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The focus of pancreatic cancer research has been shifted from pancreatic cancer cells towards their microenvironment, involving pancreatic stellate cells that interact with cancer cells and influence tumor progression. To quantitatively understand the pancreatic cancer microenvironment, we construct a computational model for intracellular signaling networks of cancer cells and stellate cells as well as their intercellular communication. We extend the rule-based BioNetGen language to depict intra- and inter-cellular dynamics using discrete and continuous variables respectively. Our framework also enables a statistical model checking procedure for analyzing the system behavior in response to various perturbations. The results demonstrate the predictive power of our model by identifying important system properties that are consistent with existing experimental observations. We also obtain interesting insights into the development of novel therapeutic strategies for pancreatic cancer.
Prediction of Overall Survival (OS) of brain cancer patients from multi-modal MRI is a challenging field of research. Most of the existing literature on survival prediction is based on Radiomic features, which does not consider either non-biological
To enable personalized cancer treatment, machine learning models have been developed to predict drug response as a function of tumor and drug features. However, most algorithm development efforts have relied on cross validation within a single study
Central nervous system (CNS) tumors come with the vastly heterogeneous histologic, molecular and radiographic landscape, rendering their precise characterization challenging. The rapidly growing fields of biophysical modeling and radiomics have shown
Cox proportional hazard model (CPH) is commonly used in clinical research for survival analysis. In quantitative medical imaging (radiomics) studies, CPH plays an important role in feature reduction and modeling. However, the underlying linear assump
Multiple myeloma is a plasma cell cancer that leads to a dysregulated bone remodeling process. We present a partial differential equation model describing the dynamics of bone remodeling with the presence of myeloma tumor cells. The model explicitly