ArticleCancer prevention research (Philadelphia, Pa.)2011
Selective PGE(2) suppression inhibits colon carcinogenesis and modifies local mucosal immunity.
Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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.
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.
Who cites it
51 citing papers in PubMed, 84 citations in OpenAlex.
- EP4 influences bortezomib resistance in multiple myeloma by modulating endoplasmic reticulum stress via the phosphatidylinositol 3-kinase/protein kinase B pathway.Anti-cancer drugs · 2026Article
- The Role of Prostaglandins as Major Inflammatory Mediators in Colorectal Cancer.International journal of molecular sciences · 2025Review
- Differential susceptibility to colonic ulceration in mice with genetic deletion ofResearch square · 2025Article
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- [Therapeutic mechanism ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promotebioRxiv : the preprint server for biology · 2023Article
- Cyclooxygenase-2-Prostaglandin E2 pathway: A key player in tumor-associated immune cells.Frontiers in oncology · 2023Review
- Specific prostaglandins are produced in the migratory cells and the surrounding substrate to promoteFrontiers in cell and developmental biology · 2023Article
- IDO/kynurenine pathway in cancer: possible therapeutic approaches.Journal of translational medicine · 2022Review
- Cytokine- and chemokine-induced inflammatory colorectal tumor microenvironment: Emerging avenue for targeted therapy.Cancer communications (London, England) · 2022Review
- Epithelial Cell-specific Deletion of Microsomal Prostaglandin E Synthase-1 Does Not Influence Colon Tumor Development in Mice.Journal of cancer prevention · 2021Article
- Transcriptome-wideCancer prevention research (Philadelphia, Pa.) · 2021Article
- Phagocytes produce prostaglandin E2 in response to cytosolic Listeria monocytogenes.PLoS pathogens · 2021Article
- Carcinogenesis: Failure of resolution of inflammation?Pharmacology & therapeutics · 2021Review
- Urinary 8-iso PGF2α and 2,3-dinor-8-iso PGF2α can be indexes of colitis-associated colorectal cancer in mice.PloS one · 2021Article
- Molecular Targets in Precision Chemoprevention of Colorectal Cancer: An Update from Pre-Clinical to Clinical Trials.International journal of molecular sciences · 2020Review
- Review
- Environmental, Neuro-immune, and Neuro-oxidative Stress Interactions in Chronic Fatigue Syndrome.Molecular neurobiology · 2020Review
- Caffeine and its main targets of colorectal cancer.World journal of gastrointestinal oncology · 2020Review
- Biological characterization of new inhibitors of microsomal PGE synthase-1 in preclinical models of inflammation and vascular tone.British journal of pharmacology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Prostaglandin E(2) (PGE(2)) is a bioactive lipid that mediates a wide range of physiologic effects and plays a central role in inflammation and cancer. PGE(2) is generated from arachidonic acid by the sequential actions of the COX and terminal synthases (PGES). Increased levels of COX-2, with a concomitant elevation of PGE(2), are often found in colorectal cancers (CRC), providing the rationale for the use of COX-2 inhibitors for chemoprevention. Despite their proven efficacy in cancer prevention, however, COX-2 inhibitors exhibit dose-dependent toxicities that are mediated in part by their nonspecific reduction of essential prostanoids, thus limiting their chemopreventive benefit. To achieve enhanced specificity, recent efforts have been directed toward targeting the inducible terminal synthase in the production of PGE(2), microsomal PGES (mPGES-1). In the present study, we show that genetic deletion of mPGES-1 affords significant protection against carcinogen-induced colon cancer. mPGES-1 gene deletion results in an about 80% decrease in tumor multiplicity and up to a 90% reduction in tumor load in the distal colon of azoxymethane (AOM)-treated mice. Associated with the striking cancer suppression, we have identified a critical role for PGE(2) in the control of immunoregulatory cell expansion (FoxP3-positive regulatory T cells) within the colon-draining mesenteric lymph nodes, providing a potential mechanism by which suppression of PGE(2) may protect against CRC. These results provide new insights into how PGE(2) controls antitumor immunity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.