Evidence map›Paper›PMID 22186256›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2012

Molecular pathways: beta-adrenergic signaling in cancer.

Steven W Cole, Anil K Sood

Open access · greenAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 397 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
397citing papers in PubMed, 5 pooled it
16.2field-weighted citation impact, top 1% 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

397 citing papers in PubMed, 5 syntheses or guidelines pooled it, 655 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Beta-blocker use and breast cancer outcomes: a meta-analysis.Breast cancer research and treatment · 2024
    Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Article
  9. Selective regulation of βMedical oncology (Northwood, London, England) · 2026
    Article
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  12. Review
  13. Review
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  15. Article
  16. Article
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  18. Article
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  20. Review

337 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Steven W ColeDivision of Hematology-Oncology, Department of Medicine, UCLA School of Medicine, Los Angeles, California 90095-1678, USA. coles@ucla.edu
Anil K Sood
The University of Texas MD Anderson Cancer Center · US

Funding

Ovarian Cancer: Mechanisms of Neuroendocrine RegulationR01CA109298 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SOOD, ANIL K · 2005 to 2017
$4.5M
Combinatorial Genomics in CancerR01CA116778 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLE, STEVE W · 2006 to 2010
$1.5M
NCI NIH HHS CA109298NCI NIH HHS CA116778NCI NIH HHS R01 CA109298NCI NIH HHS R01 CA116778
6 · The paper itself

Abstract

Beta-adrenergic signaling has been found to regulate multiple cellular processes that contribute to the initiation and progression of cancer, including inflammation, angiogenesis, apoptosis/anoikis, cell motility and trafficking, activation of tumor-associated viruses, DNA damage repair, cellular immune response, and epithelial-mesenchymal transition. In several experimental cancer models, activation of the sympathetic nervous system promotes the metastasis of solid epithelial tumors and the dissemination of hematopoietic malignancies via β-adrenoreceptor-mediated activation of protein kinase A and exchange protein activated by adenylyl cyclase signaling pathways. Within the tumor microenvironment, β-adrenergic receptors on tumor and stromal cells are activated by catecholamines from local sympathetic nerve fibers (norepinephrine) and circulating blood (epinephrine). Tumor-associated macrophages are emerging as key targets of β-adrenergic regulation in several cancer contexts. Sympathetic nervous system regulation of cancer cell biology and the tumor microenvironment has clarified the molecular basis for long-suspected relationships between stress and cancer progression, and now suggests a highly leveraged target for therapeutic intervention. Epidemiologic studies have linked the use of β-blockers to reduced rates of progression for several solid tumors, and preclinical pharmacologic and biomarker studies are now laying the groundwork for translation of β-blockade as a novel adjuvant to existing therapeutic strategies in clinical oncology.

Indexed as

Signal TransductionAdrenergic beta-AntagonistsAnimalsAntineoplastic AgentsClinical Trials as TopicHumansNeoplasmsReceptors, Adrenergic, betaTranslational Research, BiomedicalAdrenergic beta-AntagonistsAntineoplastic AgentsReceptors, Adrenergic, beta

Identifiers

PMID22186256
PMCPMC3294063
OpenAlexW2141382054

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.