Evidence map›Paper›PMID 27707976›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2016

Proliferation and Survival of Embryonic Sympathetic Neuroblasts by MYCN and Activated ALK Signaling.

Marco Kramer, Diogo Ribeiro, Marie Arsenian-Henriksson, Thomas Deller, Hermann Rohrer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 49 citations in OpenAlex.

  1. Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026
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  10. Inflammatory response to the ischaemia-reperfusion insult in the liver after major tissue trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Marco KramerMax-Planck-Institute for Brain Research, Developmental Neurobiology, 60438 Frankfurt/Main, Germany, Institute of Clinical Neuroanatomy, Goethe University Frankfurt/Main, 60590 Frankfurt/Main, Germany, Ernst-Strüngmann-Institute, 60528 Frankfurt/Main, Germany, and.
Diogo RibeiroDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden.ORCID 0000-0003-4400-8752
Marie Arsenian-HenrikssonDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden.
Thomas DellerInstitute of Clinical Neuroanatomy, Goethe University Frankfurt/Main, 60590 Frankfurt/Main, Germany.
Hermann RohrerMax-Planck-Institute for Brain Research, Developmental Neurobiology, 60438 Frankfurt/Main, Germany, Institute of Clinical Neuroanatomy, Goethe University Frankfurt/Main, 60590 Frankfurt/Main, Germany, Ernst-Strüngmann-Institute, 60528 Frankfurt/Main, Germany, and hermann.rohrer@brain.mpg.de rohrer@med.uni-frankfurt.de.
Goethe University Frankfurt · DEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroblastoma (NB) is a childhood tumor that arises from the sympathoadrenal lineage. MYCN amplification is the most reliable marker for poor prognosis and MYCN overexpression in embryonic mouse sympathetic ganglia results in NB-like tumors. MYCN cooperates with mutational activation of anaplastic lymphoma kinase (ALK), which promotes progression to NB, but the role of MYCN and ALK in tumorigenesis is still poorly understood. Here, we use chick sympathetic neuroblasts to examine the normal function of MYCN and MYC in the control of neuroblast proliferation, as well as effects of overexpression of MYCN, MYC, and activated ALK, alone and in combination. We demonstrate that MYC is more strongly expressed than MYCN during neurogenesis and is important for in vitro neuroblast proliferation. MYC and MYCN overexpression elicits increased proliferation but does not sustain neuroblast survival. Unexpectedly, long-term expression of activated ALK SIGNIFICANCE STATEMENT: MYCN overexpression combined with activated anaplastic lymphoma kinase (ALK) is sufficient to induce neuroblastoma (NB) in mouse sympathoadrenal cells. To address cellular and molecular effects elicited by MYCN/ALK cooperation, we used cultures of chick sympathetic neuroblasts. We demonstrate that MYCN increases proliferation but not survival, whereas long-term expression of ALK

Indexed as

Neural Stem CellsAnaplastic Lymphoma KinaseAnimalsApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalChick EmbryoGene Expression Regulation, NeoplasticHumansMiceNeuroblastomaNeuronsN-Myc Proto-Oncogene ProteinProto-Oncogene Proteins c-mycALK protein, humanAlk protein, mouseAnaplastic Lymphoma KinaseMYCN protein, humanMYC protein, humanN-Myc Proto-Oncogene ProteinProto-Oncogene Proteins c-mycReceptor Protein-Tyrosine KinasesALKMYCNneuroblastneuroblastomaneurogenesissympathetic

Identifiers

PMID27707976
PMCPMC6705582
OpenAlexW2528358119

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.