Evidence map›Paper›PMID 20733953›Full record

ArticleAmerican journal of translational research2010

Epoxyeicosatrienoic acids and soluble epoxide hydrolase: potential therapeutic targets for inflammation and its induced carcinogenesis.

Stephanie Norwood, Jie Liao, Bruce D Hammock, Guang-Yu Yang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Article
  3. Cell type-specific master metabolic regulators of Alzheimer's disease.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Review
  6. Green Tea Attenuates the Particulate Matter (PM)Journal of microbiology and biotechnology · 2024
    Article
  7. Article
  8. Eicosanoid profiles in an arthritis model: Effects of a soluble epoxide hydrolase inhibitor.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024
    Article
  9. Enhancing cancer immunotherapy via inhibition of soluble epoxide hydrolase.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021
    Review
  20. Article
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.

Stephanie Norwood
Jie Liao
Bruce D Hammock
Guang-Yu Yang
Northwestern University · USUniversity of California, Davis · US

Funding

Soluble epoxide hydrolase as a novel target of colitis-induced carcinogenesisR01CA137467 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YANG, GUANG-YU · 2009 to 2012
$1.2M
NCI NIH HHS R01 CA137467
6 · The paper itself

Abstract

Chronic inflammation is an important factor contributing to human carcinoma, and non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to have a preventive effect in the development of various types of carcinoma. However, NSAIDs also have adverse side effects including increased cardiovascular events, making them less than ideal for routine chemoprevention. Soluble epoxide hydrolase (sEH) is an enzyme that converts endogenous anti-inflammatory compounds, the epoxyeicosatrienoic acids (EETs), to the less anti-inflammatory dihydroxyeicosatrienoic acids (DHETs). Inhibition of sEH, by a highly selective and potent sEH inhibitor (sEHI), increases EETs leading to decreased inflammation. In our studies, administration of a sEHI in mouse colitis models led to decreased ulcer incidence and number of ulcers compared to controls, with no adverse side effects seen. In human tissue, sEH showed an increase in expression, as seen immunohistochemically, in ulcerative colitis (UC), UC-induced dysplasia, and UC-induced carcinoma. Thus, inhibition of sEH may be a novel biomarker and potential therapeutic target in inflammation and inflammation-induced carcinoma.

Indexed as

cancercarcinogenesisdihydroxyeicosatrienoic acids (DHETs)Epoxyeicosatrienoic acids (EETs)inflammationnon-steroidal anti-inflammatory drugs (NSAIDs)soluble epoxide hydrolase (sEH)therapy

Identifiers

PMID20733953
PMCPMC2923867
OpenAlexW1480185315

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.