The influence of glucocorticoid signaling on tumor progression

Paul A. Volden, Suzanne D. Conzen

Research output: Contribution to journalReview article

70 Citations (Scopus)

Abstract

The diagnosis of cancer elicits a broad range of well-characterized stress-related biobehavioral responses. Recent studies also suggest that an individual's neuroendocrine stress response can influence tumor biology. One of the major physiological pathways altered by the response to unrelenting social stressors is the hypothalamic-pituitary-adrenal or HPA axis. Initially following acute stress exposure, an increased glucocorticoid response is observed; eventually, chronic stress exposure can lead to a blunting of the normal diurnal cortisol pattern. Interestingly, recent evidence also links high primary tumor glucocorticoid receptor expression (and associated increased glucocorticoid-mediated gene expression) to more rapid estrogen-independent breast cancer progression. Furthermore, animal models of human breast cancer suggest that glucocorticoids inhibit tumor cell apoptosis. These findings provide a conceptual basis for understanding the molecular mechanisms underlying the influence of the individual's stress response, and specifically glucocorticoid action, on breast cancer and other solid tumor biology. How this increased glucocorticoid signaling might contribute to cancer progression is the subject of this review.

Original languageEnglish (US)
Pages (from-to)S26-S31
JournalBrain, Behavior, and Immunity
Volume30
Issue numberSUPPL.
DOIs
StatePublished - Mar 15 2013
Externally publishedYes

Fingerprint

Glucocorticoids
Neoplasms
Breast Neoplasms
Glucocorticoid Receptors
Hydrocortisone
Estrogens
Animal Models
Apoptosis
Gene Expression

Keywords

  • Animal models
  • Breast cancer
  • Cortisol
  • Glucocorticoid receptor
  • Glucocorticoids
  • Social environment
  • Stress response

ASJC Scopus subject areas

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience

Cite this

The influence of glucocorticoid signaling on tumor progression. / Volden, Paul A.; Conzen, Suzanne D.

In: Brain, Behavior, and Immunity, Vol. 30, No. SUPPL., 15.03.2013, p. S26-S31.

Research output: Contribution to journalReview article

@article{d661f3d9e32542478ab1b47f235236e9,
title = "The influence of glucocorticoid signaling on tumor progression",
abstract = "The diagnosis of cancer elicits a broad range of well-characterized stress-related biobehavioral responses. Recent studies also suggest that an individual's neuroendocrine stress response can influence tumor biology. One of the major physiological pathways altered by the response to unrelenting social stressors is the hypothalamic-pituitary-adrenal or HPA axis. Initially following acute stress exposure, an increased glucocorticoid response is observed; eventually, chronic stress exposure can lead to a blunting of the normal diurnal cortisol pattern. Interestingly, recent evidence also links high primary tumor glucocorticoid receptor expression (and associated increased glucocorticoid-mediated gene expression) to more rapid estrogen-independent breast cancer progression. Furthermore, animal models of human breast cancer suggest that glucocorticoids inhibit tumor cell apoptosis. These findings provide a conceptual basis for understanding the molecular mechanisms underlying the influence of the individual's stress response, and specifically glucocorticoid action, on breast cancer and other solid tumor biology. How this increased glucocorticoid signaling might contribute to cancer progression is the subject of this review.",
keywords = "Animal models, Breast cancer, Cortisol, Glucocorticoid receptor, Glucocorticoids, Social environment, Stress response",
author = "Volden, {Paul A.} and Conzen, {Suzanne D.}",
year = "2013",
month = "3",
day = "15",
doi = "10.1016/j.bbi.2012.10.022",
language = "English (US)",
volume = "30",
pages = "S26--S31",
journal = "Brain, Behavior, and Immunity",
issn = "0889-1591",
publisher = "Academic Press Inc.",
number = "SUPPL.",

}

TY - JOUR

T1 - The influence of glucocorticoid signaling on tumor progression

AU - Volden, Paul A.

AU - Conzen, Suzanne D.

PY - 2013/3/15

Y1 - 2013/3/15

N2 - The diagnosis of cancer elicits a broad range of well-characterized stress-related biobehavioral responses. Recent studies also suggest that an individual's neuroendocrine stress response can influence tumor biology. One of the major physiological pathways altered by the response to unrelenting social stressors is the hypothalamic-pituitary-adrenal or HPA axis. Initially following acute stress exposure, an increased glucocorticoid response is observed; eventually, chronic stress exposure can lead to a blunting of the normal diurnal cortisol pattern. Interestingly, recent evidence also links high primary tumor glucocorticoid receptor expression (and associated increased glucocorticoid-mediated gene expression) to more rapid estrogen-independent breast cancer progression. Furthermore, animal models of human breast cancer suggest that glucocorticoids inhibit tumor cell apoptosis. These findings provide a conceptual basis for understanding the molecular mechanisms underlying the influence of the individual's stress response, and specifically glucocorticoid action, on breast cancer and other solid tumor biology. How this increased glucocorticoid signaling might contribute to cancer progression is the subject of this review.

AB - The diagnosis of cancer elicits a broad range of well-characterized stress-related biobehavioral responses. Recent studies also suggest that an individual's neuroendocrine stress response can influence tumor biology. One of the major physiological pathways altered by the response to unrelenting social stressors is the hypothalamic-pituitary-adrenal or HPA axis. Initially following acute stress exposure, an increased glucocorticoid response is observed; eventually, chronic stress exposure can lead to a blunting of the normal diurnal cortisol pattern. Interestingly, recent evidence also links high primary tumor glucocorticoid receptor expression (and associated increased glucocorticoid-mediated gene expression) to more rapid estrogen-independent breast cancer progression. Furthermore, animal models of human breast cancer suggest that glucocorticoids inhibit tumor cell apoptosis. These findings provide a conceptual basis for understanding the molecular mechanisms underlying the influence of the individual's stress response, and specifically glucocorticoid action, on breast cancer and other solid tumor biology. How this increased glucocorticoid signaling might contribute to cancer progression is the subject of this review.

KW - Animal models

KW - Breast cancer

KW - Cortisol

KW - Glucocorticoid receptor

KW - Glucocorticoids

KW - Social environment

KW - Stress response

UR - http://www.scopus.com/inward/record.url?scp=84875370663&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84875370663&partnerID=8YFLogxK

U2 - 10.1016/j.bbi.2012.10.022

DO - 10.1016/j.bbi.2012.10.022

M3 - Review article

C2 - 23164950

AN - SCOPUS:84875370663

VL - 30

SP - S26-S31

JO - Brain, Behavior, and Immunity

JF - Brain, Behavior, and Immunity

SN - 0889-1591

IS - SUPPL.

ER -