ArticleProceedings of the National Academy of Sciences of the United States of America2008
A mouse model for EML4-ALK-positive lung cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 4 of them syntheses that pooled it.
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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
229 citing papers in PubMed, 4 syntheses or guidelines pooled it, 509 citations in OpenAlex.
- Targeted therapy for advanced anaplastic lymphoma kinase (<I>ALK</I>)-rearranged non-small cell lung cancer.The Cochrane database of systematic reviews · 2022Pooled it
- Current status and challenges of immunotherapy in ALK rearranged NSCLC.Frontiers in oncology · 2022Pooled it
- Clinicopathological characteristics of patients with non-small-cell lung cancer who harbor EML4-ALK fusion gene: a meta-analysis.PloS one · 2015Pooled it
- Clinicopathologic features of patients with non-small cell lung cancer harboring the EML4-ALK fusion gene: a meta-analysis.PloS one · 2014Pooled it
- EML4-ALK Variant-Specific Genetic Interactions Shape Lung Tumorigenesis.Cancer discovery · 2026Article
- The efficacy of targeted therapy in ALK-positive non-small-cell lung cancer patients and analysis of MET/PD-L1 expression status.Therapeutic advances in medical oncology · 2026Article
- Case report: Personalized, response-adapted neoadjuvant alectinib achieves durable remission in stage IIIB ALK-rearranged lung cancer.Frontiers in pharmacology · 2026Article
- OncogenicLung cancer management · 2025Article
- Molecular Mechanisms and Treatment Strategies of ALK-Positive Lung Cancer: A Beginner's Guide for Patients, Their Families and Carers.Thoracic cancer · 2025Review
- Preclinical Prediction of Resistance Mutations and Proposal of Sequential Treatment Strategies for ALK-positive Lung Cancer Using Next-generation ALK Inhibitors.Pharmaceutical research · 2025Article
- Middle-Out Physiologically Based Pharmacokinetic Modeling to Support Pediatric Dosing Recommendation for Alectinib.CPT: pharmacometrics & systems pharmacology · 2025Article
- ALK in cancer: from function to therapeutic targeting.Nature reviews. Cancer · 2025Review
- [A Case of Multiple Primary Pulmonary Neuroendocrine Carcinoma with EML4-ALK Fusion Gene Positive].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- CENPF (+) cancer cells promote malignant progression of early-stage TP53 mutant lung adenocarcinoma.Oncogenesis · 2025Article
- Ensartinib as a neoadjuvant therapy for stage IIIA non-small cell lung cancer patients with EML4-ALK fusion: a case report and literature review.Frontiers in oncology · 2025Article
- Establishment of potential reference measurement procedure and reference materials for EML4-ALK fusion variants measurement.Scientific reports · 2024Article
- The Genetic Analysis and Clinical Therapy in Lung Cancer: Current Advances and Future Directions.Cancers · 2024Review
- Superficial Anaplastic Lymphoma Kinase-Rearranged Myxoid Spindle Cell Neoplasm in the Buttock: A Case Report.Journal of personalized medicine · 2024Article
- [A Case of EML4-ALK Fusion V1 Subtype Lung Adenocarcinoma Detected by RNA-based NGS].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- Review
169 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EML4-ALK is a fusion-type protein tyrosine kinase that is generated in human non-small-cell lung cancer (NSCLC) as a result of a recurrent chromosome inversion, inv (2)(p21p23). Although mouse 3T3 fibroblasts expressing human EML4-ALK form transformed foci in culture and s.c. tumors in nude mice, it has remained unclear whether this fusion protein plays an essential role in the carcinogenesis of NSCLC. To address this issue, we have now established transgenic mouse lines that express EML4-ALK specifically in lung alveolar epithelial cells. All of the transgenic mice examined developed hundreds of adenocarcinoma nodules in both lungs within a few weeks after birth, confirming the potent oncogenic activity of the fusion kinase. Although such tumors underwent progressive enlargement in control animals, oral administration of a small-molecule inhibitor of the kinase activity of ALK resulted in their rapid disappearance. Similarly, whereas i.v. injection of 3T3 cells expressing EML4-ALK induced lethal respiratory failure in recipient nude mice, administration of the ALK inhibitor effectively cleared the tumor burden and improved the survival of such animals. These data together reinforce the pivotal role of EML4-ALK in the pathogenesis of NSCLC in humans, and they provide experimental support for the treatment of this intractable cancer with ALK inhibitors.
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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.