Evidence map›Paper›PMID 26517812›Full record

ArticleOncotarget2015

A combination of tyrosine kinase inhibitors, crizotinib and dasatinib for the treatment of glioblastoma multiforme.

Hayley Nehoff, Neha N Parayath, Melanie J McConnell, Sebastien Taurin, Khaled Greish

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  12. Discovery and Therapeutic Exploitation of Mechanisms of Resistance to MET Inhibitors in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. MicroRNA-137 inhibits growth of glioblastoma through EGFR suppression.American journal of translational research · 2017
    Article
  19. Article
  20. Investigational new drugs for brain cancer.Expert opinion on investigational drugs · 2016
    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 2 institutions in 1 country.

Hayley NehoffDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
Neha N ParayathDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
Melanie J McConnellSchool of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand.
Sebastien TaurinDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
Khaled GreishDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
University of Otago · NZVictoria University of Wellington · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor. Despite the advances in surgery, radiotherapy and chemotherapy, patient survival averages only 14.6 months. In most GBM tumors, tyrosine kinases show increased activity and/or expression and actively contribute to the development, recurrence and onset of treatment resistance; making their inhibition an appealing therapeutic strategy. We compared the cytotoxicity of 12 tyrosine kinase inhibitors in vitro. A combination of crizotinib and dasatinib emerged as the most cytotoxic across established and primary human GBM cell lines. The combination treatment induced apoptotic cell death and polyploidy. Furthermore, the combination treatment led to the altered expression and localization of several tyrosine kinase receptors such as Met and EGFR and downstream effectors as such as SRC. Furthermore, the combination treatment reduced the migration and invasion of GBM cells and prevented endothelial cell tube formation in vitro. Overall, our study demonstrated the broad specificity of a combination of crizotinib and dasatinib across multiple GBM cell lines. These findings provide insight into the development of alternative therapy for the treatment of GBM.

Indexed as

ApoptosisBlotting, WesternCell CycleCell MovementCell ProliferationCrizotinibDasatinibDrug Therapy, CombinationFluorescent Antibody Technique, IndirectGlioblastomaHumansProtein-Tyrosine KinasesPyrazolesPyridinesReceptor Protein-Tyrosine KinasesSignal TransductionCrizotinibDasatinibProtein-Tyrosine KinasesPyrazolesPyridinesReceptor Protein-Tyrosine Kinasesglioblastoma multiformeinvasionMetSRCtyrosine kinase inhibitors

Identifiers

PMID26517812
PMCPMC4741976
OpenAlexW2258461888

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.