ReviewOncology letters2025
EGFR mutations in non-small cell lung cancer: Classification, characteristics and resistance to third-generation EGFR-tyrosine kinase inhibitors (Review).
Review in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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
14 citing papers in PubMed.
- Central nervous system efficacy of third generationJournal of thoracic disease · 2026Article
- Natural language processing to develop a standardized lexicon for precision medicine in oncology.Journal of managed care & specialty pharmacy · 2026Article
- Tyrosine Kinase Inhibitors, Antibody-Drug Conjugates, and Bispecific Antibodies in Oncogene-Driven Non-Small-Cell Lung Cancer: Evolving Roles in Treatment Sequencing and Resistance Management.International journal of molecular sciences · 2026Review
- Targeting non-small cell lung cancer: Molecular mechanisms and clinical studies (Review).Oncology letters · 2026Review
- The potential utility of in-silico approach in identifying phytochemicals against various targets for the management of lung cancer.Discover oncology · 2026Review
- 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
- EGFR G719X + S768I co-mutations in NSCLC: genomic landscape and differential responses to EGFR-TKIs in a large real-world cohort.BMC cancer · 2026Article
- Article
- 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
- The tumor microenvironment in lung cancer: Heterogeneity, therapeutic resistance and emerging treatment strategies (Review).International journal of oncology · 2026Review
- Redefining the Diagnostic and Therapeutic Landscape of Non-Small Cell Lung Cancer in the Era of Precision Medicine.Journal of clinical medicine · 2025Review
- Role of miRNA‑214‑3p in cancer (Review).Oncology reports · 2025Review
- Innovative Amino-Functionalization of Pyrido[2,3-Pharmaceuticals (Basel, Switzerland) · 2025Article
- Treatment decision-making for leptomeningeal metastasis after TKI resistance in EGFR-mutant lung cancer: a comprehensive review on staging, resistance patterns, and multimodal interventions.Frontiers in neurologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in EGFR (mEGFRs) in non-small cell lung cancer (NSCLC) are key factors driving tumor development and treatment response. The present article aimed to review the classification, characteristics and molecular mechanisms of resistance to third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs) associated with mEGFRs. Activating mutations (such as L858R and exon 19 deletions) are the primary markers of sensitivity to EGFR-TKIs, while rare mutations (such as G719X and S768I) require individualized treatment strategies. Resistance mechanisms are categorized into EGFR-dependent (such as T790M and C797S mutations) and -independent (bypassing signaling activation, epithelial-mesenchymal transition, tumor microenvironment remodeling and epigenetic regulation). Third-generation EGFR-TKIs (such as osimertinib) markedly improve patient survival by selectively targeting the T790M mutation, but novel resistance mutations, such as C797S, limit their long-term efficacy. Combination therapies (such as MET proto-oncogene, receptor tyrosine kinase/EGFR dual-target inhibitors) and fourth-generation TKIs (such as BLU-945) offer novel directions to overcome resistance. Future research should focus on precise subtyping, dynamic monitoring of resistance mechanisms and regulation of the immune microenvironment to advance personalized treatment for NSCLC.
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Registered trials
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