ArticleOncogene2005
Microarray analysis reveals differential gene expression patterns and regulation of single target genes contributing to the opposing phenotype of TrkA- and TrkB-expressing neuroblastomas.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 77 citations in OpenAlex.
- NTRK expression and its clinical significance in pancreatic neuroendocrine tumors.Discover oncology · 2025Article
- Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours.The journal of pathology. Clinical research · 2023Review
- NTRK1/TrkA Activation Overrides the GCancers · 2021Article
- NTRK1/TrkA Signaling in Neuroblastoma Cells Induces Nuclear Reorganization and Intra-Nuclear Aggregation of Lamin A/C.Cancers · 2021Article
- Biomarkers in Neuroblastoma: An Insight into Their Potential Diagnostic and Prognostic Utilities.Current treatment options in oncology · 2021Review
- Comparison of tyrosine kinase domain properties for the neurotrophin receptors TrkA and TrkB.The Biochemical journal · 2020Article
- The Evolving Diagnostic and Treatment Landscape of NTRK-Fusion-Driven Pediatric Cancers.Paediatric drugs · 2020Review
- Tumor-Derived Extracellular Vesicles Impair CD171-Specific CD4Frontiers in immunology · 2020Article
- Chronic Intermittent Hypobaric Hypoxia Pretreatment Ameliorates Ischemia-Induced Cognitive Dysfunction Through Activation of ERK1/2-CREB-BDNF Pathway in Anesthetized Mice.Neurochemical research · 2017Article
- Trk inhibition reduces cell proliferation and potentiates the effects of chemotherapeutic agents in Ewing sarcoma.Oncotarget · 2016Article
- Mutational dynamics between primary and relapse neuroblastomas.Nature genetics · 2015Article
- N-linked glycan profiling in neuroblastoma cell lines.Journal of proteome research · 2015Article
- Article
- Neuroblastoma in dialog with its stroma: NTRK1 is a regulator of cellular cross-talk with Schwann cells.Oncotarget · 2014Article
- Robust selection of cancer survival signatures from high-throughput genomic data using two-fold subsampling.PloS one · 2014Article
- The KDM1A histone demethylase is a promising new target for the epigenetic therapy of medulloblastoma.Acta neuropathologica communications · 2013Article
- TrkB receptor signalling: implications in neurodegenerative, psychiatric and proliferative disorders.International journal of molecular sciences · 2013Review
- MYCN and ALKF1174L are sufficient to drive neuroblastoma development from neural crest progenitor cells.Oncogene · 2013Article
- LMO4 is an essential cofactor in the Snail2-mediated epithelial-to-mesenchymal transition of neuroblastoma and neural crest cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Network-based analysis of multivariate gene expression data.Methods in molecular biology (Clifton, N.J.) · 2013Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Expression of neurotrophin receptors of the tyrosine kinase receptor (Trk) family is an important prognostic factor in solid tumors including neuroblastoma. High expression of TrkA (NTRK1) is associated with a favorable biology and outcome of neuroblastoma, whereas TrkB (NTRK2) is expressed on aggressive neuroblastomas with unfavorable outcome. To gain new insights into the global gene expression program resulting in these divergent biological phenotypes, we stably expressed either TrkA or TrkB in the human SH-SY5Y neuroblastoma cell line. Gene expression profiles were obtained from parental cells and transfectants activated by their ligands in a time course over 24 h using oligonucleotide microarrays. Basal activation of Trk receptors in the absence of exogenous ligand was sufficient to induce broad and divergent genetic changes. Global gene regulation following external ligand stimulation was surprisingly similar in SY5Y-TrkA and SY5Y-TrkB cells except for the differential expression of distinct novel target genes. Consistent with their divergent biological phenotype, SY5Y-TrkA cells were characterized by upregulation of proapoptotic genes and angiogenesis inhibitors, whereas SY5Y-TrkB cells demonstrated upregulation of genes involved in invasion or therapy resistance. We suggest that the transcriptional program of neuroblastoma cells is modulated by Trk-receptor expression and basal activation rather than by ligand-induced activation. Fine-tuning of the malignant phenotype may be achieved by additional ligand stimulation with subsequent activation of a few specific genes.
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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.