Studying the emergence of invasiveness in tumours using game theory

Basanta, David; Hatzikirou, Haralampos; Deutsch, Andreas

doi:10.1140/epjb/e2008-00249-y

Cited by 80 publications

(96 citation statements)

References 27 publications

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“…Importantly, the results suggest that anti-mitotic treatments alone, despite killing cancer cells, may actually promote tumour progression if eradication of cancer stem cells cannot be achieved (Michor et al, 2005;Dingli and Michor, 2006;Yang and Wechsler-Reya, 2007). Alternatively, in line with observations of Basanta et al (2008), discouraging migration may be an important new means of cancer suppression. How this would be facilitated using agents that rely on possibly counterproductive targeting is not straightforward.…”

Section: Discussionmentioning

confidence: 94%

“…Experiments have also shown proliferation age to be higher near the outer rim in the sub-exponential populations. Basanta et al (2008) have described the interplay of proliferative and motile phenotypes in a developing tumour using game theory, applying fitness cost tradeoffs between the two phenotypes. Motile cells migrate away from cell clusters so that when they become proliferative, they promote tumour expansion.…”

Section: Discussionmentioning

confidence: 99%

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Migration rules: tumours are conglomerates of self-metastases

2009

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Tumours are heterogeneous populations composed of different cells types: stem cells with the capacity for self-renewal and more differentiated cells lacking such ability. The overall growth behaviour of a developing neoplasm is determined largely by the combined kinetic interactions of these cells. By tracking the fate of individual cancer cells using agent-based methods in silico, we apply basic rules for cell proliferation, migration and cell death to show how these kinetic parameters interact to control, and perhaps dictate defining spatial and temporal tumour growth dynamics in tumour development. When the migration rate is small, a single cancer stem cell can only generate a small, self-limited clone because of the finite life span of progeny and spatial constraints. By contrast, a high migration rate can break this equilibrium, seeding new clones at sites outside the expanse of older clones. In this manner, the tumour continually 'self-metastasises'. Counterintuitively, when the proliferation capacity is low and the rate of cell death is high, tumour growth is accelerated because of the freeing up of space for self-metastatic expansion. Changes to proliferation and cell death that increase the rate at which cells migrate benefit tumour growth as a whole. The dominating influence of migration on tumour growth leads to unexpected dependencies of tumour growth on proliferation capacity and cell death. These dependencies stand to inform standard therapeutic approaches, which anticipate a positive response to cell killing and mitotic arrest.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Migration rules: tumours are conglomerates of self-metastases

2009

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“…The production of growth factors by cancer cells therefore is an example of intra-tumor cooperation and can be studied in the framework of evolutionary game theory. Concepts from game theory have been used to describe competition between cancer cells as pairwise games [3,4] with up to four strategies [5][6][7][8][9], and more recently as multiplayer public goods games to model the interactions between different clones within a tumor in well-mixed populations [10,11], in spatially structured populations that resemble monolayers in vitro [12][13][14], and to analyse the Warburg effect [15][16][17][18]; experiments with cancer cells have been used to test the theory [2].…”

Section: From Intra-tumor Cooperation To Tumor-stroma Interactionsmentioning

confidence: 99%

Game Theory of Tumor–Stroma Interactions in Multiple Myeloma: Effect of Nonlinear Benefits

Sartakhti

Manshaei

Archetti

2018

Games

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Cancer cells and stromal cells often exchange growth factors with paracrine effects that promote cell growth: a form of cooperation that can be studied by evolutionary game theory. Previous models have assumed that interactions between cells are pairwise or that the benefit of a growth factor is a linear function of its concentration. Diffusible factors, however, affect multiple cells and generally have nonlinear effects, and these differences are known to have important consequences for evolutionary dynamics. Here, we study tumor-stroma paracrine signaling using a model with multiplayer collective interactions in which growth factors have nonlinear effects. We use multiple myeloma as an example, modelling interactions between malignant plasma cells, osteoblasts, and osteoclasts. Nonlinear benefits can lead to results not observed in linear models, including internal mixed stable equilibria and cyclical dynamics. Models with linear effects, therefore, do not lead to a meaningful characterization of the dynamics of tumor-stroma interactions. To understand the dynamics and the effect of therapies it is necessary to estimate the shape of the benefit functions experimentally and parametrize models based on these functions.

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“…To our knowledge, one of the first applications of spatial solutions in cancer modeling has been presented by Bach et al [14] as a development of angiogenic game [7]. Spatial version of the motility/evasion game is presented in [15]. Many works demonstrate, that the spatial modeling discloses altruistic and cooperative strategies, and strong discrepancies while compared with the mean-field models (e.g.…”

Section: E(p P)mentioning

confidence: 99%

Spatial evolutionary games and radiation induced bystander effect

Krzeslak¹,

Świerniak²

2011

Archives of Control Sciences

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We present an application of evolutionary game theory to modeling of some processes important from oncological point of view. A studied phenomenon is a radiation induced bystander effect, in which three different strategies (phenotypes) of cells take part. The proposed payoff table of fitness, related to environment adaptation and genetic cell behavior, contains costs/profits of bystander effect, choice of apoptotic pathway, producing growth factors and resistance against bystander effect. We consider a game theory model including spatial cells allocation (the game is played on lattice). We discuss also different polymorphic equilibrium points dependent on model parameters, types of spatial games and players distribution.

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Studying the emergence of invasiveness in tumours using game theory

Cited by 80 publications

References 27 publications

Migration rules: tumours are conglomerates of self-metastases

Migration rules: tumours are conglomerates of self-metastases

Game Theory of Tumor–Stroma Interactions in Multiple Myeloma: Effect of Nonlinear Benefits

Spatial evolutionary games and radiation induced bystander effect

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