Evidence map›Paper›PMID 26477316›Full record

ArticleOncogene2016

Expression and therapeutic targeting of dopamine receptor-1 (D1R) in breast cancer.

D C Borcherding, W Tong, E R Hugo, D F Barnard, S Fox, K LaSance, E Shaughnessy, N Ben-Jonathan

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  13. Caveolin-1, a Determinant of the Fate of MCF-7 Breast Cancer Cells.Breast cancer : basic and clinical research · 2024
    Article
  14. Review
  15. The tumor-nerve circuit in breast cancer.Cancer metastasis reviews · 2023
    Review
  16. Review
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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

8 authors at 1 institution in 1 country.

D C BorcherdingDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
W TongDepartment of Pathology, University of Cincinnati, Cincinnati, OH, USA.
E R HugoDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
D F BarnardDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
S FoxDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
K LaSanceDepartment of Radiology, University of Cincinnati, Cincinnati, OH, USA.
E ShaughnessyDepartment of Surgery, University of Cincinnati, Cincinnati, OH, USA.
N Ben-JonathanDepartment of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
University of Cincinnati · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
Prolactin as a Growth Factor in Breast CancerR01CA096613 · NCI · UNIVERSITY OF CINCINNATI · PI BEN-JONATHAN, NIRA · 2004 to 2013
$2.7M
Xenoestrogens: Genomic and Non-genomic MechanismsR01ES012212 · NIEHS · UNIVERSITY OF CINCINNATI · PI BEN-JONATHAN, NIRA · 2003 to 2006
$1.1M
Bisphenol A and the Metabolic Syndrome: Focus on Adipose Tissue FunctionsU01ES020909 · NIEHS · UNIVERSITY OF CINCINNATI · PI BEN-JONATHAN, NIRA · 2011 to 2015
$931k
NCATS NIH HHS UL1 TR001425NCI NIH HHS R01 CA096613NCI NIH HHS T32 CA117846NIEHS NIH HHS R01 ES012212NIEHS NIH HHS U01 ES020909
6 · The paper itself

Abstract

Patients with advanced breast cancer often fail to respond to treatment, creating a need to develop novel biomarkers and effective therapeutics. Dopamine (DA) is a catecholamine that binds to five G protein-coupled receptors. We discovered expression of DA type-1 receptors (D1Rs) in breast cancer, thereby identifying these receptors as novel therapeutic targets in this disease. Strong to moderate immunoreactive D1R expression was found in 30% of 751 primary breast carcinomas, and was associated with larger tumors, higher tumor grades, node metastasis and shorter patient survival. DA and D1R agonists, signaling through the cGMP/protein kinase G (PKG) pathway, suppressed cell viability, inhibited invasion and induced apoptosis in multiple breast cancer cell lines. Fenoldopam, a peripheral D1R agonist that does not penetrate the brain, dramatically suppressed tumor growth in two mouse models with D1R-expressing xenografts by increasing both necrosis and apoptosis. D1R-expressing primary tumors and metastases in mice were detected by fluorescence imaging. In conclusion, D1R overexpression is associated with advanced breast cancer and poor prognosis. Activation of the D1R/cGMP/PKG pathway induces apoptosis in vitro and causes tumor shrinkage in vivo. Fenoldopam, which is FDA (Food and Drug Administration) approved to treat renal hypertension, could be repurposed as a novel therapeutic agent for patients with D1R-expressing tumors.

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Line, TumorCell MovementDopamine AgonistsDopamine AntagonistsFemaleHEK293 CellsHeterograftsHumansMCF-7 CellsMiceMiddle AgedMolecular Targeted TherapyReceptors, DopamineDopamine AgonistsDopamine AntagonistsReceptors, Dopamine

Identifiers

PMID26477316
PMCPMC5541367
OpenAlexW1887973965

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.