Evidence map›Paper›PMID 23624019›Full record

ArticleProstaglandins & other lipid mediators2013

Genetic deletion of microsomal prostaglandin E synthase-1 suppresses mouse mammary tumor growth and angiogenesis.

Louise R Howe, Kotha Subbaramaiah, Claire V Kent, Xi K Zhou, Sung-Hee Chang, Timothy Hla, Per-Johan Jakobsson, Clifford A Hudis, Andrew J Dannenberg

Open access · greenAbstract read
In one paragraph

Article in Prostaglandins & other lipid mediators, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.9field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  8. Article
  9. Drugging cancer metabolism: Expectations vs. reality.International review of cell and molecular biology · 2019
    Review
  10. Prostaglandin terminal synthases as novel therapeutic targets.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  11. Article
  12. Article
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  16. Review
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

9 authors at 3 institutions in 2 countries.

Louise R HoweDepartment of Cell & Developmental Biology and Weill Cornell Cancer Center, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA. Electronic address: LRHOWE@MED.CORNELL.EDU.
Kotha Subbaramaiah
Claire V Kent
Xi K Zhou
Sung-Hee Chang
Timothy Hla
Per-Johan Jakobsson
Clifford A Hudis
Andrew J Dannenberg
Cornell University · USKarolinska University Hospital · SEMemorial Sloan Kettering Cancer Center · US

Funding

Targeting the Obesity-Inflammation-COX-Aromatase Axis to Lower Breast Cancer RiskR01CA154481 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DANNENBERG, ANDREW JESS · 2011 to 2015
$1.7M
NCI NIH HHS CA154481NCI NIH HHS R01 CA154481
6 · The paper itself

Abstract

The cyclooxygenase/prostaglandin (COX/PG) signaling pathway is of central importance in inflammation and neoplasia. COX inhibitors are widely used for analgesia and also have demonstrated activity for cancer prophylaxis. However, cardiovascular toxicity associated with this drug class diminishes their clinical utility and motivates the development of safer approaches both for pain relief and cancer prevention. The terminal synthase microsomal PGE synthase-1 (mPGES-1) has attracted considerable attention as a potential target. Overexpression of mPGES-1 has been observed in both colorectal and breast cancers, and gene knockout and overexpression approaches have established a role for mPGES-1 in gastrointestinal carcinogenesis. Here we evaluate the contribution of mPGES-1 to mammary tumorigenesis using a gene knockout approach. Mice deficient in mPGES-1 were crossed with a strain in which breast cancer is driven by overexpression of human epidermal growth factor receptor 2 (HER2/neu). Loss of mPGES-1 was associated with a substantial reduction in intramammary PGE2 levels, aromatase activity, and angiogenesis in mammary glands from HER2/neu transgenic mice. Consistent with these findings, we observed a significant reduction in multiplicity of tumors ≥1mm in diameter, suggesting that mPGES-1 contributes to mammary tumor growth. Our data identify mPGES-1 as a potential anti-breast cancer target.

Indexed as

Gene DeletionAnimalsAromataseCarcinogenesisCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansIntramolecular OxidoreductasesMammary Glands, AnimalMammary Neoplasms, ExperimentalMiceMice, TransgenicMicrovesselsAromataseErb-b2 Receptor Tyrosine KinasesIntramolecular OxidoreductasesProstaglandin-E SynthasesPTGES protein, humanPtges protein, mouseVascular Endothelial Growth Factor AAngiogenesisAromataseBreast cancerMousemPGES-1PGE(2)

Identifiers

PMID23624019
PMCPMC3830707
OpenAlexW2025056086

What OpenQuestion holds

Textmetadata
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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.