Evidence map›Paper›PMID 18505913›Full record

ReviewMolecular cancer research : MCR2008

Signal transducer and activator of transcription-3: a molecular hub for signaling pathways in gliomas.

Emily C Brantley, Etty N Benveniste

Open access · greenAbstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 237 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Association of immunoglobulin E levels with glioma risk and survival.Journal of the National Cancer Institute · 2025
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Association of immunoglobulin E levels with glioma risk and survival.medRxiv : the preprint server for health sciences · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Potential Therapeutic Effects of Thiazolidinedione on Malignant Glioma.International journal of molecular sciences · 2022
    Article
  17. Review
  18. Article
  19. Review
  20. Article

65 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Emily C BrantleyDepartment of Cell Biology, 1918 University Boulevard, MCLM 395A, University of Alabama at Birmingham, Birmingham, AL 35294-0005, USA.
Etty N Benveniste
University of Alabama at Birmingham · US

Funding

Viral and molecular chemotherapy of malignant CNS tumorsP50CA097247 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GILLESPIE, G. YANCEY · 2002 to 2009
$13.5M
TRADD as a Regulator of Cytokine Signaling in GliaR01NS050665 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2005 to 2009
$1.6M
The Role of ING4 in Modulating the Tumorigenic Contribution of NF-kB in GliomasR21NS054158 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N. · 2006 to 2007
$354k
NCI NIH HHS P50 CA097247NCI NIH HHS P50 CA-97247NINDS NIH HHS R01 NS050665NINDS NIH HHS R01 NS-54158NINDS NIH HHS R21 NS054158
6 · The paper itself

Abstract

Glioblastoma is the most common and severe primary brain tumor in adults. Its aggressive and infiltrative nature renders the current therapeutics of surgical resection, radiation, and chemotherapy relatively ineffective. Accordingly, recent research has focused on the elucidation of various signal transduction pathways in glioblastoma, particularly aberrant activation. This review focuses on the signal transducer and activator of transcription-3 (STAT-3) signal transduction pathway in the context of this devastating tumor. STAT-3 is aberrantly activated in human glioblastoma tissues, and this activation is implicated in controlling critical cellular events thought to be involved in gliomagenesis, such as cell cycle progression, apoptosis, angiogenesis, and immune evasion. There are no reports of gain-of-function mutations in glioblastoma; rather, the activation of STAT-3 is thought to be a consequence of either dysregulation of upstream kinases or loss of endogenous inhibitors. This review provides detailed insight into the multiple mechanisms of STAT-3 activation in glioblastoma, as well as describing endogenous and chemical inhibitors of this pathway and their clinical significance. In glioblastoma, STAT-3 acts a molecular hub to link extracellular signals to transcriptional control of proliferation, cell cycle progression, and immune evasion. Because STAT-3 plays this central role in glioblastoma signal transduction, it has significant potential as a therapeutic target.

Indexed as

Gene Expression Regulation, NeoplasticBrain NeoplasmsCell CycleCell ProliferationCytokinesErbB ReceptorsGliomaHumansImmune SystemInterleukin-6Models, BiologicalSignal TransductionSTAT3 Transcription FactorTranscriptional ActivationCytokinesErbB ReceptorsInterleukin-6STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID18505913
PMCPMC3886801
OpenAlexW2164189319

What OpenQuestion holds

Textmetadata
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.