ReviewCancer science2008
Non-solid oncogenes in solid tumors: EML4-ALK fusion genes in lung cancer.
Review in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.
- Pooled it
- Accurate and economical detection of ALK positive lung adenocarcinoma with semiquantitative immunohistochemical screening.PloS one · 2014Trial
- Cancer-associated fusion transcripts: mechanisms, functional roles, and clinical implications.Clinical and experimental medicine · 2026Review
- Systematic Targeting of Protein Complexes with Molecular COUPLrs.Cancer discovery · 2026Article
- Molecular origin, discovery, validation and application of neoantigens.Asian journal of pharmaceutical sciences · 2026Review
- Frags2Drugs: A Novel In Silico Fragment-Based Approach to the Discovery of Kinase Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Distinct size and spatial distribution patterns of ALK-inhibitor-naïve versus ALK-inhibitor exposed ALK-positive NSCLC brain metastases.Journal of neuro-oncology · 2025Article
- Preclinical Prediction of Resistance Mutations and Proposal of Sequential Treatment Strategies for ALK-positive Lung Cancer Using Next-generation ALK Inhibitors.Pharmaceutical research · 2025Article
- Machine Learning and Integrative Structural Dynamics Identify Potent ALK Inhibitors from Natural Compound Libraries.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exceptional response to brigatinib following alectinib failure in a patient withInternational cancer conference journal · 2025Article
- Presence of On-Target Resistant Mutation in Pre-Treatment Samples of ALK Fusion Gene Positive Lung Cancer Patients.Cancers · 2025Article
- Establishing a new human lung squamous cell carcinoma cell line, OMUL-1, expressing insulin-like growth factor 1 receptor and programmed cell death ligand 1.Thoracic cancer · 2025Article
- Article
- Case report: targeted therapy of malignant pleural mesothelioma with anaplastic lymphoma kinase receptor tyrosine kinase gene fusion mutation by crizotinib.The Journal of international medical research · 2024Article
- Kinase inhibitor macrocycles: a perspective on limiting conformational flexibility when targeting the kinome with small molecules.RSC medicinal chemistry · 2024Review
- EML4-ALK fusion protein in Lung cancer cells enhances venous thrombogenicity through the pERK1/2-AP-1-tissue factor axis.Journal of thrombosis and thrombolysis · 2024Article
- Discovery of novel 2-aminopyridine derivatives as ROS1 and ALK dual inhibitors to combat drug-resistant mutants including ROS1Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Multifaceted Roles of ALK Family Receptors and Augmentor Ligands in Health and Disease: A Comprehensive Review.Biomolecules · 2023Review
- Abnormal phase separation of biomacromolecules in human diseases.Acta biochimica et biophysica Sinica · 2023Review
- Therapeutic Advances of Rare ALK Fusions in Non-Small Cell Lung Cancer.Current oncology (Toronto, Ont.) · 2022Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally accepted that recurrent chromosome translocations play a major role in the molecular pathogenesis of hematological malignancies but not of solid tumors. However, chromosome translocations involving the e26 transformation-specific sequence transcription factor loci have been demonstrated recently in many prostate cancer cases. Furthermore, through a functional screening with retroviral cDNA expression libraries, we have discovered the fusion-type protein tyrosine kinase echinoderm microtubule-associated protein like-4 (EML4)-anaplastic lymphoma kinase (ALK) in non-small cell lung cancer (NSCLC) specimens. A recurrent chromosome translocation, inv(2)(p21p23), in NSCLC generates fused mRNA encoding the amino-terminal half of EML4 ligated to the intracellular region of the receptor-type protein tyrosine kinase ALK. EML4-ALK oligomerizes constitutively in cells through the coiled coil domain within the EML4 region, and becomes activated to exert a marked oncogenicity both in vitro and in vivo. Break and fusion points within the EML4 locus may diverge in NSCLC cells to generate various isoforms of EML4-ALK, which may constitute approximately 5% of NSCLC cases, at least in the Asian ethnic group. In the present review I summarize how detection of EML4-ALK cDNA may become a sensitive diagnostic means for NSCLC cases that are positive for the fusion gene, and discuss whether suppression of ALK enzymatic activity could be an effective treatment strategy against this intractable disorder.
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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.