Evidence map›Paper›PMID 25290089›Full record

ReviewBritish journal of cancer2015

IRAK signalling in cancer.

G W Rhyasen, D T Starczynowski

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 7% 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

95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. The Direction of Modern Therapies in Waldenström Macroglobulinaemia.Journal of cellular and molecular medicine · 2025
    Review
  12. Review
  13. Review
  14. Smoking-Associated Carcinogen-Induced Inflammation Promotes Lung Carcinogenesis via IRAK4 Activation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

35 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.

G W Rhyasen1] Department of Cancer Biology, University of Cincinnati, Cincinnati, OH 45267, USA [2] Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
D T Starczynowski1] Department of Cancer Biology, University of Cincinnati, Cincinnati, OH 45267, USA [2] Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
University of Cincinnati · US

Funding

Identification and characterization of genes in del(5q) myelodysplastic syndromeR01HL111103 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2012 to 2016
$1.9M
Molecular Pathogenesis of MDSR01DK102759 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI STARCZYNOWSKI, DANIEL · 2014 to 2016
$701k
NHLBI NIH HHS R01 HL111103NHLBI NIH HHS R01HL111103NIDDK NIH HHS R01 DK102759
6 · The paper itself

Abstract

Innate immune signalling has an essential role in inflammation, and the dysregulation of signalling components of this pathway is increasingly being recognised as an important mediator in cancer initiation and progression. In some malignancies, dysregulation of inflammatory toll-like receptor (TLR) and interleukin-1 receptor (IL1R) signalling is typified by increased NF-κB activity, and it occurs through somatic mutations, chromosomal deletions, and/or transcriptional deregulation. Interleukin-1 receptor-associated kinase (IRAK) family members are mediators of TLR/IL1R superfamily signalling, and mounting evidence implicates these kinases as viable cancer targets. Although there have been previous efforts aimed at the development of IRAK kinase inhibitors, this is currently an area of renewed interest for cancer drug development.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsDrug Screening Assays, AntitumorGene Expression Regulation, NeoplasticHumansImmunity, InnateInterleukin-1 Receptor-Associated KinasesMolecular Targeted TherapyNeoplasmsAntineoplastic AgentsInterleukin-1 Receptor-Associated Kinases

Identifiers

PMID25290089
PMCPMC4453441
OpenAlexW2013995112

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.