Special Issue "Mathematical Biology and Game Theory"

A special issue of Games (ISSN 2073-4336).

Deadline for manuscript submissions: closed (31 October 2018)

Special Issue Editors

Guest Editor
Dr. Mark Broom

Department of Mathematics, City University London, Northampton Square, London EC1V 0HB, UK
Website | E-Mail
Interests: evolutionary game theory; evolutionary graph theory; multiplayer games; food-stealing models; anti-predator defence and signaling; stochastic processes
Guest Editor
Dr. Igor Erovenko

Department of Mathematics and Statistics, University of North Carolina, Greensboro, NC 27402, USA
Website | E-Mail
Interests: evolution of cooperation; vaccination game theory; theoretical ecology
Guest Editor
Dr. Jan Rychtar

Department of Mathematics and Statistics, University of North Carolina, Greensboro, NC 27402, USA
Website | E-Mail
Interests: evolutionary game theory; evolutionary graph theory; stochastic processes; kleptoparasitism
Guest Editor
Dr. Shan Sun

State Key Laboratory of Grassland and Agro-Ecosystems, School of Life Sciences, Lanzhou University, Lanzhou 730000, People’s Republic of China
Website | E-Mail
Interests: evolutionary ecology; evolutionary game theory; interspecific interaction; and evolution of cooperation

Special Issue Information

Dear Colleagues,

We are seeking manuscripts that build and/or analyze game-theoretical models of biological scenarios. We welcome theoretical papers analyzing evolutionary dynamics, adaptive dynamics, evolutionarily stable strategies, and other game-theoretical notions related to mathematical biology. We also solicit papers that apply game theory directly to specific biological problems. Manuscripts applying game-theory to mating, sex allocation, signaling, food competition and foraging in general, the evolution of cooperation, hierarchy formation, predator–prey and host–parasite interactions and coevolution, coevolution of mutualists, epidemics and cancer biology modeling, and speciation are especially welcome.

Dr. Mark Broom
Dr. Igor Erovenko
Dr. Jan Rychtar
Dr. Shan Sun
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Games is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 550 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Evolutionarily stable strategy
  • Evolutionary dynamics
  • Replicator dynamics
  • Adaptive dynamics
  • Game theoretical models
  • Evolution in finite populations
  • Mating games
  • Sex allocation and sex ratio
  • Signaling games
  • Food competition
  • Kleptoparasitism
  • Foraging games
  • Predator-prey interactions and coevolution
  • Host-parasite interactions and coevolution
  • Coevolution of mutualists
  • Hierarchy formations
  • Epidemic models
  • Modeling cancer biology
  • Speciation

Published Papers (5 papers)

