Evidence map›Paper›PMID 25462899›Full record

ArticlePsychoneuroendocrinology2015

α2-Adrenergic blockade mimics the enhancing effect of chronic stress on breast cancer progression.

Donald M Lamkin, Ha Yeon Sung, Gyu Sik Yang, John M David, Jeffrey C Y Ma, Steve W Cole, Erica K Sloan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Psychoneuroendocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
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  6. Article
  7. Article
  8. The tumor-nerve circuit in breast cancer.Cancer metastasis reviews · 2023
    Review
  9. Article
  10. Effect of chronic stress on tumorigenesis and development.Cellular and molecular life sciences : CMLS · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. 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

7 authors at 2 institutions in 2 countries.

Donald M LamkinCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA. Electronic address: dlamkin@ucla.edu.
Ha Yeon SungCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA.
Gyu Sik YangCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA.
John M DavidDepartment of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, USA.
Jeffrey C Y MaCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA; Division of Hematology-Oncology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Steve W ColeCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA; Division of Hematology-Oncology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA; UCLA Molecular Biology Institute, Los Angeles, CA 90095, USA.
Erica K SloanCousins Center for PNI, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA 90095, USA; Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA 90095, USA; Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia; Department of Cancer Anaesthesia and Pain Medicine, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia.
University of California, Los Angeles · USMonash University · AU

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Melissa Fitzmaurice Neligan · 1985 to 2026
$134.5M
Adrenergic regulation of tumor inflammation and metastatic disseminationR01CA160890 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SLOAN, ERICA KATE · 2012 to 2016
$1.6M
NCI NIH HHS P30 CA016042NCI NIH HHS P30CA016042NCI NIH HHS R01 CA160890NCI NIH HHS R01CA160890
6 · The paper itself

Abstract

Experimental studies in preclinical mouse models of breast cancer have shown that chronic restraint stress can enhance disease progression by increasing catecholamine levels and subsequent signaling of β-adrenergic receptors. Catecholamines also signal α-adrenergic receptors, and greater α-adrenergic signaling has been shown to promote breast cancer in vitro and in vivo. However, antagonism of α-adrenergic receptors can result in elevated catecholamine levels, which may increase β-adrenergic signaling, because pre-synaptic α2-adrenergic receptors mediate an autoinhibition of sympathetic transmission. Given these findings, we examined the effect of α-adrenergic blockade on breast cancer progression under non-stress and stress conditions (chronic restraint) in an orthotopic mouse model with MDA-MB-231HM cells. Chronic restraint increased primary tumor growth and metastasis to distant tissues as expected, and non-selective α-adrenergic blockade by phentolamine significantly inhibited those effects. However, under non-stress conditions, phentolamine increased primary tumor size and distant metastasis. Sympatho-neural gene expression for catecholamine biosynthesis enzymes was elevated by phentolamine under non-stress conditions, and the non-selective β-blocker propranolol inhibited the effect of phentolamine on breast cancer progression. Selective α2-adrenergic blockade by efaroxan also increased primary tumor size and distant metastasis under non-stress conditions, but selective α1-adrenergic blockade by prazosin did not. These results are consistent with the hypothesis that α2-adrenergic signaling can act through an autoreceptor mechanism to inhibit sympathetic catecholamine release and, thus, modulate established effects of β-adrenergic signaling on tumor progression-relevant biology.

Indexed as

Adrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AntagonistsAnimalsBenzofuransCell ProliferationDisease ProgressionFemaleImidazolesMammary Neoplasms, ExperimentalMiceNeoplasm MetastasisPrazosinRestraint, PhysicalSignal TransductionStress, PhysiologicalStress, PsychologicalAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AntagonistsBenzofuransefaroxanImidazolesPrazosinBioluminescent imagingBreast cancerCatecholaminesMetastasisRestraint stressSympathetic nervous systemα-Adrenergic receptor

Identifiers

PMID25462899
PMCPMC4406769
OpenAlexW2107270877

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.