Evidence map›Paper›PMID 31466709›Full record

ArticleBiomedical journal2019

The beta adrenergic receptor antagonist propranolol alters mitogenic and apoptotic signaling in late stage breast cancer.

Alexa Montoya, Armando Varela-Ramirez, Erin Dickerson, Eddy Pasquier, Alireza Torabi, Renato Aguilera, Zeina Nahleh, Brad Bryan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomedical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
7.1field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  4. Review
  5. Key role of the autonomic nervous system in breast cancer (Review).Experimental and therapeutic medicine · 2026
    Review
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  20. ß-Adrenoreceptors in Human Cancers.International journal of molecular sciences · 2023
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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 5 institutions in 2 countries.

Alexa MontoyaDepartment of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX, USA; Department of Biology, University of Texas, El Paso, TX, USA.
Armando Varela-RamirezDepartment of Biology, University of Texas, El Paso, TX, USA; Border Biomedical Research Center, University of Texas, El Paso, TX, USA.
Erin DickersonDepartment of Veterinary Clinical Sciences, University of Minnesota, Saint Paul, Minnesota, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Eddy PasquierCNRS, INSERM, Aix-Marseille University, Institut Paoli-Calmettes, Cancer Research Center of Marseille, Marseille, France.
Alireza TorabiDepartment of Pathology, Texas Tech University Health Sciences Center, El Paso, TX, USA.
Renato AguileraDepartment of Biology, University of Texas, El Paso, TX, USA; Border Biomedical Research Center, University of Texas, El Paso, TX, USA.
Zeina NahlehDepartment of Hematology and Medical Oncology, Cleveland Clinic, Weston, FL, USA.
Brad BryanDepartment of Biomedical Sciences, Texas Tech University Health Sciences Center, El Paso, TX, USA. Electronic address: bradallenbryan@gmail.com.
Texas Tech University · USThe University of Texas at El Paso · USCentre National de la Recherche Scientifique · FRCleveland Clinic Florida · USUniversity of Minnesota · US

Funding

TCCG12MD007592 · NIMHD · UNIVERSITY OF TEXAS EL PASO · PI KIRKEN, ROBERT A. · 2012 to 2018
$19.4M
NIMHD NIH HHS G12 MD007592
6 · The paper itself

Abstract

backgroundSubstantial evidence supports the use of inexpensive β-AR antagonists (beta blockers) against a variety of cancers, and the β-AR antagonist propranolol was recently approved by the European Medicines Agency for the treatment of soft tissue sarcomas. Prospective and retrospective data published by our group and others suggest that non-selective β-AR antagonists are effective at reducing proliferative rates in breast cancers, however the mechanism by which this occurs is largely unknown.

methodsIn this study, we measured changes in tumor proliferation and apoptosis in a late stage breast cancer patient treated with neoadjuvant propranolol. We expounded upon these clinical findings by employing an in vitro breast cancer model, where we used cell-based assays to evaluate propranolol-mediated molecular alterations related to cell proliferation and apoptosis.

resultsNeoadjuvant propranolol decreased expression of the pro-proliferative Ki-67 and pro-survival Bcl-2 markers, and increased pro-apoptotic p53 expression in a patient with stage III breast cancer. Molecular analysis revealed that β-AR antagonism disrupted cell cycle progression and steady state levels of cyclins. Furthermore, propranolol treatment of breast cancer cells increased p53 levels, enhanced caspase cleavage, and induced apoptosis.

conclusionCollectively, these data provide support for the incorporation of β-AR antagonists into the clinical management of breast cancer, and elucidate a partial molecular mechanism explaining the efficacy of β-AR antagonists against this disease.

Indexed as

Adrenergic beta-AntagonistsApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationHumansPropranololProspective StudiesSignal TransductionTreatment OutcomeAdrenergic beta-AntagonistsPropranololApoptosisBeta adrenergic receptorBeta blockadeBreast cancerProliferationPropranolol

Identifiers

PMID31466709
PMCPMC6717753
OpenAlexW2964053772

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.