Evidence map›Paper›PMID 27542273›Full record

ArticleOncotarget2016

Sorafenib inhibits cell growth but fails to enhance radio- and chemosensitivity of glioblastoma cell lines.

Matthias Riedel, Nina Struve, Justus Müller-Goebel, Sabrina Köcher, Cordula Petersen, Ekkehard Dikomey, Kai Rothkamm, Malte Kriegs

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
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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 3 institutions in 1 country.

Matthias RiedelLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Nina StruveLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Justus Müller-GoebelLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Sabrina KöcherLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Cordula PetersenLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Ekkehard DikomeyLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Kai RothkammLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Malte KriegsLaboratory of Radiobiology & Experimental Radiooncology, University Medical Center Hamburg - Eppendorf, Hubertus Wald Tumorzentrum - University Cancer Center Hamburg, 20246 Hamburg, Germany.
Universität Hamburg · DEUniversity Cancer Center Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlioblastomas (GBM) are the most common malignant type of primary brain tumor. GBM are intensively treated with surgery and combined radiochemotherapy using X-irradiation and temozolomide (TMZ) but they are still associated with an extremely poor prognosis, urging for the development of new treatment strategies. To improve the outcome of GBM patients, the small molecule multi-kinase inhibitor sorafenib has moved into focus of recent research. Sorafenib has already been shown to enhance the radio- and radiochemosensitivity of other tumor entities. Whether sorafenib is also able to sensitize GBM cells to radio- and chemotherapy is still an unsolved question which we have addressed in this study.

methodsThe effect of sorafenib on signaling, proliferation, radiosensitivity, chemosensitivity and radiochemosensitivity was analyzed in six glioblastoma cell lines using Western blot, proliferation- and colony formation assays.

resultsIn half of the cell lines sorafenib clearly inhibited MAPK signaling. We also observed a strong blockage of proliferation, which was, however, not associated with MAPK pathway inhibition. Sorafenib had only minor effects on cell survival when administered alone. Most importantly, sorafenib treatment failed to enhance GBM cell killing by irradiation, TMZ or combined treatment, and instead rather caused resistance in some cell lines.

conclusionOur data suggest that sorafenib treatment may not improve the efficacy of radiochemotherapy in GBM.

Indexed as

Antineoplastic AgentsApoptosisBrain NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDose-Response Relationship, RadiationDrug Resistance, NeoplasmGlioblastomaHumansMAP Kinase Signaling SystemNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsRadiation ToleranceSignal TransductionAntineoplastic AgentsNiacinamidePhenylurea CompoundsProtein Kinase InhibitorsSorafenibglioblastomaradiochemosensitivitysorafenibtemozolomideX-irradiation

Identifiers

PMID27542273
PMCPMC5308705
OpenAlexW2515231642

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.