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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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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