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Research

Open AccessFeature PaperArticle
Including Blood Vasculature into a Game-Theoretic Model of Cancer Dynamics
Games 2019, 10(1), 13; https://doi.org/10.3390/g10010013
Received: 23 December 2018 / Revised: 10 February 2019 / Accepted: 25 February 2019 / Published: 11 March 2019
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Abstract
For cancer, we develop a 2-D agent-based continuous-space game-theoretical model that considers cancer cells’ proximity to a blood vessel. Based on castrate resistant metastatic prostate cancer (mCRPC), the model considers the density and frequency (eco-evolutionary) dynamics of three cancer cell types: those that [...] Read more.
For cancer, we develop a 2-D agent-based continuous-space game-theoretical model that considers cancer cells’ proximity to a blood vessel. Based on castrate resistant metastatic prostate cancer (mCRPC), the model considers the density and frequency (eco-evolutionary) dynamics of three cancer cell types: those that require exogenous testosterone ( T + ), those producing testosterone ( T P ), and those independent of testosterone ( T ). We model proximity to a blood vessel by imagining four zones around the vessel. Zone 0 is the blood vessel. As rings, zones 1–3 are successively farther from the blood vessel and have successively lower carrying capacities. Zone 4 represents the space too far from the blood vessel and too poor in nutrients for cancer cell proliferation. Within the other three zones that are closer to the blood vessel, the cells’ proliferation probabilities are determined by zone-specific payoff matrices. We analyzed how zone width, dispersal, interactions across zone boundaries, and blood vessel dynamics influence the eco-evolutionary dynamics of cell types within zones and across the entire cancer cell population. At equilibrium, zone 3’s composition deviates from its evolutionary stable strategy (ESS) towards that of zone 2. Zone 2 sees deviations from its ESS because of dispersal from zones 1 and 3; however, its composition begins to resemble zone 1’s more so than zone 3’s. Frequency-dependent interactions between cells across zone boundaries have little effect on zone 2’s and zone 3’s composition but have decisive effects on zone 1. The composition of zone 1 diverges dramatically from both its own ESS, but also that of zone 2. That is because T + cells (highest frequency in zone 1) benefit from interacting with T P cells (highest frequency in zone 2). Zone 1 T + cells interacting with cells in zone 2 experience a higher likelihood of encountering a T P cell than when restricted to their own zone. As expected, increasing the width of zones decreases these impacts of cross-boundary dispersal and interactions. Increasing zone widths increases the persistence likelihood of the cancer subpopulation in the face of blood vessel dynamics, where the vessel may die or become occluded resulting in the “birth” of another blood vessel elsewhere in the space. With small zone widths, the cancer cell subpopulations cannot persist. With large zone widths, blood vessel dynamics create cancer cell subpopulations that resemble the ESS of zone 3 as the larger area of zone 3 and its contribution to cells within the necrotic zone 4 mean that zones 3 and 4 provide the likeliest colonizers for the new blood vessel. In conclusion, our model provides an alternative modeling approach for considering density-dependent, frequency-dependent, and dispersal dynamics into cancer models with spatial gradients around blood vessels. Additionally, our model can consider the occurrence of circulating tumor cells (cells that disperse into the blood vessel from zone 1) and the presence of live cancer cells within the necrotic regions of a tumor. Full article
(This article belongs to the Special Issue Mathematical Biology and Game Theory)
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Open AccessArticle
When and How Does Mutation-Generated Variation Promote the Evolution of Cooperation?
Games 2019, 10(1), 4; https://doi.org/10.3390/g10010004
Received: 31 October 2018 / Revised: 16 December 2018 / Accepted: 25 December 2018 / Published: 14 January 2019
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Abstract
Mutation-generated variation in behavior is thought to promote the evolution of cooperation. Here, we study this by distinguishing two effects of mutation in evolutionary games of the finitely repeated Prisoner’s Dilemma in infinite asexual populations. First, we show how cooperation can evolve through [...] Read more.
Mutation-generated variation in behavior is thought to promote the evolution of cooperation. Here, we study this by distinguishing two effects of mutation in evolutionary games of the finitely repeated Prisoner’s Dilemma in infinite asexual populations. First, we show how cooperation can evolve through the direct effect of mutation, i.e., the fitness impact that individuals experience from interactions with mutants before selection acts upon these mutants. Whereas this direct effect suffices to explain earlier findings, we question its generality because mutational variation usually generates the highest direct fitness impact on unconditional defectors (AllD). We identify special conditions (e.g., intermediate mutation rates) for which cooperation can be favored by an indirect effect of mutation, i.e., the fitness impact that individuals experience from interactions with descendants of mutants. Simulations confirm that AllD-dominated populations can be invaded by cooperative strategies despite the positive direct effect of mutation on AllD. Thus, here the indirect effect of mutation drives the evolution of cooperation. The higher level of cooperation, however, is not achieved by individuals triggering reciprocity (‘genuine cooperation’), but by individuals exploiting the willingness of others to cooperate (‘exploitative cooperation’). Our distinction between direct and indirect effects of mutation provides a new perspective on how mutation-generated variation alters frequency-dependent selection. Full article
(This article belongs to the Special Issue Mathematical Biology and Game Theory)
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Open AccessArticle
Evolution of Cooperation in Public Goods Games with Stochastic Opting-Out
Games 2019, 10(1), 1; https://doi.org/10.3390/g10010001
Received: 13 December 2018 / Accepted: 19 December 2018 / Published: 21 December 2018
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Abstract
