We propose a model of cancer initiation and progression where tumor growth is modulated by an evolutionary coordination game. Evolutionary games of cancer are widely used to model frequency-dependent cell interactions with the most studied games being the Prisoner's Dilemma and public goods games. Coordination games, by their more obscure and less evocative nature, are left understudied, despite the fact that, as we argue, they offer great potential in understanding and treating cancer. In this paper we present the conditions under which coordination games between cancer cells evolve, we propose aspects of cancer that can be modeled as results of coordination games, and explore the ways through which coordination games of cancer can be exploited for therapy. @en

This paper develops and analyzes a Markov chain model for the treatment of cancer. Cancer therapy is modeled as the patient's Markov Decision Problem, with the objective of maximizing the patient's discounted expected quality of life years. Patients make decisions on the duration of therapy based on the progression of the disease as well as their own preferences. We obtain a powerful analytic decision tool through which patients may select their preferred treatment strategy. We illustrate the tradeoffs patients in a numerical example and calculate the value lost to a cohort in suboptimal strategies. In a second model patients may make choices to include drug holidays. By delaying therapy, the patient temporarily forgoes the gains of therapy in order to delay its side effects. We obtain an analytic tool that allows numerical approximations of the optimal times of delay.

@en

We propose a model with two types of cancer cells differentiated by their defense mechanisms against the immune system. “Selfish” cancer cells develop defense mechanisms that benefit the individual cell, whereas “cooperative” cells deploy countermeasures that increase the chance of survival of every cell. Our phenotypes capture the two main features of the tumor's efforts to avoid immune destruction, crypticity against immune cells for the selfish cells, and tumor-induced immunosuppression for the cooperative cells. We identify steady states of the system and show that only homogeneous tumors can be stable in both size and composition. We show that under generic parameter values, a tumor of selfish cells is more benign than a tumor of cooperative cells, and that a treatment against cancer crypticity may promote immunosuppression and increase cancer growth.

@en