Mathematical modelling of the innate and adaptive immune response to solid tumours
type: CreativeWork
description: In this thesis mathematical models describing the growth of a solid tumour in the presence of an immune response are presented. Specifically, attention is focused on the interactions between cytotoxic T-lymphocytes (CTLs) and tumour cells in a small, avascular multicellular tumour. At this stage of the disease the CTLs and the tumour cells are considered to be in a state of dynamic equilibrium or cancer dormancy. The precise biochemical and cellular mechanisms by which CTLs can control a cancer and keep it in a dormant state are still not completely understood from a biological and immunological point of view. The mathematical models focus on the spatio-temporal dynamics of tumour cells, immune cells, chemokines and “chemo-repellors” in an immunogenic tumour. The CTLs and tumour cells are assumed to migrate and interact with each other in such a way that lymphocyte-tumour cell complexes are formed. These complexes result in either the death of the tumour cells (the normal situation) or the inactivation of the lymphocytes and consequently the survival of the tumour cells. In the latter case, we assume that each tumour cell which survives its “brief encounter” with the CTLs undergoes certain beneficial phenotypic changes. We explore the dynamics of the model under these assumptions and show that the process of the immuno-evasion can arise as a consequence of these encounters.Our computational simulations suggest that the proposed mechanism is able to mimic various dynamics of immunoevasion during the lifespan of a mouse. We also highlight the differential spatiotemporal contributions to evasion due, respectively, to: i) a decrease in the probability pi of being lethally hit; ii) a decrease in the probability, embedded in k+ i , that a tumour cell is recognized by a CTL. In particular, our model suggests that a decrease in the parameters pi is needed to produce evasion, which does not occur in the case where pi remains constant at its baseline level inferred from the e…
abstract: In this thesis mathematical models describing the growth of a solid tumour in the presence of an immune response are presented. Specifically, attention is focused on the interactions between cytotoxic T-lymphocytes (CTLs) and tumour cells in a small, avascular multicellular tumour. At this stage of the disease the CTLs and the tumour cells are considered to be in a state of dynamic equilibrium or cancer dormancy. The precise biochemical and cellular mechanisms by which CTLs can control a cancer and keep it in a dormant state are still not completely understood from a biological and immunological point of view. The mathematical models focus on the spatio-temporal dynamics of tumour cells, immune cells, chemokines and “chemo-repellors” in an immunogenic tumour. The CTLs and tumour cells are assumed to migrate and interact with each other in such a way that lymphocyte-tumour cell complexes are formed. These complexes result in either the death of the tumour cells (the normal situation) or the inactivation of the lymphocytes and consequently the survival of the tumour cells. In the latter case, we assume that each tumour cell which survives its “brief encounter” with the CTLs undergoes certain beneficial phenotypic changes. We explore the dynamics of the model under these assumptions and show that the process of the immuno-evasion can arise as a consequence of these encounters.Our computational simulations suggest that the proposed mechanism is able to mimic various dynamics of immunoevasion during the lifespan of a mouse. We also highlight the differential spatiotemporal contributions to evasion due, respectively, to: i) a decrease in the probability pi of being lethally hit; ii) a decrease in the probability, embedded in k+ i , that a tumour cell is recognized by a CTL. In particular, our model suggests that a decrease in the parameters pi is needed to produce evasion, which does not occur in the case where pi remains constant at its baseline level inferred from the e…
author: Al-Tameemi, Mohannad Musa Eisa
language: eng
keywords: Cancer, Immune response, Mathematical model
date published: 2011
date modified: 2026-07-24T02:07:25Z
provider: University of Dundee
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Dundee