Evidence map›Paper›PMID 8987776›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997

Nerve growth factor induces apoptosis in human medulloblastoma cell lines that express TrkA receptors.

Y Muragaki, T T Chou, D R Kaplan, J Q Trojanowski, V M Lee

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
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  8. Review
  9. Dependence receptor TrkC is a putative colon cancer tumor suppressor.Proceedings of the National Academy of Sciences of the United States of America · 2013
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  20. Recent advances in embryonal tumours of the central nervous system.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2005
    Review
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 3 institutions in 2 countries.

Y MuragakiDepartment of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104-4283, USA.
T T Chou
D R Kaplan
J Q Trojanowski
V M Lee
University of Pennsylvania · USNational Cancer Institute · USTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotrophins act through their cognate receptors to promote the differentiation and/or survival of neuronal progenitor cells, immature neurons, and other cells. Here, we examined the effects of nerve growth factor (NGF) and its cognate receptor (Trk or TrkA) on the survival of a common childhood brain tumor, i.e., medulloblastoma, a tumor that resembles CNS neuroepithelial progenitor cells. To do this, we engineered two human medulloblastoma cell lines (i.e., D283MED and DAOY cells) to express human TrkA using a retroviral expression vector. Surprisingly, NGF-treated medulloblastoma cells expressing the TrkA receptor (D283trk and DAOYtrk cells) grown in the presence or absence of serum underwent massive apoptosis, but similar treatment did not induce apoptosis in wild-type uninfected cells, cells expressing an empty vector, or cells expressing the TrkC receptor. Furthermore, D283MED cells engineered to express the human p75 NGF receptor (D283p75) also did not undergo apoptosis. Significantly, NGF-induced apoptosis in D283trk and DAOYtrk cells can be inhibited by anti-NGF antibodies and by K-252a, an inhibitor of TrkA tyrosine phosphorylation and mimicked by high concentrations of NT3. Because NGF treatment primarily eliminated D283trk cells from the S phase of the cell cycle, this form of NGF-mediated apoptosis is cell cycle-dependent. These findings suggest that a NGF/TrkA signal transduction pathway could activate apoptotic cell death programs in CNS neuroepithelial progenitor cells and in childhood brain tumors.

Indexed as

3T3 CellsAnimalsApoptosisBrain NeoplasmsCell CycleHumansMedulloblastomaMiceNerve Growth FactorsNerve Tissue ProteinsPhosphorylationProtein Processing, Post-TranslationalProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Nerve Growth FactorReceptor, trkANerve Growth FactorsNerve Tissue ProteinsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Nerve Growth FactorReceptor, trkARecombinant Fusion Proteins

Identifiers

PMID8987776
PMCPMC6573234
OpenAlexW1953570960

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.