A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy

Prostate cancer is commonly treated by a form of hormone therapy called androgen suppression. This form of treatment, while successful at reducing the cancer cell population, adversely affects quality of life and typically leads to a recurrence of the cancer in an androgen-independent form. Intermit...

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Main Authors: Travis Portz, Yang Kuang, John D. Nagy
Format: Article
Language:English
Published: AIP Publishing LLC 2012-03-01
Series:AIP Advances
Online Access:http://dx.doi.org/10.1063/1.3697848
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spelling doaj-4c21829816f6400cbe8d0977f3265c602020-11-24T20:42:56ZengAIP Publishing LLCAIP Advances2158-32262012-03-0121011002011002-1410.1063/1.3697848078201ADVA clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapyTravis Portz0Yang Kuang1John D. Nagy2School of Computing and Informatics, Arizona State University, Tempe, Arizona 85281, USASchool of Mathematical and Statistical Sciences, Arizona State University, Tempe, Arizona 85287, USADepartment of Biology, Scottsdale Community College, Scottsdale, Arizona 85256, USAProstate cancer is commonly treated by a form of hormone therapy called androgen suppression. This form of treatment, while successful at reducing the cancer cell population, adversely affects quality of life and typically leads to a recurrence of the cancer in an androgen-independent form. Intermittent androgen suppression aims to alleviate some of these adverse affects by cycling the patient on and off treatment. Clinical studies have suggested that intermittent therapy is capable of maintaining androgen dependence over multiple treatment cycles while increasing quality of life during off-treatment periods. This paper presents a mathematical model of prostate cancer to study the dynamics of androgen suppression therapy and the production of prostate-specific antigen (PSA), a clinical marker for prostate cancer. Preliminary models were based on the assumption of an androgen-independent (AI) cell population with constant net growth rate. These models gave poor accuracy when fitting clinical data during simulation. The final model presented hypothesizes an AI population with increased sensitivity to low levels of androgen. It also hypothesizes that PSA production is heavily dependent on androgen. The high level of accuracy in fitting clinical data with this model appears to confirm these hypotheses, which are also consistent with biological evidence.http://dx.doi.org/10.1063/1.3697848
collection DOAJ
language English
format Article
sources DOAJ
author Travis Portz
Yang Kuang
John D. Nagy
spellingShingle Travis Portz
Yang Kuang
John D. Nagy
A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
AIP Advances
author_facet Travis Portz
Yang Kuang
John D. Nagy
author_sort Travis Portz
title A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
title_short A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
title_full A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
title_fullStr A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
title_full_unstemmed A clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
title_sort clinical data validated mathematical model of prostate cancer growth under intermittent androgen suppression therapy
publisher AIP Publishing LLC
series AIP Advances
issn 2158-3226
publishDate 2012-03-01
description Prostate cancer is commonly treated by a form of hormone therapy called androgen suppression. This form of treatment, while successful at reducing the cancer cell population, adversely affects quality of life and typically leads to a recurrence of the cancer in an androgen-independent form. Intermittent androgen suppression aims to alleviate some of these adverse affects by cycling the patient on and off treatment. Clinical studies have suggested that intermittent therapy is capable of maintaining androgen dependence over multiple treatment cycles while increasing quality of life during off-treatment periods. This paper presents a mathematical model of prostate cancer to study the dynamics of androgen suppression therapy and the production of prostate-specific antigen (PSA), a clinical marker for prostate cancer. Preliminary models were based on the assumption of an androgen-independent (AI) cell population with constant net growth rate. These models gave poor accuracy when fitting clinical data during simulation. The final model presented hypothesizes an AI population with increased sensitivity to low levels of androgen. It also hypothesizes that PSA production is heavily dependent on androgen. The high level of accuracy in fitting clinical data with this model appears to confirm these hypotheses, which are also consistent with biological evidence.
url http://dx.doi.org/10.1063/1.3697848
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