Evidence map›Paper›PMID 30578415›Full record

ReviewNature reviews. Cancer2019

Therapeutically exploiting STAT3 activity in cancer - using tissue repair as a road map.

Jennifer Huynh, Ashwini Chand, Daniel Gough, Matthias Ernst

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
304citing papers in PubMed, 3 pooled it
19.8field-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

304 citing papers in PubMed, 3 syntheses or guidelines pooled it, 511 citations in OpenAlex.

  1. Pooled it
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  6. Targeting the JAK/STAT signalling axis in cancer: chemopreventive potential of natural compounds with emerging focus on retinoids.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  20. Coronary artery disease and cancer: Shared risk factors, pathogenesis, and treatment effects.American heart journal plus : cardiology research and practice · 2026
    Review

244 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

4 authors at 2 institutions in 1 country.

Jennifer HuynhOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, Victoria, Australia.ORCID http://orcid.org/0000-0002-2638-8352
Ashwini ChandOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, Victoria, Australia.ORCID http://orcid.org/0000-0002-1245-729X
Daniel GoughCentre for Cancer Research, Hudson Institute of Medical Research, Clayton, Victoria, Australia. Daniel.Gough@monash.edu.ORCID http://orcid.org/0000-0001-6479-1735
Matthias ErnstOlivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, Victoria, Australia. Matthias.Ernst@onjcri.org.au.ORCID http://orcid.org/0000-0002-6399-1177
La Trobe University · AUHudson Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tightly orchestrated temporal and spatial control of signal transducer and activator of transcription 3 (STAT3) activity in epithelial, immune and stromal cells is critical for wound healing and tissue repair. Excessive STAT3 activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that collectively promotes tumour progression. In addition to the canonical transcriptional pathways by which STAT3 promotes stem cell-like characteristics, survival, proliferation, metastatic potential and immune evasion, cytoplasmic STAT3 activity fuels tumour growth by metabolic and other non-transcriptional mechanisms. Here, we review the tumour-modulating activities of STAT3 in light of its role as a signalling node integrating inflammatory responses during wound healing. Accordingly, many of the cytokines that contribute to the para-inflammatory state of most solid malignancies converge on and underpin dysregulated STAT3 activity. Targeting of these cytokines, their cognate receptors and associated signalling cascades in clinical trials is beginning to demonstrate therapeutic efficacy, given that interference with STAT3 activity is likely to simultaneously curb the growth of cancer cells and augment antitumour immunity.

Indexed as

AnimalsCell Transformation, NeoplasticCytokinesHumansInflammationNeoplasmsSignal TransductionSTAT3 Transcription FactorTumor MicroenvironmentCytokinesSTAT3 Transcription Factor

Identifiers

PMID30578415
OpenAlexW2906052725

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.