Evidence map›Paper›PMID 25268132›Full record

ArticlePloS one2014

Aurora kinases as targets in drug-resistant neuroblastoma cells.

Martin Michaelis, Florian Selt, Florian Rothweiler, Nadine Löschmann, Benedikt Nüsse, Wilhelm G Dirks, Richard Zehner, Jindrich Cinatl

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.6field-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

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
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  11. Aurora B Inhibitors as Cancer Therapeutics.Molecules (Basel, Switzerland) · 2023
    Review
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  13. Article
  14. Review
  15. Review
  16. Article
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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

8 authors at 2 institutions in 2 countries.

Martin MichaelisInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany; Centre for Molecular Processing and School of Biosciences, University of Kent, Canterbury, United Kingdom.
Florian SeltInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Florian RothweilerInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Nadine LöschmannInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Benedikt NüsseInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Wilhelm G DirksLeibniz-Institute Deutsche Sammlung für Mikroorganismen und Zellkulturen GmbH, Braunschweig, Germany.
Richard ZehnerInstitut für Rechtsmedizin, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Jindrich CinatlInstitut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
Goethe University Frankfurt · DELeibniz Institute DSMZ – German Collection of Microorganisms and Cell Cultures · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aurora kinase inhibitors displayed activity in pre-clinical neuroblastoma models. Here, we studied the effects of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) and the aurora kinase inhibitor alisertib (MLN8237) that shows some specificity for aurora kinase A over aurora kinase B in a panel of neuroblastoma cell lines with acquired drug resistance. Both compounds displayed anti-neuroblastoma activity in the nanomolar range. The anti-neuroblastoma mechanism included inhibition of aurora kinase signalling as indicated by decreased phosphorylation of the aurora kinase substrate histone H3, cell cycle inhibition in G2/M phase, and induction of apoptosis. The activity of alisertib but not of tozasertib was affected by ABCB1 expression. Aurora kinase inhibitors induced a p53 response and their activity was enhanced in combination with the MDM2 inhibitor and p53 activator nutlin-3 in p53 wild-type cells. In conclusion, aurora kinases are potential drug targets in therapy-refractory neuroblastoma, in particular for the vast majority of p53 wild-type cases.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BAurora Kinase AAurora Kinase BAzepinesBrain NeoplasmsCell Cycle CheckpointsCell ProliferationCyclopropanesDrug Resistance, NeoplasmDrug SynergismHistonesHumansImidazolesABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BAURKA protein, humanAURKB protein, humanAurora Kinase AAurora Kinase BAzepinesCyclopropanesHistonesImidazolesMDM2 protein, humanMLN 8237nutlin 3PiperazinesProtein Kinase InhibitorsProto-Oncogene Proteins c-mdm2PyrazolesPyrimidinestozasertibTumor Suppressor Protein p53

Identifiers

PMID25268132
PMCPMC4182628
OpenAlexW2027057177

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.