Evidence map›Paper›PMID 29661238›Full record

ArticleBMC cancer2018

EP3 (prostaglandin E2 receptor 3) expression is a prognostic factor for progression-free and overall survival in sporadic breast cancer.

Anna Semmlinger, Viktoria von Schoenfeldt, Verena Wolf, Alexandra Meuter, Theresa Maria Kolben, Thomas Kolben, Christine Zeder-Goess, Florian Weis, Julia Gallwas, Rachel Wuerstlein and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  12. EP3 receptor is a prognostic factor in TA-MUC1-negative ovarian cancer.Journal of cancer research and clinical oncology · 2019
    Article
  13. The role of EP3-receptor expression in cervical dysplasia.Journal of cancer research and clinical oncology · 2019
    Article
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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

17 authors at 4 institutions in 2 countries.

Anna SemmlingerDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Viktoria von SchoenfeldtDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Maistrasse 11, 80337, Munich, Germany.
Verena WolfDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Maistrasse 11, 80337, Munich, Germany.
Alexandra MeuterDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Theresa Maria KolbenDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Thomas KolbenDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Christine Zeder-GoessDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Florian WeisDepartment of Anaesthesiology, Klinikum Fuerstenfeldbruck, Dachauer Strasse 33, 82256, Fuerstenfeldbruck, Germany.
Julia GallwasDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Rachel WuerstleinDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Kerstin HermelinkDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Elisa SchmoeckelDepartment of Pathology, LMU Munich, Thalkirchnerstrasse 36, 80337, Munich, Germany.
Nadia HarbeckDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Doris MayrDepartment of Pathology, LMU Munich, Thalkirchnerstrasse 36, 80337, Munich, Germany.
Sven MahnerDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.
Udo JeschkeDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany.ORCID 0000-0003-2623-3235
Nina DitschDepartment of Obstetrics and Gynecology & Breast Center, University Hospital, LMU Munich, Marchioninistrasse 15, 81377, Munich, Germany. nina.ditsch@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DELMU Klinikum · DEBreast Center · CHKlinikum Osnabrück · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn various cancers, overexpression of cyclooxygenase (COX)-2 and elevated prostaglandin (PG) E2 synthesis have been associated with tumor development and progression. The potential of COX-2 inhibitors in cancer prevention and treatment has been shown repeatedly; however, their clinical use is limited due to toxicity. PGE2 signals via EP receptors 1-4, whose functions are analyzed in current research in search for targeted anti-PG therapies. EP2 and EP4 rather promote tumorigenesis, while the role of EP3, especially in breast cancer, is not yet clear and both pro- and anti-tumorigenic effects have been described. Our study evaluates EP3 receptor expression in sporadic breast cancer and its association with clinicopathological parameters, progression-free and overall survival.

methodsTwo hundred eighty-nine sporadic breast cancer samples without primary distant metastasis were immunohistochemically analyzed for EP3 receptor expression. Tissue was stained with primary anti-EP3-antibodies. Immunoreactivity was quantified by the immunoreactivity-score (IRS); samples with an IRS ≥ 2 scored as EP3 positive. Chi-squared and Mann-Whitney-U test were used for comparison of data; Kaplan-Meier estimates and Cox-regression were used for survival analyses.

resultsEP3 receptor was expressed in 205 of 289 samples analyzed (70.9%). EP3 receptor expression was not associated with clinicopathological parameters (e. g. tumor size, hormone receptors, lymph node status). Kaplan-Meier estimates showed a significant association of EP3 positivity with improved progression-free survival (p = 0.002) and improved overall survival (p = 0.001) after up to 10 years. Cox regression analysis confirmed EP3 positivity as a significant prognostic factor even when other known prognosticators were accounted for.

conclusionsIn sporadic breast cancer, EP3 receptor expression is not significantly associated with clinicopathological parameters but is a significant prognostic factor for improved progression-free and overall survival. However, the functional aspects of EP3 receptor in breast cancer and the way how EP3 may oppose the pro-tumorigenic effects of PGE2 elevation and COX-2 overexpression are not fully understood so far. Further studies aiming at identification of the factors regulated by EP3 are necessary to evaluate the possibility of targeting EP3 in future anti-tumor therapy in breast cancer.

Indexed as

PrognosisAgedAnimalsBreast NeoplasmsCarcinogenesisCyclooxygenase 2 InhibitorsDinoprostoneDisease-Free SurvivalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMiddle AgedReceptors, Prostaglandin E, EP3 SubtypeCyclooxygenase 2 InhibitorsDinoprostonePTGER3 protein, humanReceptors, Prostaglandin E, EP3 SubtypeBreast cancerCOX-2EP3EP-receptorPGE2Prognostic factorProstaglandin E2

Identifiers

PMID29661238
PMCPMC5902996
OpenAlexW2803432641

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.