ArticleOncogene2002
Activation of anaplastic lymphoma kinase is responsible for hyperphosphorylation of ShcC in neuroblastoma cell lines.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- The autocrine loop of ALK receptor and ALKAL2 ligand is an actionable target in consensus molecular subtype 1 colon cancer.Journal of experimental & clinical cancer research : CR · 2022Pooled it
- Oncogenic alterations in advanced NSCLC: a molecular super-highway.Biomarker research · 2024Review
- ALK fusions in the pan-cancer setting: another tumor-agnostic target?NPJ precision oncology · 2023Review
- Unlocking the power of precision medicine for pediatric low-grade gliomas: molecular characterization for targeted therapies with enhanced safety and efficacy.Frontiers in oncology · 2023Review
- Non-Small Cell Lung Cancer Targeted Therapy: Drugs and Mechanisms of Drug Resistance.International journal of molecular sciences · 2022Review
- Defining Pathological Activities of ALK in Neuroblastoma, a Neural Crest-Derived Cancer.International journal of molecular sciences · 2021Review
- Biomarkers in Neuroblastoma: An Insight into Their Potential Diagnostic and Prognostic Utilities.Current treatment options in oncology · 2021Review
- A review of the biological and clinical implications of RAS-MAPK pathway alterations in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2021Review
- Molecular targeting therapies for neuroblastoma: Progress and challenges.Medicinal research reviews · 2021Review
- Unproductive Effects of ALK Gene Amplification and Copy Number Gain in Non-Small-Cell Lung Cancer. ALK Gene Amplification and Copy Gain in NSCLC.International journal of molecular sciences · 2020Article
- Pediatric low-grade glioma in the era of molecular diagnostics.Acta neuropathologica communications · 2020Review
- Opportunities and challenges of circulating biomarkers in neuroblastoma.Open biology · 2019Review
- Integrated proximal proteomics reveals IRS2 as a determinant of cell survival in ALK-driven neuroblastoma.Science signaling · 2018Article
- Leukocyte receptor tyrosine kinase interacts with secreted midkine to promote survival of migrating neural crest cells.Development (Cambridge, England) · 2018Article
- The ALK receptor in sympathetic neuron development and neuroblastoma.Cell and tissue research · 2018Review
- Review
- ALK-rearrangement in non-small-cell lung cancer (NSCLC).Thoracic cancer · 2018Review
- ALK Protein Expression Is Related to Neuroblastoma Aggressiveness But Is Not Independent Prognostic Factor.Cancer research and treatment · 2018Article
- The p53 activator overcomes resistance to ALK inhibitors by regulating p53-target selectivity in ALK-driven neuroblastomas.Cell death discovery · 2018Article
- ALK Inhibitor Response in Melanomas ExpressingMolecular cancer therapeutics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shc family of docking proteins, ShcA, ShcB and ShcC, play roles in cellular signal transduction by binding to phosphotyrosine residues of various activated receptor tyrosine kinases. Both ShcB and ShcC proteins are selectively expressed in the neural system of adult mouse tissues. In most of neuroblastoma cells, obvious tyrosine phosphorylation of ShcC was observed, whereas expression of ShcB was considerably low. Phosphoproteins associated with hyperphosphorylated ShcC were purified from neuroblastoma cell lines, and identified by mass-spectrometry. Anaplastic lymphoma kinase (ALK), which turned out to be one of these phosphoproteins, was constitutively activated and associated with the PTB domain of ShcC in three neuroblastoma cells. In vitro kinase assay revealed that ShcC is a potent substrate of the activated ALK kinase. The ALK gene locus was significantly amplified in both of these cell lines, suggesting that gene amplification leads to constitutive activation of the ALK kinase, which results in hyperphosphorylation of ShcC. Constitutive activation of ALK appeared to interfere with signals from other receptor tyrosine kinases. ALK-ShcC signal activation, possibly caused by co-amplification with the N-myc gene, might give additional effects on malignant tumor progression of neuroblastoma.
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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.