Pancreatic Cancer

Cancer of the pancreas is the fourth-leading cause of cancer death in the United States [1]. This solid malignancy is almost always detected late, and five-year survival rates are only 4% and have not substantially improved over the past 30 years. New insights into the dynamics of this lethal disease are urgently needed.

Pancreatic Cancer, like all cancers, is a failure mode whereby tumor cells ignore or otherwise inappropriately respond to the normal biochemical signals that control growth and maintain homeostasis in normal tissue. The transmission of these biochemical signals can be modeled as a reaction-diffusion system, and each cell can be modeled as a state machine consisting of a number of interacting and interdependent signaling pathways. We will use MCAI 2.0, in collaboration with our colleagues at the Translational Genomics Research Institute, to develop new tools for formally reasoning about the dynamics of several biochemical pathways that are known to be critical in pancreatic cancer (see for example Jones et al.’s work [2]).

[1] A. Maitra and R. Hruban. Pancreatic cancer. Annu. Rev. of Patho. Mech. Dis., 3:157 – 188, 2008.

[2] S. Jones et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science, 321(5897):1801-1806, 2008.

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nsfSupported by an Expeditions in Computing award from the National Science Foundation