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The Estradiol-Dihydrotestosterone model of prostate cancer

A Edward Friedman email

Department of Mathematics, University of Chicago, 5734 S. University Avenue, Chicago, IL 60637, USA

author email corresponding author email

Theoretical Biology and Medical Modelling 2005, 2:10doi:10.1186/1742-4682-2-10

Published: 18 March 2005

Abstract

Background

The exact relationship between hormonal activity and prostate cancer(PCa) has not yet been clearly defined. One of the key hormones associated with PCa is testosterone(T). However, both in vitro and in vivo studies have shown that under some conditions T is capable of either promoting PCa growth or death. This article proposes a theory which resolves this apparent paradox.

Model

The Estradiol-Dihydrotestosterone(E-D) model introduced in this paper proposes that 17β-estradiol(E2) is essential for initiating the growth of PCa cells through the formation of telomeres. It also proposes that T is responsible for increasing the expression of proteins which cause apoptosis, or programmed cell death, and that 5α-dihydrotestosterone(DHT) is essential for preventing this. In addition, it is known that some T is converted to both E2 and DHT, which means that depending on the conditions, T is capable of either promoting the growth of or the killing of PCa.


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