Evidence map›Paper›PMID 25458015›Full record

ArticleCancer science2015

Sunitinib impedes brain tumor progression and reduces tumor-induced neurodegeneration in the microenvironment.

Gökçe Hatipoglu, Stefan W Hock, Ruth Weiss, Zheng Fan, Tina Sehm, Ali Ghoochani, Michael Buchfelder, Nicolai E Savaskan, Ilker Y Eyüpoglu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Guanabenz Sensitizes Glioblastoma Cells to Sunitinib by Inhibiting GADD34-Mediated Autophagic Signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
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  10. Review
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  14. Tumor Microenvironment in Treatment of Glioma.Open medicine (Warsaw, Poland) · 2017
    Article
  15. Article
  16. Review
  17. Article
  18. 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

9 authors at 2 institutions in 1 country.

Gökçe HatipogluDepartment of Neurosurgery, Universitätsklinikum Erlangen, Friedrich Alexander University Erlangen-Nürnberg (FAU), Erlangen, Germany.
Stefan W Hock
Ruth Weiss
Zheng Fan
Tina Sehm
Ali Ghoochani
Michael Buchfelder
Nicolai E Savaskan
Ilker Y Eyüpoglu
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Erlangen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant gliomas can be counted to the most devastating tumors in humans. Novel therapies do not achieve significant prolonged survival rates. The cancer cells have an impact on the surrounding vital tissue and form tumor zones, which make up the tumor microenvironment. We investigated the effects of sunitinib, a small molecule multitargeted receptor tyrosine kinase inhibitor, on constituents of the tumor microenvironment such as gliomas, astrocytes, endothelial cells, and neurons. Sunitinib has a known anti-angiogenic effect. We found that sunitinib normalizes the aberrant tumor-derived vasculature and reduces tumor vessel pathologies (i.e. auto-loops). Sunitinib has only minor effects on the normal, physiological, non-proliferating vasculature. We found that neurons and astrocytes are protected by sunitinib against glutamate-induced cell death, whereas sunitinib acts as a toxin towards proliferating endothelial cells and tumor vessels. Moreover, sunitinib is effective in inducing glioma cell death. We determined the underlying pathways by which sunitinib operates as a toxin on gliomas and found vascular endothelial growth factor receptor 2 (VEGFR2, KDR/Flk1) as the main target to execute gliomatoxicity. The apoptosis-inducing effect of sunitinib can be mimicked by inhibition of VEGFR2. Knockdown of VEGFR2 can, in part, foster the resistance of glioma cells to receptor tyrosine kinase inhibitors. Furthermore, sunitinib alleviates tumor-induced neurodegeneration. Hence, we tested whether temozolomide treatment could be potentiated by sunitinib application. Here we show that sunitinib can amplify the effects of temozolomide in glioma cells. Thus, our data indicate that combined treatment with temozolomide does not abrogate the effects of sunitinib. In conclusion, we found that sunitinib acts as a gliomatoxic agent and at the same time carries out neuroprotective effects, reducing tumor-induced neurodegeneration. Thus, this report uncovered sunitinib's actions on the brain tumor microenvironment, revealing novel aspects for adjuvant approaches and new clinical assessment criteria when applied to brain tumor patients.

Indexed as

Angiogenesis InhibitorsAnimalsAntineoplastic AgentsApoptosisAstrocytesBrain NeoplasmsCell DeathCell Line, TumorCell ProliferationDisease ProgressionEndothelial CellsGliomaHumansIndolesMiceNeovascularization, PathologicAngiogenesis InhibitorsAntineoplastic AgentsIndolesNeuroprotective AgentsPyrrolesSunitinibVascular Endothelial Growth Factor Receptor-2Angiogenesis modulatorscell deathcytoprotectiongliomatyrosine kinase-type cell surface receptor

Identifiers

PMID25458015
PMCPMC4399021
OpenAlexW2020605686

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LicenceCC BY-NC
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Registered trials

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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.