ReviewTranslational lung cancer research2025
Molecular mechanisms and clinical insights in transformed small cell lung cancer: a narrative review.
Review in Translational lung cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Small-cell transformation of advanced non-small-cell lung cancer harboring driver mutations following tyrosine kinase inhibitor therapy: a multicenter real-world study.Journal of thoracic disease · 2026Article
- ALK rearrangements and resistance mutations in non-small cell lung cancer: molecular mechanisms and therapeutic implications.Cancer chemotherapy and pharmacology · 2026Review
- Plasticity inFrontiers in oncology · 2026Article
- Advanced and underlying therapeutic strategies in transformed small cell lung cancer.Frontiers in medicine · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Objective: In recent years, the application of targeted therapies has significantly improved survival rates in patients with driver gene-positive non-small cell lung cancer (NSCLC). However, one mechanism underlying acquired resistance is the histological transformation from NSCLC to small cell lung cancer (SCLC). NSCLC-to-SCLC transformation is thought to occur due to selective pressure from targeted therapies, yet this shift has also been observed in patients receiving non-targeted treatments, raising questions about its underlying mechanisms. This review aims to identify key molecular biomarkers predictive of this transformation to optimize clinical management strategies for transformed SCLC (T-SCLC). Methods: We systematically searched PubMed, EMBASE, the Cochrane Library, and major international conference proceedings for all English-language articles published up to December 31, 2024. This review synthesizes current evidence on the mechanisms of T-SCLC transformation, its genomic and transcriptomic alterations, and related therapeutic approaches. Key Content and Findings: T-SCLC is hypothesized to involve tumor heterogeneity and lineage plasticity. Key molecular players include dysregulation of the phosphatidylinositol 3-kinase ( Conclusions: Current T-SCLC research is limited by retrospective designs and small sample sizes, leaving transformation mechanisms incompletely understood. This phenotypic shift highlights lung cancer plasticity as a novel resistance mechanism rooted in lineage plasticity and tumor heterogeneity. Personalized therapies guided by molecular profiling may represent a future direction for improving outcomes.
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Registered trials
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