Dataset Information

Wilkie2013r - immune-induced cancer dormancy and immune evasion-resistance

ABSTRACT: The paper describes a model of immune-induced cancer dormancy and immune evasion with resistance. Created by COPASI 4.25 (Build 207) This model is described in the article: Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion Kathleen P. Wilkie and Philip Hahnfeldt Interface Focus 3: 20130010 Abstract: Cancer dormancy, a state in which cancer cells persist in a host without sig- nificant growth, is a natural forestallment of progression to manifest disease and is thus of great clinical interest. Experimental work in mice suggests that in immune-induced dormancy, the longer a cancer remains dormant in a host, the more resistant the cancer cells become to cytotoxic T-cell-mediated killing. In this work, mathematical models are used to analyse the possible causative mechanisms of cancer escape from immune-induced dormancy. Using a data-driven approach, both decaying efficacy in immune predation and immune recruitment are analysed with results suggesting that decline in recruitment is a stronger determinant of escape than increased resistance to predation. Using a mechanistic approach, the existence of an immune- resistant cancer cell subpopulation is considered, and the effects on cancer dormancy and potential immunoediting mechanisms of cancer escape are analysed and discussed. The immunoediting mechanism assumes that the immune system selectively prunes the cancer of immune-sensitive cells, which is shown to cause an initially heterogeneous population to become a more homogeneous, and more resistant, population. The fact that this selec- tion may result in the appearance of decreasing efficacy in T-cell cytotoxic effect with time in dormancy is also demonstrated. This work suggests that through actions that temporarily delay cancer growth through the targeted removal of immune-sensitive subpopulations, the immune response may actually progress the cancer to a more aggressive state. 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.

SUBMITTER: Jinghao Men

PROVIDER: BIOMD0000000752 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000752?filename=Wilkie2013r-biopax2.owl	Owl
	BIOMD0000000752?filename=Wilkie2013r-biopax3.owl	Owl
	BIOMD0000000752?filename=Wilkie2013r-matlab.m	Other
	BIOMD0000000752?filename=Wilkie2013r-octave.m	Other
	BIOMD0000000752?filename=Wilkie2013r.cps	Other

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Publications

Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion.

Wilkie Kathleen P KP Hahnfeldt Philip P

Interface focus 20130801 4

Cancer dormancy, a state in which cancer cells persist in a host without significant growth, is a natural forestallment of progression to manifest disease and is thus of great clinical interest. Experimental work in mice suggests that in immune-induced dormancy, the longer a cancer remains dormant in a host, the more resistant the cancer cells become to cytotoxic T-cell-mediated killing. In this work, mathematical models are used to analyse the possible causative mechanisms of cancer escape from ...[more]

PMID: 24511375

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Project description:The paper describes a basic model of immune-induced cancer dormancy and immune evasion. Created by COPASI 4.25 (Build 207) This model is described in the article: Mathematical models of immune-induced cancer dormancy and the emergence of immune evasion Kathleen P. Wilkie and Philip Hahnfeldt Interface Focus 3: 20130010 Abstract: Cancer dormancy, a state in which cancer cells persist in a host without sig- nificant growth, is a natural forestallment of progression to manifest disease and is thus of great clinical interest. Experimental work in mice suggests that in immune-induced dormancy, the longer a cancer remains dormant in a host, the more resistant the cancer cells become to cytotoxic T-cell-mediated killing. In this work, mathematical models are used to analyse the possible causative mechanisms of cancer escape from immune-induced dormancy. Using a data-driven approach, both decaying efficacy in immune predation and immune recruitment are analysed with results suggesting that decline in recruitment is a stronger determinant of escape than increased resistance to predation. Using a mechanistic approach, the existence of an immune- resistant cancer cell subpopulation is considered, and the effects on cancer dormancy and potential immunoediting mechanisms of cancer escape are analysed and discussed. The immunoediting mechanism assumes that the immune system selectively prunes the cancer of immune-sensitive cells, which is shown to cause an initially heterogeneous population to become a more homogeneous, and more resistant, population. The fact that this selec- tion may result in the appearance of decreasing efficacy in T-cell cytotoxic effect with time in dormancy is also demonstrated. This work suggests that through actions that temporarily delay cancer growth through the targeted removal of immune-sensitive subpopulations, the immune response may actually progress the cancer to a more aggressive state. 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.