ArticleNeoplasia (New York, N.Y.)2011
Evaluation of EML4-ALK fusion proteins in non-small cell lung cancer using small molecule inhibitors.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- Transcriptomic Profile of Isocitrate Dehydrogenase Mutant Type of Lower-Grade Glioma Reveals Molecular Changes for Prognosis.Biomedicines · 2025Article
- Low-rank regression models for multiple binary responses and their applications to cancer cell-line encyclopedia data.Journal of the American Statistical Association · 2024Article
- Silibinin Suppresses the Hyperlipidemic Effects of the ALK-Tyrosine Kinase Inhibitor Lorlatinib in Hepatic Cells.International journal of molecular sciences · 2022Article
- SMPD3-ALK: A novel ALK fusion gene in lung adenocarcinoma.Clinical genetics · 2021Article
- Notch Transduction in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2020Review
- ALK Inhibitors-Induced M Phase Delay Contributes to the Suppression of Cell Proliferation.Cancers · 2020Article
- Elevated levels of pre-treatment lactate dehydrogenase are an unfavorable predictor factor in patients with EML4-ALK rearrangement non-small cell lung cancer treated with crizotinib.Cancer management and research · 2019Article
- Primary resistance to crizotinib treatment in a non-small cell lung cancer patient with an EML4-ALK rearrangement: a case report.Cancer biology & medicine · 2018Article
- Histology-dependent prognostic role of pERK and p53 protein levels in early-stage non-small cell lung cancer.Oncotarget · 2018Article
- Treating ALK-positive non-small cell lung cancer.Annals of translational medicine · 2018Review
- The function and therapeutic targeting of anaplastic lymphoma kinase (ALK) in non-small cell lung cancer (NSCLC).Molecular cancer · 2018Review
- Oncogene addiction and radiation oncology: effect of radiotherapy with photons and carbon ions in ALK-EML4 translocated NSCLC.Radiation oncology (London, England) · 2018Article
- Effects of SMYD2-mediated EML4-ALK methylation on the signaling pathway and growth in non-small-cell lung cancer cells.Cancer science · 2017Article
- AZD0530 sensitizes drug-resistant ALK-positive lung cancer cells by inhibiting SRC signaling.FEBS open bio · 2017Article
- ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017Review
- Anilinoquinazoline inhibitors of the RET kinase domain-Elaboration of the 7-position.Bioorganic & medicinal chemistry letters · 2016Article
- EMT is associated with, but does not drive resistance to ALK inhibitors among EML4-ALK non-small cell lung cancer.Molecular oncology · 2016Article
- Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.Cellular and molecular life sciences : CMLS · 2016Review
- Molecular Pathology and Personalized Medicine: The Dawn of a New Era in Companion Diagnostics-Practical Considerations about Companion Diagnostics for Non-Small-Cell-Lung-Cancer.Journal of personalized medicine · 2016Review
- Profile of ceritinib in the treatment of ALK+ metastatic non-small-cell lung cancer.Lung Cancer (Auckland, N.Z.) · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene resulting from an inversion within chromosome 2p occurs in approximately 5% of non-small cell lung cancer and is mutually exclusive with Ras and EGFR mutations. In this study, we have used a potent and selective ALK small molecule inhibitor, NPV-TAE684, to assess the oncogenic role of EML4-ALK in non-small cell lung cancer (NSCLC). We show here that TAE684 inhibits proliferation and induces cell cycle arrest, apoptosis, and tumor regression in two NSCLC models that harbor EML4-ALK fusions. TAE684 inhibits EML4-ALK activation and its downstream signaling including ERK, AKT, and STAT3. We used microarray analysis to carry out targeted pathway studies of gene expression changes in H2228 NSCLC xenograft model after TAE684 treatment and identified a gene signature of EML4-ALK inhibition. The gene signature represents 1210 known human genes, and the top biologic processes represented by these genes are cell cycle, DNA synthesis, cell proliferation, and cell death. We also compared the effect of TAE684 with PF2341066, a c-Met and ALK small molecule inhibitor currently in clinical trial in cancers harboring ALK fusions, and demonstrated that TAE684 is a much more potent inhibitor of EML4-ALK. Our data demonstrate that EML4-ALK plays an important role in the pathogenesis of a subset of NSCLC and provides insight into the mechanism of EML4-ALK inhibition by a small molecule inhibitor.
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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.