Evidence map›Paper›PMID 24270349›Full record

ReviewCancer journal (Sudbury, Mass.)

An inflammatory mediator, prostaglandin E2, in colorectal cancer.

Dingzhi Wang, Raymond N DuBois

Open access · greenAbstract readReview
In one paragraph

Review in Cancer journal (Sudbury, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 3 pooled it
5.5field-weighted citation impact, top 4% 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

66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Metabolomics and Biomarker Discovery.Advances in experimental medicine and biology · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Investigating the role of the mPGES-PGE₂-EP4 pathway inFrontiers in veterinary science · 2025
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

6 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.

Dingzhi WangFrom the *Center for Inflammation and Cancer, the Biodesign Institute of Arizona State University, and †Department of Chemistry and Biology, Arizona State University, Tempe, AZ.
Raymond N DuBois
Office of the Director · US

Funding

THE ROLE OF ENDOCANNABINOIDS AND THEIR RECEPTORS IN COLORECTAL CANCERP01CA077839 · NCI · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 1999 to 2016
$17.8M
Eicosanoids and Intestinal Epithelial Growth RegulationR37DK047297 · NIDDK · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 2003 to 2012
$3.8M
Role of Eicosanoids in Intestinal BiologyR01DK047297 · NIDDK · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 1994 to 2018
$2.6M
(PQA1)The Molecular Mechanisms Underlying Effects of Aspirin on Colorectal CancerR01CA184820 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DUBOIS, RAYMOND N. · 2014 to 2017
$1.6M
NCI NIH HHS P01 CA077839NCI NIH HHS P01-CA-77839NCI NIH HHS R01 CA184820NIDDK NIH HHS R01 DK047297NIDDK NIH HHS R37 DK047297NIDDK NIH HHS R37-DK47297
6 · The paper itself

Abstract

It is widely accepted that intake of dietary fats and chronic inflammation are risk factors for developing colorectal cancer. Arachidonic acid is a major component of animal fats, and the bioactive lipids produced from this substrate play critical roles in a variety of biologic processes, including cancer. Cyclooxygenase-derived prostaglandin E2 is a known proinflammatory lipid mediator that promotes tumor progression. Metabolism of arachidonic acid by the cyclooxygenase pathway provides one mechanism for the contribution of dietary fats and chronic inflammation to carcinogenesis. In this review, we highlight recent advances in our understanding of how a proinflammatory mediator prostaglandin E2 promotes colorectal cancer immune evasion. These findings may provide a rationale for the development of new therapeutic approaches to subvert tumor-induced immunosuppression.

Indexed as

AnimalsColorectal NeoplasmsDinoprostoneHumansRisk FactorsTumor EscapeTumor MicroenvironmentDinoprostone

Identifiers

PMID24270349
PMCPMC4797645
OpenAlexW2324559253

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.