ArticleScientific reports2018
MET or NRAS amplification is an acquired resistance mechanism to the third-generation EGFR inhibitor naquotinib.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Precision navigation through the labyrinth: overcoming EGFR resistance in non-Small cell lung cancer.Annals of medicine · 2025Review
- Wild-type RAS signaling is an essential therapeutic target inScience signaling · 2025Article
- Prognostic model for lung adenocarcinoma based on experimental drug-resistant cell lines and clinical patients.Frontiers in molecular biosciences · 2025Article
- Targeting NRAS via miR-1304-5p or farnesyltransferase inhibition confers sensitivity to ALK inhibitors in ALK-mutant neuroblastoma.Nature communications · 2024Article
- Small molecule agents for triple negative breast cancer: Current status and future prospects.Translational oncology · 2024Review
- Third-generation EGFR and ALK inhibitors: mechanisms of resistance and management.Nature reviews. Clinical oncology · 2022Review
- Artificial Intelligence-Assisted Serial Analysis of Clinical Cancer Genomics Data Identifies Changing Treatment Recommendations and Therapeutic Targets.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Preclinical Models for Acquired Resistance to Third-Generation EGFR Inhibitors in NSCLC: Functional Studies and Drug Combinations Used to Overcome Resistance.Frontiers in oncology · 2022Review
- Evolution of MET and NRAS gene amplification as acquired resistance mechanisms in EGFR mutant NSCLC.NPJ precision oncology · 2021Article
- Has programmed cell death ligand-1Translational lung cancer research · 2021Review
- Single-cell transcriptional changes associated with drug tolerance and response to combination therapies in cancer.Nature communications · 2021Article
- LncRNA SNHG15 regulates EGFR-TKI acquired resistance in lung adenocarcinoma through sponging miR-451 to upregulate MDR-1.Cell death & disease · 2020Article
- STAT3 induces G9a to exacerbate HER3 expression for the survival of epidermal growth factor receptor-tyrosine kinase inhibitors in lung cancers.BMC cancer · 2019Article
- Liquid Biopsy by Next-Generation Sequencing: a Multimodality Test for Management of Cancer.Current hematologic malignancy reports · 2019Review
- Cell signaling and cancer: a mechanistic insight into drug resistance.Molecular biology reports · 2019Review
- Understanding the Mechanisms of Resistance inInternational journal of molecular sciences · 2019Review
- MET inhibitors for targeted therapy of EGFR TKI-resistant lung cancer.Journal of hematology & oncology · 2019Review
- Third generation EGFR inhibitor osimertinib combined with pemetrexed or cisplatin exerts long-lasting anti-tumor effect in EGFR-mutated pre-clinical models of NSCLC.Journal of experimental & clinical cancer research : CR · 2019Article
- Non-canonical cMet regulation by vimentin mediates Plk1 inhibitor-induced apoptosis.EMBO molecular medicine · 2019Article
- Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase inhibitors for EGFR-mutant lung cancer.Biomarker research · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), osimeritnib is the standard treatment for patients with non-small cell lung cancer harboring the EGFR T790M mutation; however, acquired resistance inevitably develops. Therefore, a next-generation treatment strategy is warranted in the osimertinib era. We investigated the mechanism of resistance to a novel EGFR-TKI, naquotinib, with the goal of developing a novel treatment strategy. We established multiple naquotinib-resistant cell lines or osimertinib-resistant cells, two of which were derived from EGFR-TKI-naïve cells; the others were derived from gefitinib- or afatinib-resistant cells harboring EGFR T790M. We comprehensively analyzed the RNA kinome sequence, but no universal gene alterations were detected in naquotinib-resistant cells. Neuroblastoma RAS viral oncogene homolog (NRAS) amplification was detected in naquotinib-resistant cells derived from gefitinib-resistant cells. The combination therapy of MEK inhibitors and naquotinib exhibited a highly beneficial effect in resistant cells with NRAS amplification, but the combination of MEK inhibitors and osimertinib had limited effects on naquotinib-resistant cells. Moreover, the combination of MEK inhibitors and naquotinib inhibited the growth of osimertinib-resistant cells, while the combination of MEK inhibitors and osimertinib had little effect on osimertinib-resistant cells. Clinical assessment of this novel combination (MEK inhibitors and naquotinib) is worth considering in osimertinib-resistant lung tumors.
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