scholarly journals Mathematical models of therapeutical actions related to tumour and immune system competition

2005 ◽  
Vol 28 (17) ◽  
pp. 2061-2083 ◽  
Author(s):  
Elena De Angelis ◽  
Pierre-Emmanuel Jabin
Author(s):  
Abdulkareem Ibrahim Afolabi ◽  
Normah Maan

<p class="0abstract">Biomedical literature suggested that the tumor-immune system physical phenomenon usually climaxes into either tumor elimination or escape. In retort to the phenomenological mechanics of tumor-immune system interaction, researchers had used Mathematical models mostly prey-predator and competitive extensively, to model the dynamics of tumor immune system interaction. However, these models had not accounted for total elimination and, or escape of tumor as hypothesizes by immunoediting hypotheses. In this work, we propose a dual aggressive model based on the biological narration of tumor-immune system interactions. The stability analyses of tumor-negative steady state are stable if the rate at which body cells dies is less than their proliferation rate a confirmation of biological listed causes of the tumor. The tumor-positive steady state is always unstable and saddle with the likelihood of either elimination or escape of tumor. Numerical analysis validates our analytical results and provides insight into the dynamics of the benignant and malignant tumor. The immunosuppression by tumor is not only visible but also validated by both analytical and numerical analysis.</p>


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Filippo Castiglione ◽  
Francesco Pappalardo ◽  
Carlo Bianca ◽  
Giulia Russo ◽  
Santo Motta

It is coming nowadays more clear that in order to obtain a unified description of the different mechanisms governing the behavior and causality relations among the various parts of a living system, the development of comprehensive computational and mathematical models at different space and time scales is required. This is one of the most formidable challenges of modern biology characterized by the availability of huge amount of high throughput measurements. In this paper we draw attention to the importance of multiscale modeling in the framework of studies of biological systems in general and of the immune system in particular.


2010 ◽  
Vol 73 (1) ◽  
pp. 2-32 ◽  
Author(s):  
Raluca Eftimie ◽  
Jonathan L. Bramson ◽  
David J. D. Earn

2018 ◽  
Vol 9 (2) ◽  
pp. 106-118 ◽  
Author(s):  
Diletta Burini ◽  
Elena De Angelis ◽  
Miroslaw Lachowicz

Abstract In the present paper we propose two mathematical models describing, respectively at the microscopic level and at the mesoscopic level, a system of interacting tumor cells and cells of the immune system. The microscopic model is in terms of a Markov chain defined by the generator, the mesoscopic model is developed in the framework of the kinetic theory of active particles. The main result is to prove the transition from the microscopic to mesoscopic level of description.


Author(s):  
И.А. Шаповалова

Современная иммунология не может успешно развиваться без помощи математического моделирования. Математические модели являются эффективным фильтром идей и индикатором правильности выбранных предположений, позволяют дать правильную интерпретацию результатам и выбирать критерии для оценки правильности, могут быть использованы как средство для визуализации результатов вычисления, что помогает дальнейшему развитию вычислительных алгоритмов. Исследование математической модели иммунной системы позволяет сравнивать теоретические и экспериментальные результаты и уточнять предположения, положенные в основу математического моделирования. Иммунная система является высокоразвитой биологической системой, функция которой заключается в выявлении и уничтожении чужеродного агента, поэтому она должна распознавать разнообразных возбудителей. Иммунная система способна к обучению, запоминанию, распознаванию образов, аналогичными свойствами обладают искусственные нейронные сети. Искусственные нейронные сети, подобно биологическим, являются вычислительной системой с огромным числом параллельно функционирующих простых процессоров с огромным числом связей. Нейросетевые алгоритмы используются в кластеризации, визуализации данных, контроле и оптимизации управляемых процессов, разработке искусственных нейронных сетей. В работе исследуется математическая модель иммунной системы, которая моделируется с помощью искусственной нейронной сети и описывается системой дифференциальных уравнений с запаздыванием. При анализе модели используется аппарат математической теории оптимального управления, а именно принцип максимума для систем дифференциальных уравнений с запаздыванием в аргументе функции состояния и аппарат методов оптимизации, базирующийся на методе быстрого автоматического дифференцирования. Вместо традиционных методов программирования используется обучение полносвязной искусственной нейронной сети с помощью метода распространения ошибки. Modern immunology can not be developed successfully without the help of mathematical modeling. Mathematical models are an effective way filter and indicator of the correctness of the selected assumptions. Mathematical models allow us to give a correct interpretation of the results, to select criteria for evaluating the correctness and that help the development of the numerical methods and algorithm. The research of the mathematical model of the immune system allow to compare theoretical and experimental results and clarified mathematical assumptions laid down in the basis of mathematical modeling. The immune system is a highly developed biological system, whose function is to detect and destroy foreign substance, so it needs to recognize a variety of pathogens.The immune system is capable of learning to remember the recognitions of images. The similar properties possess artificial neural networks. Similar to biological ones artificial neural networks are computer systems with a huge number of parallel functioning simple processors and with a large number of connections. Neural networks algorithms are used in clustering, data visualization, control and optimization of processes, the development of artificial neural networks. In the article we consider mathematical model of immune system modeled with the help of artificial multi layer neural net described by the system of differential equations with delay in argument of state functions. The model is analyzed with the help of the theory of optimal control namely the maximum principle of Pontrjagin for the systems of differential equations with delay in argument of the state functions. The method of optimization is based on the method of fast automatic differentiations. Instead of traditional methods of programming the training of the fully connected neural networks and the error propagation method are used.


