Research

Can a single model explain both breast cancer and prostate cancer?

A Edward Friedman

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

author email corresponding author email

Theoretical Biology and Medical Modelling 2007, 4:28doi:10.1186/1742-4682-4-28

Published:	1 August 2007

Abstract

Background

The Estradiol-Dihydrotestosterone model of prostate cancer (PC) showed how the interaction of hormones with specific hormone receptors affected apoptosis. The same hormone can produce different effects, depending on which hormone receptor it interacts with.

Model

This model proposes that the first step in the development of most PC and breast cancer (BC) occurs when aromatase converts testosterone to estradiol (E2). A sufficiently high enough local level of E2 results in telomerase activity. The telomerase activity allows cell division and may lead to BC or PC, which will proliferate if the rate of cell division is greater than the rate of cell death. The effect of hormones on their hormone receptors will affect the rate of cell death and determine whether or not the cancer proliferates.

Conclusion

By minimizing bcl-2 and maximizing apoptotic proteins, new systemic treatments for BC and PC can be developed that may be more effective than existing treatments.