Evidence map›Paper›PMID 19723038›Full record

ReviewAnnals of the New York Academy of Sciences2009

Signal transducer and activator of transcription-3, inflammation, and cancer: how intimate is the relationship?.

Bharat B Aggarwal, Ajaikumar B Kunnumakkara, Kuzhuvelil B Harikumar, Shan R Gupta, Sheeja T Tharakan, Cemile Koca, Sanjit Dey, Bokyung Sung

Open access · bronzeAbstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 329 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
329citing papers in PubMed, 1 pooled it
19.5field-weighted citation impact, top 1% 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

329 citing papers in PubMed, 1 synthesis or guideline pooled it, 644 citations in OpenAlex.

  1. Pooled it
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  17. Hydrogen sulfide and its role in female reproduction.Frontiers in veterinary science · 2024
    Review
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269 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

8 authors at 1 institution in 1 country.

Bharat B AggarwalDepartment of Experimental Therapeutics, Cytokine Research Laboratory, University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA. aggarwal@mdanderson.org
Ajaikumar B Kunnumakkara
Kuzhuvelil B Harikumar
Shan R Gupta
Sheeja T Tharakan
Cemile Koca
Sanjit Dey
Bokyung Sung
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DIANE BODURKA · 1985 to 2026
$290.8M
TARGETING NF-KB ACTIVATION IN REGULATION OF SYMPTOMS IN PATIENTS WITH MULTIPLEP01CA124787 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI REUBEN, JAMES MARTIN · 2008 to 2012
$10.6M
NCI NIH HHS CA-124787-01A2NCI NIH HHS CA-16 672NCI NIH HHS P01 CA124787
6 · The paper itself

Abstract

Signal transducer and activator of transcription-3 (STAT-3) is one of six members of a family of transcription factors. It was discovered almost 15 years ago as an acute-phase response factor. This factor has now been associated with inflammation, cellular transformation, survival, proliferation, invasion, angiogenesis, and metastasis of cancer. Various types of carcinogens, radiation, viruses, growth factors, oncogenes, and inflammatory cytokines have been found to activate STAT-3. STAT-3 is constitutively active in most tumor cells but not in normal cells. Phosphorylation of STAT-3 at tyrosine 705 leads to its dimerization, nuclear translocation, DNA binding, and gene transcription. The phosphorylation of STAT-3 at serine 727 may regulate its activity negatively or positively. STAT-3 regulates the expression of genes that mediate survival (survivin, bcl-xl, mcl-1, cellular FLICE-like inhibitory protein), proliferation (c-fos, c-myc, cyclin D1), invasion (matrix metalloproteinase-2), and angiogenesis (vascular endothelial growth factor). STAT-3 activation has also been associated with both chemoresistance and radioresistance. STAT-3 mediates these effects through its collaboration with various other transcription factors, including nuclear factor-kappaB, hypoxia-inducible factor-1, and peroxisome proliferator activated receptor-gamma. Because of its critical role in tumorigenesis, inhibitors of this factor's activation are being sought for both prevention and therapy of cancer. This has led to identification of small peptides, oligonucleotides, and small molecules as potential STAT-3 inhibitors. Several of these small molecules are chemopreventive agents derived from plants. This review discusses the intimate relationship between STAT-3, inflammation, and cancer in more detail.

Indexed as

AnimalsAntineoplastic AgentsCell ProliferationHumansInflammationModels, BiologicalNeoplasmsPhosphorylationSignal TransductionSTAT3 Transcription FactorAntineoplastic AgentsSTAT3 Transcription Factor

Identifiers

PMID19723038
PMCPMC3141289
OpenAlexW2003681585

What OpenQuestion holds

Textmetadata
LicenceTDM
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.