ReviewTherapeutic advances in medical oncology2025
Histologic transformation after targeted therapy resistance in driver gene-positive NSCLC: mechanisms and therapeutic challenges.
Review in Therapeutic advances in medical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Co-mutation landscape and prognostic impact of genomic complexity in EGFR-mutant non-small cell lung cancer.BMC cancer · 2026Article
- Hypoxia/Reoxygenation-Induced Mitochondrial Reverse Electron Transfer: A Targetable Mechanism to Enhance Radiosensitivity in Non-Small Cell Lung Cancer.Antioxidants (Basel, Switzerland) · 2026Article
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- Nanotechnology-Enabled Precision Therapy for Lung Cancer in Never-Smokers.Pharmaceutics · 2026Review
- Transformation from lung adenocarcinoma to pulmonary giant cell carcinoma following targeted therapy: a case report.Frontiers in oncology · 2026Article
- Squamous transformation of EGFR-mutant lung adenocarcinoma after EGFR-TKI therapy: clonal continuity, tissue-based diagnosis, and therapeutic evidence gaps.Frontiers in oncology · 2026Review
- Clinicopathologic features and therapeutic outcomes in EGFR/ALK-aberrations NSCLC with histologic transformation.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeted therapies have significantly improved the prognosis and productivity of non-small-cell lung cancer (NSCLC) patients carrying driver mutations, but drug resistance is inevitable. Histological transformation, an important resistance mechanism, is often manifested as transformation into small-cell lung cancer, large-cell neuroendocrine carcinoma, squamous cell carcinoma, and sarcomatoid carcinoma. The mechanisms involved are complex, including RB1/TP53 inactivation, epithelial-mesenchymal transition, and microenvironmental changes. Post-transformation tumors are often more aggressive and drug-resistant, with limited therapeutic options and poorer prognosis. In this paper, we systematically review the histological transformation types, molecular mechanisms, and therapeutic strategies of NSCLC after resistance to targeted therapy, with the aim of providing a reference for clinical decision-making and promoting the development of individualized therapy.
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Registered trials
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