The presence of driver mutations and subsequent clonal expansion by Darwinian evolution does not explain dormancy and re-emergence of cancer from a community of cancer and host cells (including stromal… Click to show full abstract
The presence of driver mutations and subsequent clonal expansion by Darwinian evolution does not explain dormancy and re-emergence of cancer from a community of cancer and host cells (including stromal and immune cells). Dormancy appears to be a slow-driven, interaction-dominated, threshold system which is poorly prognosed. At the simplest level, we view cancer cells interacting with host cells via complex, non-linear population dynamics, which can lead to very non-intuitive but perhaps deterministic and understandable progression dynamics of cancer. We explore here the dynamics of host-cancer cell populations in the presence of (1) payoffs gradients and (2) perturbation due to cell migration to determine to what extent the time-dependence of the populations can be quantitatively understood in spite of the underlying complexity of the individual agents. The population dynamics presented here provide a model system for the clinic to map the payoffs matrices and suggest new avenues to predict drug dosages. Citation Format: Robert H. Austin. Game theory and personalized cancer treatment. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr IA04.
               
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