ArticleInternational journal of cancer2019
Clinical outcomes of EGFR kinase domain duplication to targeted therapies in NSCLC.
Article in International journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Acquired Resistance to Afatinib Mediated by EGFR T790M in Lung Adenocarcinoma Patients Harboring EGFR-KDD: A Case Report and Literature Review.Current oncology (Toronto, Ont.) · 2026Review
- Peritoneal Metastasis in Advanced Lung Adenocarcinoma Harboring EGFR Exon 19 Deletion/T790M with STRN::ALK Fusion and EGFR Kinase Domain Duplication: Two Case Reports and a Narrative Literature Summary.Cancer management and research · 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
- Comprehensive multi-omics analysis of tandem duplicator phenotypes in non-small cell lung cancer.Frontiers in medicine · 2025Article
- 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
- Article
- Clinical and molecular characteristics of kinase domain duplications across diverse cancer types in the Chinese population.Cancer medicine · 2023Article
- Structure-Guided Strategies of Targeted Therapies for Patients withBiomolecules · 2023Review
- Hyperprogression under treatment with immune-checkpoint inhibitors in patients with gastrointestinal cancer: A natural process of advanced tumor progression?World journal of clinical oncology · 2022Review
- Role of the EGFR-KDD mutation as a possible mechanism of acquired resistance of non-small cell lung cancer to EGFR tyrosine kinase inhibitors: A case report.Molecular and clinical oncology · 2022Article
- Acquired Resistance Mechanism of EGFR Kinase Domain Duplication to EGFR TKIs in Non-Small Cell Lung Cancer.Cancer research and treatment · 2022Article
- Therapeutic advances in non-small cell lung cancer: Focus on clinical development of targeted therapy and immunotherapy.MedComm · 2021Review
- Durable response to EGFR tyrosine kinase inhibitors in a patient with non-small cell lung cancer harboring an EGFR kinase domain duplication.Thoracic cancer · 2021Article
- The Genomics of Young Lung Cancer: Comprehensive Tissue Genomic Analysis in Patients Under 40 With Lung Cancer.JTO clinical and research reports · 2021Article
- Structure-function analysis of oncogenic EGFR Kinase Domain Duplication reveals insights into activation and a potential approach for therapeutic targeting.Nature communications · 2021Article
- Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer.Frontiers in pharmacology · 2021Review
- Lung Adenocarcinoma Patient HarboringFrontiers in oncology · 2021Article
- The landscape of kinase domain duplication in Chinese lung cancer patients.Annals of translational medicine · 2020Article
- Hyperprogression: A novel response pattern under immunotherapy.Clinical and translational medicine · 2020Review
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kinase domain duplications of the epidermal growth factor receptor (EGFR-KDD) have been identified and implicated to be oncogenic in nonsmall cell lung cancers (NSCLCs). However, its prevalence and clinical contributions in lung cancer are largely unknown. Here, we conducted a multicenter record review of 10,759 NSCLC patients who underwent genetic testing using next-generation sequencing (NGS) targeting EGFR exons and the introns involved in EGFR-KDD rearrangements. EGFR-KDDs were identified in a total of 13 patients, which is approximately 0.12% of the total population reviewed, and also consisted of 0.24% (13/5394) of EGFR mutation-positive patients. A total of 85% of patients (11/13) were identified with the canonical EGFR-KDD duplication of exons 18-25, while the remaining two cases harbored duplications of EGFR exons 14-26 and exons 17-25, which have not been previously described. Importantly, none of the 13 patients had other coexisting driver mutations, highlighting the potential oncogenic role of this type of alteration. Three out of five patients who had exon 18-25 duplications showed partial antitumor responses to targeted therapies, while the other two patients demonstrated no clinical improvement. Furthermore, our data suggested that the EGFR T790 M mutation and EGFR amplification may represent the major resistance mechanisms against targeted therapies in tumors bearing EGFR-KDD. In summary, our findings provide valuable insight into the prevalence of EGFR-KDDs in NSCLCs and their clinical outcomes to targeted therapies.
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