Computational modeling of cell signaling and mutations in pancreatic cancer
Telmer, C. A.; Sayed, K.; Butchy, A. A.; Bocan, K.; Kaltenmeier, C.; Lotze, M. T.; Miskov-Zivanov, N.
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Published research articles are rich sources of data when the knowledge is incorporated into models. Complex biological systems benefit from computational modelings ability to elucidate dynamics, explain data and address hypotheses. Modeling of pancreatic cancer could guide treatment of this devastating disease that has a known mutational profile disrupting signaling pathways but no reliable therapies. The approach described here is to utilize discrete modeling of the major signaling pathways, metabolism and the tumor microenvironment including macrophages. This modeling approach allows for abstraction in order to assemble large networks to capture numerous facets of the biological system under investigation. The Hallmarks of Cancer are represented as the processes of apoptosis, autophagy, cell cycle progression, inflammation, immune response, oxidative phosphorylation and proliferation. The model is initialized with pancreatic cancer receptors and mutations and simulated in time. The model portrays the hallmarks of cancer and suggests combinations of inhibitors as therapies.
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