ReviewJournal of cancer research and clinical oncology2021
Drug resistance of targeted therapy for advanced non-small cell lung cancer harbored EGFR mutation: from mechanism analysis to clinical strategy.
Review in Journal of cancer research and clinical oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Review
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- Targeting inflammatory microenvironments: overcoming therapy resistance and immunosuppression.Molecular cancer · 2026Review
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- Harmine suppresses the malignant phenotypes of Lewis lung carcinoma cells by inhibiting EGFR phosphorylation.American journal of translational research · 2026Article
- Cancer-associated fibroblasts: central players in cancer hallmarks and therapeutic resistance.Cell communication and signaling : CCS · 2025Review
- Synergistic camrelizumab therapy inhibits P53-mutant osimertinib-resistant solid lung adenocarcinoma via the TGF-β signaling pathway.Translational lung cancer research · 2025Article
- First-line immunotherapy in advanced non-squamous non-small cell lung cancer patients with rare mutations: a retrospective cohort study.Translational lung cancer research · 2025Article
- Efficacy and safety of furmonertinib in patients with EGFR‑mutant advanced lung adenocarcinoma after failure of multiple lines of therapy: A single‑center retrospective study.Oncology letters · 2025Article
- A Structural Insight Into Two Important ErbB Receptors (EGFR and HER2) and Their Relevance to Non-Small Cell Lung Cancer.Archiv der Pharmazie · 2025Review
- Unlocking the therapeutic potential of antibody-drug conjugates in targeting molecular biomarkers in non-small cell lung cancer.Journal of the Egyptian National Cancer Institute · 2025Review
- Advances in the study of reversing tumor drug resistance by targeting cancer-associated fibroblasts with nanomaterials.Frontiers in immunology · 2025Review
- Review
- Ze-Qi decoction inhibits non-small cell lung cancer growth and metastasis by modulating the PI3K/Akt/p53 signaling pathway.Journal of traditional and complementary medicine · 2023Article
- Real-World Data on Combined EGFR-TKI and Crizotinib Treatment for Acquired and De NovoInternational journal of molecular sciences · 2023Article
- Inhibition of the mitochondria-shaping protein Opa1 restores sensitivity to Gefitinib in a lung adenocarcinomaresistant cell line.Cell death & disease · 2023Article
- A radiomics-based deep learning approach to predict progression free-survival after tyrosine kinase inhibitor therapy in non-small cell lung cancer.Cancer imaging : the official publication of the International Cancer Imaging Society · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeNon-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6-13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC.
methodsRelevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as "NSCLC", "EGFR-TKIs resistance", "EGFR mutations", "human epidermal growth factor receptor-2 (HER2/erbB-2)", "hepatocyte growth factor (HGF)", "vascular endothelial growth factor (VEGF)", "insulin-like growth factor 1 (IGF-1)", "epithelial-mesenchymal transition (EMT)", "phosphatase and tensin homolog (PTEN)", "RAS mutation", "BRAF mutation", "signal transducer and activator of transcription 3 (STAT3)", and "tumor microenvironment", etc.
resultsThe mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC.
conclusionIn this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
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