Evidence map›Paper›PMID 23348742›Full record

ArticleThe Journal of clinical investigation2013

Behavioral stress accelerates prostate cancer development in mice.

Sazzad Hassan, Yelena Karpova, Daniele Baiz, Dana Yancey, Ashok Pullikuth, Anabel Flores, Thomas Register, J Mark Cline, Ralph D'Agostino, Nika Danial and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
13.4field-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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 229 citations in OpenAlex.

  1. Pooled it
  2. Molecular mechanisms and therapeutic targets in lung cancer-nerve crosstalk.Chinese medical journal pulmonary and critical care medicine · 2026
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102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Sazzad HassanDepartment of Cancer Biology, Wake Forest School of Medicine, Medical Center Blvd., Winston-Salem, North Carolina 27157, USA.
Yelena Karpova
Daniele Baiz
Dana Yancey
Ashok Pullikuth
Anabel Flores
Thomas Register
J Mark Cline
Ralph D'Agostino
Nika Danial
Sandeep Robert Datta
George Kulik
Wake Forest University · USDana-Farber Cancer Institute · USHarvard University · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Wake Forest University School of Medicine PREP ScholarsR25GM064249 · NIGMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DIZ, DEBRA I · 2001 to 2017
$4.8M
Stress-activated signaling in prostate cancerR01CA118329 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI KULIK, GEORGE A · 2008 to 2012
$2.5M
NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA118329NCI NIH HHS R01CA118329NIGMS NIH HHS R25 GM064249
6 · The paper itself

Abstract

Prostate cancer patients have increased levels of stress and anxiety. Conversely, men who take beta blockers, which interfere with signaling from the stress hormones adrenaline and noradrenaline, have a lower incidence of prostate cancer; however, the mechanisms underlying stress-prostate cancer interactions are unknown. Here, we report that stress promotes prostate carcinogenesis in mice in an adrenaline-dependent manner. Behavioral stress inhibited apoptosis and delayed prostate tumor involution both in phosphatase and tensin homolog-deficient (PTEN-deficient) prostate cancer xenografts treated with PI3K inhibitor and in prostate tumors of mice with prostate-restricted expression of c-MYC (Hi-Myc mice) subjected to androgen ablation therapy with bicalutamide. Additionally, stress accelerated prostate cancer development in Hi-Myc mice. The effects of stress were prevented by treatment with the selective β2-adrenergic receptor (ADRB2) antagonist ICI118,551 or by inducible expression of PKA inhibitor (PKI) or of BCL2-associated death promoter (BAD) with a mutated PKA phosphorylation site (BADS112A) in xenograft tumors. Effects of stress were also blocked in Hi-Myc mice expressing phosphorylation-deficient BAD (BAD3SA). These results demonstrate interactions between prostate tumors and the psychosocial environment mediated by activation of an adrenaline/ADRB2/PKA/BAD antiapoptotic signaling pathway. Our findings could be used to identify prostate cancer patients who could benefit from stress reduction or from pharmacological inhibition of stress-induced signaling.

Indexed as

Adrenergic beta-AntagonistsAnimalsApoptosisbcl-Associated Death ProteinCell Line, TumorDisease Models, AnimalEpinephrineHumansHypothalamo-Hypophyseal SystemMaleMiceMice, Inbred BALB CMice, NudePituitary-Adrenal SystemPropanolaminesProstatic NeoplasmsAdrenergic beta-AntagonistsBad protein, mousebcl-Associated Death ProteinEpinephrineICI 118551Myc protein, mousePropanolaminesProto-Oncogene Proteins c-mycPTEN PhosphohydrolasePten protein, mouseReceptors, Adrenergic, beta-2

Identifiers

PMID23348742
PMCPMC3561807
OpenAlexW2095612053

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.