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Beta blockers, norepinephrine, and cancer: an epidemiological viewpoint

Paul J Fitzgerald1

  • 1The Zanvyl Krieger Mind/Brain Institute, Solomon H Snyder, Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.

Clinical Epidemiology
|July 19, 2012
PubMed

Insights

Norepinephrine (NE) and epinephrine (EPI) influence cancer development and progression. Drugs targeting these stress hormones, like beta blockers, show promise in reducing cancer recurrence and mortality.

Area of Science:

  • Oncology
  • Neuroendocrinology
  • Pharmacology

Background:

  • Growing evidence links neurotransmitters norepinephrine (NE) and epinephrine (EPI) to cancer.
  • Epidemiological studies suggest beta blockers (antagonizing NE/EPI receptors) reduce breast cancer and melanoma recurrence, progression, and mortality.
  • Psychological stress, mediated by NE/EPI via the sympathetic nervous system, may contribute to cancer etiology.

Purpose of the Study:

  • To explore the role of NE and EPI in cancer.
  • To investigate the impact of NE/EPI pathway modulation on cancer.
  • To identify potential therapeutic strategies targeting NE/EPI in cancer treatment.

Main Methods:

  • Review of epidemiological studies on beta blocker use and cancer outcomes.
  • Analysis of preclinical studies on NE/EPI manipulation in experimental cancers.
  • Exploration of molecular pathways (e.g., P38/MAPK) and oxidative stress in NE/EPI's effect on cancer.

Main Results:

  • Beta blockers are associated with improved outcomes in breast cancer and melanoma.
  • Drug-induced modulation of NE/EPI levels or receptors impacts experimentally induced cancers.
  • NE/EPI may influence cancer via P38/MAPK pathways and oxidative stress.

Conclusions:

  • NE and EPI play a significant role in cancer biology.
  • Targeting the NE/EPI system, including with non-beta blocker drugs or cholinesterase inhibitors, presents potential cancer prevention and treatment avenues.
  • Further epidemiological studies are warranted to validate these findings.
Keywords:
acetylcholineadrenalineaspirinclonidineepinephrineguanfacineinflammationparasympathetic nervous systemsympathetic nervous system

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