Evidence map›Paper›PMID 28736522›Full record

ArticleFrontiers in pharmacology2017

Gliotoxin Targets Nuclear NOTCH2 in Human Solid Tumor Derived Cell Lines

Rainer Hubmann, Wolfgang Sieghart, Susanne Schnabl, Mohammad Araghi, Martin Hilgarth, Marlies Reiter, Dita Demirtas, Peter Valent, Christoph Zielinski, Ulrich Jäger and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. The Intricate Notch Signaling Dynamics in Therapeutic Realms of Cancer.ACS pharmacology & translational science · 2023
    Review
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  7. Article
  8. Article
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  10. Article
  11. Long Noncoding RNA (lncRNA) MIR22HG Suppresses Gastric Cancer Progression through Attenuating NOTCH2 Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Review
  13. Review
  14. Article
  15. Article
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

11 authors at 3 institutions in 1 country.

Rainer HubmannDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Wolfgang SieghartDepartment of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of ViennaVienna, Austria.
Susanne SchnablDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Mohammad AraghiDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Martin HilgarthDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Marlies ReiterDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Dita DemirtasDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Peter ValentDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Christoph ZielinskiDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Ulrich JägerDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Medhat ShehataDepartment of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of ViennaVienna, Austria.
Medical University of Vienna · ATComprehensive Cancer Center Vienna · ATLudwig Boltzmann Cluster for Cardiovascular Research · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of NOTCH2 signaling is implicated in a wide variety of human neoplasias. The current concept of targeting NOTCH is based on using gamma secretase inhibitors (GSI) to regulate the release of the active NOTCH intracellular domain. However, the clinical outcome of GSI remains unsatisfactory. Therefore we analyzed human solid tumor derived cell lines for their nuclear NOTCH activity and evaluated the therapeutic potential of the NOTCH2 transactivation inhibitor gliotoxin in comparison to the representative GSI DAPT. Electrophoretic mobility shift assays (EMSA) were used as a surrogate method for the detection of NOTCH/CSL transcription factor complexes. The effect of gliotoxin on cell viability and its clinical relevance was evaluated

Indexed as

gliotoxinhepatocellular carcinomamelanomaNOTCH2pancreas carcinomaγ-secretase inhibitors

Identifiers

PMID28736522
PMCPMC5500618
OpenAlexW2730103785

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.