ReviewCancers2022
Resistance to TKIs in EGFR-Mutated Non-Small Cell Lung Cancer: From Mechanisms to New Therapeutic Strategies.
Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 73 citations in OpenAlex.
- Resistance Mutation Profiles Associated with Current Treatments for Epidermal Growth Factor Receptor-Mutated Non-Small-Cell Lung Cancer in the United States: A Systematic Literature Review.Current oncology (Toronto, Ont.) · 2025Pooled it
- A Bayesian meta-analysis on MRI-based radiomics for predicting EGFR mutation in brain metastasis of lung cancer.BMC medical imaging · 2025Pooled it
- Chinese herbal injections combined with EGFR-TKIs for intervention of non-small cell lung cancer: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- A four‑gene signature identifies TKI‑induced persister cells and uncovers a ZLN005‑induced pyroptotic vulnerability via the GSDME pathway in EGFR‑mutant lung cancer.Molecular medicine reports · 2026Article
- Review
- Review
- Integrated hypoxia and metabolic gene signature to predict clinical outcomes and therapeutic vulnerabilities in lung adenocarcinoma.Journal of thoracic disease · 2026Article
- Machine learning-guided drug repurposing for EGFR inhibition using scaffold-split validation, docking, and molecular dynamics.Journal of computer-aided molecular design · 2026Article
- Evaluating datopotamab deruxtecan (Dato-DXd) as a novel treatment option for EGFR-mutated non-small cell lung cancer.Future oncology (London, England) · 2026Review
- Leveraging mitochondrial dynamics-related risk signatures to predict the prognosis and tumor microenvironment of lung adenocarcinoma.Discover oncology · 2026Article
- Dual-Targeting Strategy in Cancer Therapy: The Emerging Role of Pyrrolopyrimidine Scaffolds.Chemistry & biodiversity · 2026Review
- Therapeutic Targeting of VEGFR-2, PD-L1, and EGFR-MET Pathways in Non-Small Cell Lung Cancer: Clinical Progress with Ramucirumab, Atezolizumab, and Amivantamab.Journal of clinical medicine · 2026Review
- Real-World Outcomes of Sequential Afatinib and Osimertinib Versus Afatinib and Chemotherapy in EGFR-Mutant NSCLC: Taiwan Multicenter GIANT Study.Targeted oncology · 2026Article
- Indenoquinoxaline-Based Spiro-Heterocycles: Synthesis, Structural Characterization, MEDT Study, and Dual Inhibition of Kinase-Related Enzymes EGFR and VEGFR2.Chemistry & biodiversity · 2026Article
- A Comparative Review of Methods for Detecting Epidermal Growth Factor Receptor Mutations in Cell-free DNA from Lung Cancer Patients.Current molecular medicine · 2026Review
- Bufalin: a potential drug for regulating EGFR-TKIs resistance in lung cancer via the EGFR-PI3K/Akt-mTOR signaling.Translational cancer research · 2025Article
- Decoding the molecular mechanism via systems biology-based insights into neoschaftoside from Ailanthus altissima targeting lung cancer.Scientific reports · 2025Article
- Click synthesis of some novel benzo[RSC medicinal chemistry · 2025Article
- DUSP11 is an Intracellular Innate Immune Checkpoint in Lung Adenocarcinoma.Cancer immunology research · 2025Article
- Long non-coding RNAs and signaling networks in non-small cell lung cancer: mechanistic insights into tumor pathogenesis.Cancer gene therapy · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to tyrosine kinase inhibitors (TKIs) of the epidermal growth factor receptor (EGFR) in advanced mutant Non-Small Cell Lung Cancer (NSCLC) constitutes a therapeutic challenge. This review intends to summarize the existing knowledge about the mechanisms of resistance to TKIs in the context of EGFR mutant NSCLC and discuss its clinical and therapeutic implications. EGFR-dependent and independent molecular pathways have the potential to overcome or circumvent the activity of EGFR-targeted agents including the third-generation TKI, osimertinib, negatively impacting clinical outcomes. CNS metastases occur frequently in patients on EGFR-TKIs, due to the inability of first and second-generation agents to overcome both the BBB and the acquired resistance of cancer cells in the CNS. Newer-generation TKIs, TKIs targeting EGFR-independent resistance mechanisms, bispecific antibodies and antibody-drug conjugates or combinations of TKIs with other TKIs or chemotherapy, immunotherapy and Anti-Vascular Endothelial Growth Factors (anti-VEGFs) are currently in use or under investigation in EGFR mutant NSCLC. Liquid biopsies detecting mutant cell-free DNA (cfDNA) provide a window of opportunity to attack mutant clones before they become clinically apparent. Overall, EGFR TKIs-resistant NSCLC constitutes a multifaceted therapeutic challenge. Mapping its underlying mutational landscape, accelerating the detection of resistance mechanisms and diversifying treatment strategies are essential for the management of the disease.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.