Evidence map›Paper›PMID 27709364›Full record

ReviewJournal of cancer research and clinical oncology2017

β-Adrenergic modulation of cancer cell proliferation: available evidence and clinical perspectives.

Marisa Coelho, Cátia Soares-Silva, Daniela Brandão, Franca Marino, Marco Cosentino, Laura Ribeiro

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 2 pooled it
5.8field-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

65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.

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  14. Cancer and neurotransmitter receptors.Chinese medical journal · 2025
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5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Marisa CoelhoDepartment of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal.
Cátia Soares-SilvaDepartment of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal.
Daniela BrandãoDepartment of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal.
Franca MarinoCenter for Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Marco CosentinoCenter for Research in Medical Pharmacology, University of Insubria, Varese, Italy.
Laura RibeiroDepartment of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal. lribeiro@med.up.pt.
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTUniversity of Insubria · ITUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeIn this review, we aimed to present and discuss the available preclinical and epidemiological evidences regarding the modulation of cancer cell proliferation by β-adrenoceptors (β-AR), with a specific focus on the putative effects of β-blockers according to their pharmacological properties.

methodsA comprehensive review of the published literature was conducted, and the evidences concerning the involvement of β-AR in cancer as well as the possible role of β-blockers were selected and discussed.

resultsThe majority of reviewed studies show that: (1) All the cancer types express both β1- and β2-AR, with the exception of neuroblastoma only seeming to express β2-AR; (2) adrenergic agonists are able to increase proliferation of several types of cancers; (3) the proliferative effect seems to be mediated by both β1- and β2-AR; (4) binding to β-AR results in a cAMP transient flux which activates two major downstream effector systems: protein kinase A and EPAC and (5) β-blockers might be putative adjuvants for cancer treatment.

conclusionsOverall, the reviewed studies show strong evidences that β-AR activation, through several intracellular mechanisms, modulate tumor cell proliferation suggesting β-blockers can be a feasible therapeutic approach to antagonize β-adrenergic response or have a protective effect per se. This review highlight the need for intensifying the research not only on the molecular mechanisms underlying the β-adrenergic influence in cancer, but also on the implications of biased agonism of β-blockers as potential antitumor agents.

Indexed as

Adrenergic beta-AntagonistsAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationClinical Trials as TopicHumansNeoplasmsNorepinephrineReceptors, Adrenergic, betaSignal TransductionTumor MicroenvironmentAdrenergic beta-AntagonistsAntineoplastic AgentsNorepinephrineReceptors, Adrenergic, betaAdrenergic systemCancerCatecholaminesProliferationβ-Blockers

Identifiers

PMID27709364
PMCPMC11819197
OpenAlexW2528320990

What OpenQuestion holds

Textmetadata
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.