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Therapeutic delivery within the tumor is attenuated bystatic pressure and the permeability of the tissue, which ismediated by the extent of ECM remodeling. Additionally, cellularsignaling from stromal fibroblasts limits the efficacy oftreatment. This phenomenon is of particular relevance at the tumorborder, where there is a transitional region from predominantlycancer cells to predominantly stromal cells. These factors promotecancer growth and select for a potentially metastaticsubpopulation. Furthermore, interstitial fluid flow at the tumorborder affects the migration characteristics of cancer cells.Interstitial fluid flow has been implicated in an increase incancer cell invasion, which is the major effector of cancer spreadand decreased patient viability. In brain cancer, two differentmechanisms have been implicated in this increased invasion, andthis invasion is mediated by both CXCR4 and CD44. Therefore, TMEcomplexity necessitates utilization of robust models to elucidatethe effects of the TME on cancer development and progression. Thecurrent work defines two novel agent-based models that describe andpredict cancer specific outcomes within in vitro TME mimeticsystems. Our models indicate that brain cancer cell invasion isincreased in the presence of interstitial flow, and this increasedinvasion is driven by two specific mechanisms, CXCR4-CXCL12autologous chemotaxis and CD44 mechanotransduction. Additionally,in vitro and in silico models of the tumor border transition zonepredict that regional viability within the breast tumor border isaffected by both fibroblast signaling and transport mechanisms, andthis affect could be selecting for important resistantsubpopulations.

Agent-Based Models of the Tumor Microenvironment: Predicting Flow-Mediated Invasion and Cancer Viability in Response to Interstitial Flow, Chemotherapy, and Stromal Cell Density