ReviewCancer drug resistance (Alhambra, Calif.)2020
Non-small cell lung cancer-small cell lung cancer transformation as mechanism of resistance to tyrosine kinase inhibitors in lung cancer.
Review in Cancer drug resistance (Alhambra, Calif.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 15 citations in OpenAlex.
- 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
- Baseline retinoblastoma transcriptional corepressor 1 (Rb1) functional inactivation is a pre-requisite but not sufficient for small-cell histological transformation in epidermal growth factor receptor (EGFR) mutant lung adenocarcinomas post-tyrosine kinase inhibitor therapy.Virchows Archiv : an international journal of pathology · 2025Article
- Identification of STAT3 phosphorylation inhibitors using generative deep learning, virtual screening, molecular dynamics simulations, and biological evaluation for non-small cell lung cancer therapy.Molecular diversity · 2025Article
- A Comparative Study on CT-guided Radiofrequency Ablation and Targeted Therapy: Intervention Efficacy and Survival Rates in Lung Cancer PatientsCurrent medical imaging · 2025Article
- TIPRL Regulates Stemness and Survival in Lung Cancer Stem Cells through CaMKK2-CaMK4-CREB Feedback Loop Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Understanding the treatment response and resistance to targeted therapies in non-small cell lung cancer: clinical insights and perspectives.Frontiers in oncology · 2024Review
- Top 20Lung Cancer (Auckland, N.Z.) · 2024Article
- Non-Small Cell Lung Cancer Targeted Therapy: Drugs and Mechanisms of Drug Resistance.International journal of molecular sciences · 2022Review
- Review
- Comparative characteristics of small cell lung cancer and Ewing's sarcoma: a narrative review.Translational lung cancer research · 2022Review
- Small Cell Lung Cancer Transformation following Treatment in EGFR-Mutated Non-Small Cell Lung Cancer.Journal of clinical medicine · 2022Article
- T790M and Acquired Resistance of Epidermal Growth Factor Receptor to Tyrosine Kinase Inhibitors in Patients with Lung Adenocarcinoma.Tanaffos · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutated or rearranged driver kinases in non-small cell lung cancer (NSCLC) cells are clinically amenable to treatment with tyrosine kinase inhibitors (TKIs) resulting in prolonged survival and significant benefit compared to cytotoxic chemotherapy. The most frequent genomic alterations are observed for epidermal growth factor receptor and anaplastic lymphoma kinase, which can be blocked by a range of specific TKIs in sequence. In clinics, resistance to TKIs emerges after approximately one year and comprises secondary mutations of the kinases (on-target) or alternative pathways circumventing the original kinase (off-target) alterations. A special feature of NSCLC is the occurrence of histological transformation to small cell lung cancer (SCLC) in up to 14% of cases, which, in general, is accompanied by resistance to the original TKIs. SCLC transformed tumors may be treated with the classical platinum/etoposide regimen but thus far there are no definitive guidelines. Four transformed pleural SCLC lines in our lab indicate the presence of a gradual NSCLC-SCLC shift with overlapping drug sensitivities. In conclusion, the treatment of NSCLC-SCLC transformed cancer cells would need a better chemosensitivity assessment using functional genomics to guide further therapy.
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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.