The influence of glucocorticoid signaling on tumor progression

Paul A. Volden, Suzanne D. Conzen

Research output: Contribution to journalReview articlepeer-review

104 Scopus citations


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
Issue numberSUPPL.
StatePublished - Mar 15 2013
Externally publishedYes


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

ASJC Scopus subject areas

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience


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