Evidence map›Paper›PMID 24311630›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2014

NSAIDs inhibit tumorigenesis, but how?

Evrim Gurpinar, William E Grizzle, Gary A Piazza

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed, 1 pooled it
10.7field-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

110 citing papers in PubMed, 1 synthesis or guideline pooled it, 211 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. High-throughput screening identifies ibuprofen as an sEV PD-L1 inhibitor for synergistic cancer immunotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  12. The Past and Future of Inflammation as a Target to Cancer Prevention.Cancer prevention research (Philadelphia, Pa.) · 2024
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Cyclooxygenase and Cancer: Fundamental Molecular Investigations.International journal of molecular sciences · 2023
    Article
  18. Article
  19. Article
  20. Review

50 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

3 authors at 2 institutions in 1 country.

Evrim GurpinarAuthors' Affiliations: Department of Pharmacology and Toxicology; Department of Pathology, The University of Alabama at Birmingham, Birmingham; and Drug Discovery Research Center, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
William E Grizzle
Gary A Piazza
University of Alabama at Birmingham · USUniversity of South Alabama · US

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
Selective anti-cancer activity of sulindac derivatives on KRAS mutant colon tumor cells by inducing ROSR01CA131378 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2008 to 2019
$5.2M
Development of a novel sulindac amide for colorectal cancer chemopreventionR01CA148817 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2010 to 2015
$2.4M
Phosphodiesterase 5: A Novel Target and Inhibitor for Breast Cancer ChemopreventionR01CA155638 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI PIAZZA, GARY A · 2012 to 2017
$2.3M
NCI NIH HHS 1R01CA131378NCI NIH HHS 1R01CA148817-01A1NCI NIH HHS 1R01CA155638-01ANCI NIH HHS R01 CA131378NCI NIH HHS R01 CA148817NCI NIH HHS R01 CA155638NIAMS NIH HHS P30 AR048311
6 · The paper itself

Abstract

Numerous epidemiologic studies have reported that the long-term use of nonsteroidal anti-inflammatory drugs (NSAID) is associated with a significant decrease in cancer incidence and delayed progression of malignant disease. The use of NSAIDs has also been linked with reduced risk from cancer-related mortality and distant metastasis. Certain prescription-strength NSAIDs, such as sulindac, have been shown to cause regression of precancerous lesions. Unfortunately, the extended use of NSAIDs for chemoprevention results in potentially fatal side effects related to their COX-inhibitory activity and suppression of prostaglandin synthesis. Although the basis for the tumor growth-inhibitory activity of NSAIDs likely involves multiple effects on tumor cells and their microenvironment, numerous investigators have concluded that the underlying mechanism is not completely explained by COX inhibition. It may therefore be possible to develop safer and more efficacious drugs by targeting such COX-independent mechanisms. NSAID derivatives or metabolites that lack COX-inhibitory activity, but retain or have improved anticancer activity, support this possibility. Experimental studies suggest that apoptosis induction and suppression of β-catenin-dependent transcription are important aspects of their antineoplastic activity. Studies show that the latter involves phosphodiesterase inhibition and the elevation of intracellular cyclic GMP levels. Here, we review the evidence for COX-independent mechanisms and discuss progress toward identifying alternative targets and developing NSAID derivatives that lack COX-inhibitory activity but have improved antineoplastic properties.

Indexed as

ChemopreventionAnimalsAnticarcinogenic AgentsAnti-Inflammatory Agents, Non-SteroidalCell Transformation, NeoplasticCyclooxygenase InhibitorsGene Expression Regulation, NeoplasticHumansNeoplasmsProstaglandin-Endoperoxide SynthasesSignal TransductionAnticarcinogenic AgentsAnti-Inflammatory Agents, Non-SteroidalCyclooxygenase InhibitorsProstaglandin-Endoperoxide Synthases

Identifiers

PMID24311630
PMCPMC3947450
OpenAlexW2153825864

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.