ArticleTranslational lung cancer research2016
Kinase inhibitor-responsive genotypes in EGFR mutated lung adenocarcinomas: moving past common point mutations or indels into uncommon kinase domain duplications and rearrangements.
Article in Translational lung cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- Trial
- Osimertinib for Patients With Non-Small-Cell Lung Cancer Harboring Uncommon EGFR Mutations: A Multicenter, Open-Label, Phase II Trial (KCSG-LU15-09).Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020Trial
- Opportunities and challenges in the development of evolving EGFR inhibitors to overcome EGFR TKIs resistance.Acta pharmacologica Sinica · 2026Review
- Lung cancer withTranslational lung cancer research · 2026Review
- Congenital mesoblastic nephroma: a single-center retrospective study.Translational pediatrics · 2026Article
- Molecular Subtyping Based on EGFR Mutation-Associated Genes and the Prognostic Role of TRAF2 in Lung Adenocarcinoma.Human mutation · 2026Article
- Colorectal cancer harboring EGFR kinase domain duplication response to EGFR tyrosine kinase inhibitors.The oncologist · 2025Article
- Epidermal Growth Factor Receptor Kinase Domain Duplication in Lung Adenocarcinoma with Sensitive Response to Afatinib: A Case Report and Literature Review.Lung Cancer (Auckland, N.Z.) · 2025Article
- Receptor Pharmacogenomics: Deciphering Genetic Influence on Drug Response.International journal of molecular sciences · 2024Review
- Article
- Tumor-suppressive action of miR-30a-5p in lung adenocarcinoma correlates with ABL2 inhibition and PI3K/AKT pathway inactivation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- EGFR kinase domain duplication in lung adenocarcinoma with systemic and intracranial response to a double-dose of furmonertinib: a case report and literature review.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
- Adjuvant therapies in stages I-III epidermal growth factor receptor-mutated lung cancer: current and future perspectives.Translational lung cancer research · 2023Review
- TAS2940, a novel brain-penetrable pan-ERBB inhibitor, for tumors with HER2 and EGFR aberrations.Cancer science · 2023Article
- Structure-Guided Strategies of Targeted Therapies for Patients withBiomolecules · 2023Review
- Mathematical analysis identifies the optimal treatment strategy for epidermal growth factor receptor-mutated non-small cell lung cancer.Frontiers in oncology · 2023Article
- A Primary Lung and Breast Cancer Patient with GermlineOncoTargets and therapy · 2023Article
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Abstract
The most frequent epidermal growth factor receptor (EGFR) mutations found by traditional or comprehensive molecular profiling of lung adenocarcinomas include indels of exon 19 (the exon 19 deletion delE746_A750 being the most common) and the exon 21 L858R point mutation. The current approval labels for first line palliative gefitinib 250 mg/day, erlotinib 150 mg/day and afatinib 40 mg/day for advanced lung cancers require the presence of the aforementioned classical/sensitizing EGFR mutations. Other gefitinib, erlotinib and afatinib sensitizing mutations include exon 18 indels, G719X, exon 19 insertions, A763_Y764insFQEA, S768I and L861Q; for which off-label EGFR kinase inhibitor use is generally agreed upon by thoracic oncologists. The main biological mechanism of resistance to approved first line EGFR inhibitors is the selection/acquisition of EGFR-T790M that in itself can be inhibited by osimertinib 80 mg/day, a 3(rd) generation EGFR inhibitor that is bypassed by EGFR-C797X mutations. Another class of de novo inhibitor insensitive mutation includes EGFR exon 20 insertions. More recently, the dichotomy of only point mutations or indels explaining aberrant kinase activation of EGFR plus inhibitor response has been shattered by the discovery of uncommon (<0.5% of all EGFR mutations) genomic events involving exon 18-25 kinase domain duplications (KDD) and rearrangements (EGFR-RAD51 or EGFR-PURB). The latter lead to oncogene addiction, enhanced sensitivity to kinase inhibitors in vitro and clinical responses to approved EGFR inhibitors. The enhanced landscape of EGFR inhibitor-responsive genotypes highlights that comprehensive molecular profiling may be necessary to maximize the identification of all cases that can benefit from precision oncology.
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