BIOMATH ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 1905147 ◽  
Author(s):  
Jean Clairambault ◽  
Camille Pouchol

This article is a proceeding survey (deepening a talk given by the first author at the Biomath 2019 International Conference on Mathematical Models and Methods, held in Bedlewo, Poland) of mathematical models of cancer and healthy cell population adaptive dynamics exposed to anticancer drugs, to describe how cancer cell populations evolve toward drug resistance.Such mathematical models consist of partial differential equations (PDEs) structured in continuous phenotypes coding for the expression of drug resistance genes; they involve different functions representing targets for different drugs, cytotoxic and cytostatic, with complementary effects in limiting tumour growth. These phenotypes evolve continuously under drug exposure, and their fate governs the evolution of the cell population under treatment. Methods of optimal control are used, taking inevitable emergence of drug resistance into account, to achieve the best strategies to contain the expansion of a tumour.This evolutionary point of view, which relies on biological observations and resulting modelling assumptions, naturally extends to questioning the very nature of cancer as evolutionary disease, seen not only at the short time scale of a human life, but also at the billion year-long time scale of Darwinian evolution, from unicellular organisms to evolved multicellular organs such as animals and man. Such questioning, not so recent, but recently revived, in cancer studies, may have consequences for understanding and treating cancer.Some open and challenging questions may thus be (non exhaustively) listed as:- May cancer be defined as a spatially localised loss of coherence between tissues in the same multicellular organism, `spatially localised' meaning initially starting from a given organ in the body, but also possibly due to flaws in an individual's rms of evolution towards drug resistance governed by the phenotypes which determine landscape such as imperfect epigenetic control of differentiation genes?- If one assumes that ''The genes of cellular cooperation that evolved with multicellularity about a billion years ago arethe same genes that malfunction in cancer.'', how can these genes besystematically investigated, looking for zones of fragility - that depend on individuals - in the 'tinkering' evolution is made of, tracking local defaults of coherence?- What is such coherence made of and to what extent is the immune system responsible for it (the self and differentiation within the self)?Related to this question of self, what parallelism can be established between the development of multicellularity in different species proceeding from the same origin and the development of the immune system in these different species?


2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Gennady Bocharov ◽  
Jordi Argilaguet ◽  
Andreas Meyerhans

Virus infections represent complex biological systems governed by multiple-level regulatory processes of virus replication and host immune responses. Understanding of the infection means an ability to predict the systems behaviour under various conditions. Such predictions can only rely upon quantitative mathematical models. The model formulations should be tightly linked to a fundamental step called “coordinatization” (Hermann Weyl), that is, the definition of observables, parameters, and structures that enable the link with a biological phenotype. In this review, we analyse the mathematical modelling approaches to LCMV infection in mice that resulted in quantification of some fundamental parameters of the CTL-mediated virus control including the rates of T cell turnover, infected target cell elimination, and precursor frequencies. We show how the modelling approaches can be implemented to address diverse aspects of immune system functioning under normal conditions and in response to LCMV and, importantly, make quantitative predictions of the outcomes of immune system perturbations. This may highlight the notion that data-driven applications of meaningful mathematical models in infection biology remain a challenge.


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