We study the evolution of cooperation in group interactions where players are randomly drawn from well-mixed populations of finite size to participate in a public goods game. However, due to the possibility of unforeseen circumstances, each player has a fixed probability of being [...] Read more.
We study the evolution of cooperation in group interactions where players are randomly drawn from well-mixed populations of finite size to participate in a public goods game. However, due to the possibility of unforeseen circumstances, each player has a fixed probability of being unable to participate in the game, unlike previous models which assume voluntary participation. We first study how prescribed stochastic opting-out affects cooperation in finite populations, and then generalize for the limiting case of large populations. Because we use a pairwise comparison updating rule, our results apply to both genetic and behavioral evolution mechanisms. Moreover, in the model, cooperation is favored by natural selection over both neutral drift and defection if the return on investment exceeds a threshold value depending on the population size, the game size, and a player’s probability of opting-out. Our analysis further shows that, due to the stochastic nature of the opting-out in finite populations, the threshold of return on investment needed for natural selection to favor cooperation is actually greater than the one corresponding to compulsory games with the equal expected game size. We also use adaptive dynamics to study the co-evolution of cooperation and opting-out behavior. Indeed, given rare mutations minutely different from the resident population, an analysis based on adaptive dynamics suggests that over time the population will tend towards complete defection and non-participation, and subsequently cooperators abstaining from the public goods game will stand a chance to emerge by neutral drift, thereby paving the way for the rise of participating cooperators. Nevertheless, increasing the probability of non-participation decreases the rate at which the population tends towards defection when participating. Our work sheds light on understanding how stochastic opting-out emerges in the first place and on its role in the evolution of cooperation. Full article
(This article belongs to the Special Issue Mathematical Biology and Game Theory)
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Open AccessArticle
Game Theoretical Model of Cancer Dynamics with Four Cell Phenotypes
Games 2018, 9(3), 61; https://doi.org/10.3390/g9030061
Received: 30 June 2018 / Revised: 25 August 2018 / Accepted: 29 August 2018 / Published: 2 September 2018
Cited by 1 | PDF Full-text (558 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
The development of a cancerous tumor requires affected cells to collectively display an assortment of characteristic behaviors that contribute differently to its growth. A heterogeneous population of tumor cells is far more resistant to treatment than a homogeneous one as different cell types [...] Read more.
The development of a cancerous tumor requires affected cells to collectively display an assortment of characteristic behaviors that contribute differently to its growth. A heterogeneous population of tumor cells is far more resistant to treatment than a homogeneous one as different cell types respond dissimilarly to treatments; yet, these cell types are also in competition with one another. This paper models heterogeneous cancer cell interactions within the tumor mass through several game theoretic approaches including classical normal form games, replicator dynamics, and spatial games. Our concept model community consists of four cell strategies: an angiogenesis-factor-producing cell, a proliferative cell, a cytotoxin producing cell, and a neutral stromal cell. By comparing pairwise strategic interactions, invasibility and counter-invasibility, we establish conditions for dominance and the existence of both monomorphic and polymorphic equilibria. The spatial game supports co-occurrence among multiple subpopulations in accordance with biological observations of developing tumors. As the tumor progresses from primarily stromal cells to a more malignant state, angiogenic and cytotoxic cells form clusters while proliferative cells are widespread. The clustering of certain subpopulations suggests insight into the behaviors of cancer cells that could influence future treatment strategies. Full article
(This article belongs to the Special Issue Mathematical Biology and Game Theory)
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Open AccessArticle
Computation of Sparse and Dense Equilibrium Strategies of Evolutionary Games
Games 2018, 9(3), 46; https://doi.org/10.3390/g9030046
Received: 8 May 2018 / Revised: 1 July 2018 / Accepted: 4 July 2018 / Published: 7 July 2018
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Abstract
The evolution of social or biological species can be modeled as an evolutionary game with the equilibrium strategies of the game as prediction for the ultimate distributions of species in population, when some species may survive with positive proportions, while others become extinct. [...] Read more.
The evolution of social or biological species can be modeled as an evolutionary game with the equilibrium strategies of the game as prediction for the ultimate distributions of species in population, when some species may survive with positive proportions, while others become extinct. We say a strategy is dense if it contains a large and diverse number of positive species, and is sparse if it has only a few dominant ones. Sparse equilibrium strategies can be found relatively easily, while dense ones are more computationally costly. Here we show that by formulating a “complementary” problem for the computation of equilibrium strategies, we are able to reduce the cost for computing dense equilibrium strategies much more efficiently. We describe the primary and complementary algorithms for computing dense as well as sparse equilibrium strategies, and present test results on randomly generated games as well as a more biologically related one. In particular, we demonstrate that the complementary algorithm is about an order of magnitude faster than the primary algorithm to obtain the dense equilibrium strategies for all our test cases. Full article
(This article belongs to the Special Issue Mathematical Biology and Game Theory)
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