Evidence map›Paper›PMID 22006370›Full record

ArticleMolecular carcinogenesis2012

Transgenic insulin-like growth factor-1 stimulates activation of COX-2 signaling in mammary glands.

Jie Tian, Isabel Lambertz, Thomas R Berton, Joyce E Rundhaug, Kaoru Kiguchi, Stephanie H Shirley, John Digiovanni, Claudio J Conti, Susan M Fischer, Robin Fuchs-Young

Open access · greenAbstract read
In one paragraph

Article in Molecular carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Urinary prostaglandin E2 metabolite and breast cancer risk.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2014
    Article
  8. Resistance and escape from antiangiogenesis therapy: clinical implications and future strategies.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012
    Review
  9. 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

10 authors at 1 institution in 1 country.

Jie TianDepartment of Molecular Carcinogenesis, Science Park, The University of Texas MD Anderson Cancer Center, Smithville, Texas 78957, USA.
Isabel Lambertz
Thomas R Berton
Joyce E Rundhaug
Kaoru Kiguchi
Stephanie H Shirley
John Digiovanni
Claudio J Conti
Susan M Fischer
Robin Fuchs-Young
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
SHARED RESOUCES COREP60MD000503 · NIMHD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI JONES, LOVELL ALLAN · 2003 to 2011
$12.4M
IGF-1 Signaling &ER crosstalk in mammary cancer in vivoR01CA104114 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FUCHS-YOUNG, ROBIN S · 2005 to 2008
$1.2M
NCI NIH HHS CA016672NCI NIH HHS CA104114NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA104114NIEHS NIH HHS ES007784NIEHS NIH HHS P30 ES007784NIMHD NIH HHS P60 MD000503
6 · The paper itself

Abstract

Studies show that elevated insulin-like growth factor-1 (IGF-1) levels are associated with an increased risk of breast cancer; however, mechanisms through which IGF-1 promotes mammary tumorigenesis in vivo have not been fully elucidated. To assess the possible involvement of COX-2 signaling in the pro-tumorigenic effects of IGF-1 in mammary glands, we used the unique BK5.IGF-1 mouse model in which transgenic (Tg) mice have significantly increased incidence of spontaneous and DMBA-induced mammary cancer compared to wild type (WT) littermates. Studies revealed that COX-2 expression was significantly increased in Tg mammary glands and tumors, compared to age-matched WTs. Consistent with this, PGE(2) levels were also increased in Tg mammary glands. Analysis of expression of the EP receptors that mediate the effects of PGE(2) showed that among the four G-protein-coupled receptors, EP3 expression was elevated in Tg glands. Up-regulation of the COX-2/PGE(2) /EP3 pathway was accompanied by increased expression of VEGF and a striking enhancement of angiogenesis in IGF-1 Tg mammary glands. Treatment with celecoxib, a selective COX-2 inhibitor, caused a 45% reduction in mammary PGE(2) levels, attenuated the influx of mast cells and reduced vascularization in Tg glands. These findings indicate that the COX-2/PGE(2) /EP3 signaling pathway is involved in IGF-1-stimulated mammary tumorigenesis and that COX-2-selective inhibitors may be useful in the prevention or treatment of breast cancer associated with elevated IGF-1 levels in humans. © 2011 Wiley Periodicals, Inc.

Indexed as

AnimalsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsEnzyme ActivationEnzyme-Linked Immunosorbent AssayFemaleInsulin-Like Growth Factor IMammary Glands, AnimalMiceMice, TransgenicNeovascularization, PathologicPyrazolesReal-Time Polymerase Chain ReactionReceptors, Prostaglandin ESignal TransductionCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsInsulin-Like Growth Factor IPyrazolesReceptors, Prostaglandin ESulfonamides

Identifiers

PMID22006370
PMCPMC3790642
OpenAlexW2057132360

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.