ReviewFrontiers in oncology2019
EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies.
Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
151 citing papers in PubMed.
- Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Early-Phase Activation of Epithelial-Mesenchymal Transition in Lung Cancer Cells Treated with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.International journal of molecular sciences · 2026Article
- Opportunities and challenges in the development of evolving EGFR inhibitors to overcome EGFR TKIs resistance.Acta pharmacologica Sinica · 2026Review
- Expression of Transforming Growth Factor Beta 1 in Lung Adenocarcinoma and Its Relationship with Circulating Tumour Cells.Biochemical genetics · 2026Article
- Organoids: From Bench to Bedside Applications.MedComm · 2026Review
- scRADAR: Dissecting intratumoral drug response heterogeneity at single-cell resolution via mechanism-guided prototype routing.PLoS computational biology · 2026Article
- C-terminal interleukin 1 alpha (IL-1α) overexpression drives EMT and a vulnerability to ferroptosis in HNSCC.Redox biology · 2026Article
- USP7-dependent stabilization of FKBP4 contributes to acquired osimertinib resistance through glycolytic remodeling in NSCLC.Scientific reports · 2026Article
- Mitochondrial translocation of MDM2 and TFAM reprograms metabolism in treatment-refractory cancers.NPJ precision oncology · 2026Article
- Therapy-induced cholesterol biosynthesis drives lung cancer dormancy and drug resistance.The Journal of clinical investigation · 2026Article
- sc-rDSeq: a robust and cost-effective full-length total RNA sequencing method for single cells reveals multilayered heterogeneity in drug-resistant lung cancer cells.Nucleic acids research · 2026Article
- First Line and Treatment Sequencing in EGFR-Mutated Metastatic NSCLC: What is Right for Which Patient?Drugs · 2026Review
- CST4 promotes EMT and tumor progression in ovarian cancer via Wnt/β-catenin signaling.Discover oncology · 2026Article
- Is Immunotherapy a Contraindication for Treating Lung Cancer Patients with Interstitial Lung Diseases? A Review of the Literature.Journal of clinical medicine · 2026Review
- Advances in understanding the mechanisms underlying acquired resistance to third-generation tyrosine kinase inhibitors in non-small cell lung cancer.Frontiers in cell and developmental biology · 2026Review
- Taxanes Versus Pemetrexed After Osimertinib Resistance in EGFR-Mutated NSCLC: A Retrospective Cohort with Two-Model In Vitro Validation.Cancer management and research · 2026Article
- Astragaloside IV Co-Loaded Osimertinib Liposomes Alleviate EGFR-TKI Resistance in Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Article
- The Activity of EGFR CAR NK and CAR T Cells against EGFR Inhibitor-Resistant NSCLC and Drug-Tolerant Persister Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Knockdown of Inhibin Beta A Reversed the Epithelial Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance and Enhanced the Therapeutic Effect of Radiotherapy in Non-Small Cell Lung Cancer.Biochemical genetics · 2025Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice.
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Registered trials
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