Dataset Information

Frascoli2014 - A dynamical model of tumour immunotherapy

ABSTRACT: This is a coupled ordinary differential equation model of tumour-immune dynamics, accounting for biological and clinical factors which regulate the interaction rates of cytotoxic T lymphocytes on the surface of the tumour mass.

SUBMITTER: Johannes Meyer

PROVIDER: BIOMD0000000787 | BioModels | 2019-08-12

REPOSITORIES: BioModels

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A dynamical model of tumour immunotherapy.

Frascoli Federico F Kim Peter S PS Hughes Barry D BD Landman Kerry A KA

Mathematical biosciences 20140420

A coupled ordinary differential equation model of tumour-immune dynamics is presented and analysed. The model accounts for biological and clinical factors which regulate the interaction rates of cytotoxic T lymphocytes on the surface of the tumour mass. A phase plane analysis demonstrates that competition between tumour cells and lymphocytes can result in tumour eradication, perpetual oscillations, or unbounded solutions. To investigate the dependence of the dynamic behaviour on model parameters ...[more]

PMID: 24759513

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Project description:Webb2002 - Fas/FasL mediated tumor T-cell interaction This deterministic model of immunological surveillance involving tumour cell–T-lymphocyte interaction, cell surface expression of Fas/FasL, and their secreted soluble forms. This model is described in the article: Cells behaving badly: a theoretical model for the Fas/FasL system in tumour immunology. Webb SD, Sherratt JA, Fish RG. Math Biosci 2002 Sep-Oct; 179(2): 113-129 Abstract: One proposed mechanism of tumour escape from immune surveillance is tumour up-regulation of the cell surface ligand FasL, which can lead to apoptosis of Fas receptor (Fas) positive lymphocytes. Based upon this 'counterattack', we have developed a mathematical model involving tumour cell-lymphocyte interaction, cell surface expression of Fas/FasL, and their secreted soluble forms. The model predicts that (a) the production of soluble forms of Fas and FasL will lead to the down-regulation of the immune response; (b) matrix metalloproteinase (MMP) inactivation should lead to increased membrane FasL and result in a higher rate of Fas-mediated apoptosis for lymphocytes than for tumour cells. Recent studies on cancer patients lend support for these predictions. The clinical implications are two-fold. Firstly, the use of broad spectrum MMP inhibitors as anti-angiogenic agents may be compromised by their adverse effect on tumour FasL up-regulation. Also, Fas/FasL interactions may have an impact on the outcome of numerous ongoing immunotherapeutic trials since the final common pathway of all these approaches is the transduction of death signals within the tumour cell. This model is hosted on BioModels Database and identified by: BIOMD0000000661. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. 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.

Dataset Information

Frascoli2014 - A dynamical model of tumour immunotherapy

Publications

A dynamical model of tumour immunotherapy.

Similar Datasets

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