Evidence map›Paper›PMID 25342631›Full record

ReviewNature reviews. Cancer2014

Revisiting STAT3 signalling in cancer: new and unexpected biological functions.

Hua Yu, Heehyoung Lee, Andreas Herrmann, Ralf Buettner, Richard Jove

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,276 papers.

0numbers the graph read from it
0cells of the map it votes in
1,276citing papers in PubMed
67.7field-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

1,276 citing papers in PubMed, 2,100 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. 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
    Review
  10. Article
  11. Article
  12. STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

1,216 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

5 authors at 1 institution in 1 country.

Hua YuDepartment of Cancer Immunotherapeutics and Tumor Immunology, Beckman Research Institute, City of Hope Comprehensive Cancer Center, Duarte, California 91010, USA.
Heehyoung LeeDepartment of Cancer Immunotherapeutics and Tumor Immunology, Beckman Research Institute, City of Hope Comprehensive Cancer Center, Duarte, California 91010, USA.
Andreas HerrmannDepartment of Cancer Immunotherapeutics and Tumor Immunology, Beckman Research Institute, City of Hope Comprehensive Cancer Center, Duarte, California 91010, USA.
Ralf BuettnerDepartment of Molecular Medicine, Beckman Research Institute, City of Hope Comprehensive Cancer Center, Duarte, California 91010, USA.
Richard JoveVaccine and Gene Therapy Institute of Florida, Port St. Lucie, Florida 34987, USA.
Vaccine & Gene Therapy Institute of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Janus kinases (JAKs) and signal transducer and activator of transcription (STAT) proteins, particularly STAT3, are among the most promising new targets for cancer therapy. In addition to interleukin-6 (IL-6) and its family members, multiple pathways, including G-protein-coupled receptors (GPCRs), Toll-like receptors (TLRs) and microRNAs were recently identified to regulate JAK-STAT signalling in cancer. Well known for its role in tumour cell proliferation, survival, invasion and immunosuppression, JAK-STAT3 signalling also promotes cancer through inflammation, obesity, stem cells and the pre-metastatic niche. In addition to its established role as a transcription factor in cancer, STAT3 regulates mitochondrion functions, as well as gene expression through epigenetic mechanisms. Newly identified regulators and functions of JAK-STAT3 in tumours are important targets for potential therapeutic strategies in the treatment of cancer.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsEpigenesis, GeneticGene Expression Regulation, NeoplasticHumansNeoplasmsSTAT3 Transcription FactorAntineoplastic AgentsSTAT3 Transcription Factor

Identifiers

PMID25342631
OpenAlexW2028544780

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.