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Admon2017 - Modelling tumor growth with immune response and drug using ordinary differential equations

ABSTRACT: Modelling tumor growth with immune response and drug using ordinary differential equations Mohd Rashid Admon, Normah Maan This is a mathematical study about tumor growth from a different perspective, with the aim of predicting and/or controlling the disease. The focus is on the effect and interaction of tumor cell with immune and drug. This paper presents a mathematical model of immune response and a cycle phase specific drug using a system of ordinary differential equations. Stability analysis is used to produce stability regions for various values of certain parameters during mitosis. The stability region of the graph shows that the curve splits the tumor decay and growth regions in the absence of immune response. However, when immune response is present, the tumor growth region is decreased. When drugs are considered in the system, the stability region remains unchanged as the system with the presence of immune response but the population of tumor cells at interphase and metaphase is reduced with percentage differences of 1.27 and 1.53 respectively. The combination of immunity and drug to fight cancer provides a better method to reduce tumor population compared to immunity alone.

SUBMITTER: Mohammad Umer Sharif Shohan

PROVIDER: BIOMD0000000904 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000904?filename=Admon2017.cps	Other
	BIOMD0000000904?filename=Admon2017.sedml	Other
	BIOMD0000000904?filename=Admon2017.xml	Xml

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Project description:The paper describes a simple model of tumor immunotherapy. Created by COPASI 4.25 (Build 207) This model is described in the article: Predicting success or failure of immunotherapy for cancer: insights from a clinically applicable mathematical model Charles F Babbs Am J Cancer Res 2012;2(2):204-213 Abstract: The objective of this study was to create a clinically applicable mathematical model of immunotherapy for cancer and use it to explore differences between successful and unsuccessful treatment scenarios. The simplified predator-prey model includes four lumped parameters: tumor growth rate, g; immune cell killing efficiency, k; immune cell signaling factor, λ; and immune cell half-life decay, μ. The predator-prey equations as functions of time, t, for nor- malized tumor cell numbers, y, (the prey) and immunocyte numbers, x, (the predators) are: dy/dt = gy – kx and dx/dt = λxy – μx. A parameter estimation procedure that capitalizes on available clinical data and the timing of clinically observable phenomena gives mid-range benchmarks for parameters representing the unstable equilibrium case in which the tumor neither grows nor shrinks. Departure from this equilibrium results in oscillations in tumor cell num- bers and in many cases complete elimination of the tumor. Several paradoxical phenomena are predicted, including increasing tumor cell numbers prior to a population crash, apparent cure with late recurrence, one or more cycles of tumor growth prior to eventual tumor elimination, and improved tumor killing with initially weaker immune parame- ters or smaller initial populations of immune cells. The model and the parameter estimation techniques are easily adapted to various human cancers that evoke an immune response. They may help clinicians understand and predict certain strange and unexpected effects in the world of tumor immunity and lead to the design of clinical trials to test improved treatment protocols for patients. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Admon2017 - Modelling tumor growth with immune response and drug using ordinary differential equations

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