Evidence map›Paper›PMID 27732951›Full record

ArticleOncotarget2016

IKK/NF-κB signaling contributes to glioblastoma stem cell maintenance.

Amanda L Rinkenbaugh, Patricia C Cogswell, Barbara Calamini, Denise E Dunn, Anders I Persson, William A Weiss, Donald C Lo, Albert S Baldwin

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 47 citations in OpenAlex.

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  6. Translational cancer research · 2025
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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 6 institutions in 1 country.

Amanda L RinkenbaughDepartment of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA.
Patricia C CogswellLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
Barbara CalaminiCenter for Drug Discovery and Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
Denise E DunnCenter for Drug Discovery and Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
Anders I PerssonHelen Diller Family Comprehensive Cancer Center and Department of Neurology, University of California, San Francisco, CA, USA.
William A WeissHelen Diller Family Comprehensive Cancer Center and Department of Neurology, University of California, San Francisco, CA, USA.
Donald C LoCenter for Drug Discovery and Department of Neurobiology, Duke University Medical Center, Durham, NC, USA.
Albert S BaldwinLineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.
Duke Medical Center · USUniversity of California, San Francisco · USChordoma Foundation · USDuke University Hospital · USUNC Lineberger Comprehensive Cancer CenterUniversity of North Carolina at Chapel Hill · US

Funding

IKK/NF-kappaB Signaling in Cancer: Therapy, Resistance, and Tumor Initiating CellsR35CA197684 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BALDWIN, ALBERT SIDNEY · 2016 to 2022
$5.8M
NCI NIH HHS R35 CA197684
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) carries a poor prognosis and continues to lack effective treatments. Glioblastoma stem cells (GSCs) drive tumor formation, invasion, and drug resistance and, as such, are the focus of studies to identify new therapies for disease control. Here, we identify the involvement of IKK and NF-κB signaling in the maintenance of GSCs. Inhibition of this pathway impairs self-renewal as analyzed in tumorsphere formation and GBM expansion as analyzed in brain slice culture. Interestingly, both the canonical and non-canonical branches of the NF-κB pathway are shown to contribute to this phenotype. One source of NF-κB activation in GBM involves the TGF-β/TAK1 signaling axis. Together, our results demonstrate a role for the NF-κB pathway in GSCs and provide a mechanistic basis for its potential as a therapeutic target in glioblastoma.

Indexed as

Cell Self RenewalSignal TransductionAnimalsBrain NeoplasmsCell Line, TumorGlioblastomaHumansI-kappa B KinaseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNeoplastic Stem CellsNF-kappa BRatsRNA InterferenceSpheroids, CellularTissue Culture TechniquesI-kappa B KinaseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BTransforming Growth Factor betacancer stem cellsglioblastomaNF-κBtumor-initiating cells

Identifiers

PMID27732951
PMCPMC5342468
OpenAlexW2529071390

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.