ArticleClinical & experimental metastasis1997
Modulation of N-myc expression alters the invasiveness of neuroblastoma.
Article in Clinical & experimental metastasis, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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
21 citing papers in PubMed, 52 citations in OpenAlex.
- A multi-omics approach for biomarker discovery in neuroblastoma: a network-based framework.NPJ systems biology and applications · 2024Article
- Identification of MYCN non-amplified neuroblastoma subgroups points towards molecular signatures for precision prognosis and therapy stratification.British journal of cancer · 2024Article
- Metabolic protein kinase signalling in neuroblastoma.Molecular metabolism · 2023Review
- The MYCN inhibitor BGA002 restores the retinoic acid response leading to differentiation or apoptosis by the mTOR block in MYCN-amplified neuroblastoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Article
- Down-regulation of MYCN protein by CX-5461 leads to neuroblastoma tumor growth suppression.Journal of pediatric surgery · 2019Article
- Opportunities and challenges of circulating biomarkers in neuroblastoma.Open biology · 2019Review
- Inhibition of cathepsin proteases attenuates migration and sensitizes aggressive N-Myc amplified human neuroblastoma cells to doxorubicin.Oncotarget · 2015Article
- MycN promotes TRPM7 expression and cell migration in neuroblastoma through a process that involves polyamines.FEBS open bio · 2014Article
- ALK is a MYCN target gene and regulates cell migration and invasion in neuroblastoma.Scientific reports · 2013Article
- Neuroblastoma and MYCN.Cold Spring Harbor perspectives in medicine · 2013Review
- FAK inhibition decreases cell invasion, migration and metastasis in MYCN amplified neuroblastoma.Clinical & experimental metastasis · 2013Article
- Anaplastic Lymphoma Kinase (ALK) regulates initiation of transcription of MYCN in neuroblastoma cells.Oncogene · 2012Article
- MYCN, neuroblastoma and focal adhesion kinase (FAK).Frontiers in bioscience (Elite edition) · 2011Review
- Article
- Novel c-MYC target genes mediate differential effects on cell proliferation and migration.EMBO reports · 2007Article
- Inhibition of phosphatidylinositol 3-kinase destabilizes Mycn protein and blocks malignant progression in neuroblastoma.Cancer research · 2006Article
- Functional analysis of the actin-binding protein, tropomyosin 1, in neuroblastoma.British journal of cancer · 2003Article
- MYC oncogenes and human neoplastic disease.Oncogene · 1999Review
- Primary orbital neuroblastoma: Case report and literature review.Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 7 institutions in 1 country.
Funding
Abstract
N-myc oncogene expression plays a pivotal role in the biology of neuroblastoma, a common childhood tumor. High N-myc expression is associated with advanced disease stage, and in animal models, increased expression results in increased metastatic potential. In normal embryologic development, N-myc expression is associated with neuroblast migration out from the neural crest. To further define the relationship between N-myc and metastasis, an in vitro assay was adapted to measure tumor cell attachment, motility, and proteolytic ability in neuroblastoma cell lines. These parameters were examined in a non-amplified, uniformly N-myc overexpressing cell line and its anti-sense N-myc expressing clones. These lines have been characterized previously, and have a decrease in N-myc expression, growth rate, and tumorigenicity relative to the parent line and vector-only control transfectant. Decrease in N-myc expression resulted in a non-proportional increase of tumor cell attachment, and a proportional decrease in both tumor cell motility and proteolytic ability. In further experiments, assay of a N-myc-amplified overexpressing cell line with an intrinsic heterogeneous pattern of expression demonstrated that motile cells expressed higher amounts of N-myc relative to the general population. Together these relationships indicate that N-myc plays a causative role in the invasive phenotype, and suggest that metastasis may, in part, result from the disruption of a developmentally important normal process.
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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.