ba/F3 cells to assess oncogenicity and in vitro sensitivity to EGFR-TKIs. In patients receiving TKI, response magnitude was assessed with serial computed tomographic (CT) measurement.
resultsTwelve tumors harboring EGFR exon 19 insertions were identified; patients were predominately female (92%) and never-smokers (75%). The 11 specimens available for full sequencing all showed an 18-bp insertion that resulted in the substitution of a Pro for Leu at residue 747. The mutant EGFR transformed the Ba/F3 cells, which were then sensitive to EGFR-TKI. Six patients with measurable disease received TKI and five had a response on serial CT.
conclusionsEGFR exon 19 insertions are a newly appreciated family of EGFR-TKI-sensitizing mutations, and patients with tumors harboring these mutations should be treated with EGFR-TKI. While these mutations may be missed through the use of some mutation-specific assays, the addition of PCR product size analysis to multigene assays allows sensitive detection of both exon 19 insertion and deletion mutations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.