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Cardiac and Renal Hormones
  1. David L. Vesely, MD, PhD
  1. From the Departments of Medicine, Molecular Pharmacology and Physiology, and Cardiac Hormone Center, University of South Florida Health Sciences Center and James A. Haley Veterans Medical Center, Tampa, FL.
  1. Received August 28, 2008, and in revised form October 2, 2008.
  2. Accepted for publication October 2, 2008.
  3. Reprints: David L. Vesely, MD, PhD, Molecular Pharmacology and Physiology, University of South Florida Cardiac Hormone Center, 13000 Bruce B. Downs Blvd., Tampa, FL 33612 (e-mail: david.vesely{at}va.gov).
  4. This work supported in part by Merit Review Grants from the United States Department of Veterans Affairs and a grant from the Darren Malenski Foundation.
  5. This article was presented in part at the EB 2008 Symposium "Cardiac hormones: For the treatment of acute myocardial infarction, congestive hart failure, acute renal failure, and cancer, held in San Diego, CA, USA on April 9, 2008.

Anticancer Effects In Vitro and In Vivo

Abstract

Background Four cardiovascular hormones, ie, vessel dilator, long-acting natriuretic peptide, kaliuretic peptide, and atrial natriuretic peptide each at 1 mmol/L, decrease up to 97% of human breast, ovarian, pancreatic, colon, kidney, and prostate adenocarcinoma cells, as well as small cell and squamous cell lung cancer cells within 24 hours.

Methods Vessel dilator, long-acting natriuretic peptide, and kaliuretic peptide were investigated in vivo.

Results These cardiac hormones completely stop the growth of human pancreatic adenocarcinomas in athymic mice and decrease their tumor volume by 49%, 28%, and 11%, respectively, in 1 week. When these cardiac hormones are given subcutaneously for 1 month via osmotic pumps with the pumps changed weekly, up to 80% of the human pancreatic adenocarcinomas growing in athymic mice can be completely eliminated. Similarly, two thirds of human breast cancers in athymic mice can be eliminated without surgery with these cardiac hormones. Natriuretic peptide receptors A-, B-, and C- are present on the cancer cells to mediate atrial natriuretic peptide's effects.

Conclusions The cardiac hormones' anticancer mechanism of action(s) include a strong inhibition of mitogen (epidermal growth factor and insulin) activated extracellular signal-regulated kinases (ERK) 1/2 and as well as inhibition of basal extracellular-signal regulated kinase 1/2 and upstream MEK 1/2 phosphorylation. They cause 80% to 90% inhibition of DNA synthesis in the nucleus where these cardiac hormones have been demonstrated to localize by immunocytochemical techniques.

Key Words
  • cancer
  • natriuretic peptides
  • metastasis

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