Affiliations: [a] Department of Medicine, Section of Hematology/Oncology, The University of Chicago, Chicago, IL, USA | [b] Ben May Department for Cancer Biology, The University of Chicago, Chicago, IL, USA | [x] Department of Breast medical Oncology, M.D. Anderson Cancer Center, Houston, TX, USA | [y] Department of Gynecologic Oncology, M.D. Anderson Cancer Center, Houston, TX, USA
Correspondence:
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Corresponding author: Suzanne D. Conzen, Ben May Department for Cancer Biology, The University of Chicago, Chicago, IL 60637, USA. E-mail: sconzen@medicine.bsd.uchicago.edu.
Abstract: Adrenergic signaling results from the effects of the catecholamines epinephrine and norepinephrine, on alpha- and beta-adrenergic receptors. In breast cancer, preclinical models suggest that this pathway may influence breast cancer progression through 1) increasing tumor cell survival after exposure to chemotherapeutic agents; 2) increasing breast cancer cell proliferation; and 3) altering the tumor microenvironment in angiogenesis and the inflammatory response. Epidemiologic data have suggested a correlation between drugs that indirectly affect the adrenergic pathway and breast cancer incidence. In addition, there is retrospective evidence suggesting that the use of β-adrenergic blockers in early stage breast cancer patients correlates with an increased time to recurrence. Here we review evidence from both pre-clinical models and epidemiological studies that have examined the question of whether adrenergic signaling may modify breast cancer biology.
Keywords: Breast cancer, stress, adrenergic signaling, HPA axis, glucocorticoids
