Department of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry; and the University of Maryland Greenebaum Comprehensive Cancer Center, Baltimore, Maryland, USA

*Corresponding author: Dr. Leslie C Costello, PhD, Distinguished University Professor, Department of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry; and the University of Maryland Greenebaum Comprehensive Cancer Center, Baltimore, Maryland 21201. Email: [email protected]  

Received Date: Aug 26, 2022

Published Date: Sep 22, 2022

Citation: Costello LC. (2022). The Genetic Evolution of “Decreased Zinc” Malignancies and Their Treatment. Mathews J Cancer Sci. 7(3):34.

Copyrights: Costello LC, et al. © (2022). 

ABSTRACT

The development of zinc malignancies is dependent on the relationship that “The initiation of malignancy is the evolutionary genetic transformation of normal cells to “decreased zinc” malignant cells.” The reason is the zinc concentration that exists in normal cells is cytotoxic in malignant cells. That transformation applies to the initial evolution of all malignancies. There are no exceptions! The “normal zinc” malignant cells develop in accordance with Darwin’s “Natural Selection” and the “survival of the fittest”. The human prostate gland exhibits those relationships. Testosterone-dependent acinar epithelial cells are “decreased zinc” cells; and “prolactin-dependent” acinar epithelial are “normal zinc” Natural Selection/survival of the fittest cells.

Treatment with clioquinol zinc ionophore increases the transport of zinc in the “decreased zinc” testosterone-dependent malignant cells and induces cytotoxic effects. Cabergoline prolactin agonist inhibits pituitary production and induces hypoprolactinemia, which terminates prolactin-dependent malignancy.

Keywords: decreased zinc, zinc malignancy, genetic evolution, treatment