Akman Yıldız, Tuğba

Elliott, Samantha L.

Köse, Emek

English

ISU ReD: Research and eData

Presentation for the Symposium on BEER November 2020Mathematical Modeling of Pancreatic Cancer withClinical DataTuğba Akman Yıldız1,*, Emek Köse2, Samantha L. Elliott31Department of Industrial Engineering, Faculty of Engineering, University of Turkish Aeronautical Association,06790 Ankara, Turkey2Department of Mathematics and Computer Science, St. Mary’s College of Maryland, St. Mary’s City, MD 20619,U.S.A.3Department of Biology, St. Mary’s College of Maryland, St. Mary’s City, MD 20619, U.S.A.takman@thk.edu.trPancreatic cancer is a highly fatal disease and difficulties in diagnosis result in poor survival outcomes.Indeed, five-year survival rate is approximately 8%. In this study, the model proposed by He and Xu [2] hasbeen considered where different cell types, such as pancreatic cancer cells, pancreatic stellate cells and someimmune cells, and some cytokines, such as IL-2 concentration, IFN-γ concentration and TGF-β concentrationhave been included. We extend this model with the cancer stem cells to follow cancer progression. Moreover,the experimental data presented by Cioffi et al. [1] have been used to find the patient specific parameters suchas tumor growth rate, inverse carrying capacity and activation rate of pancreatic stellate cells. As treatmentchoices, chemotherapy (with Abraxane and Gemcitabine) and immunotherapy (with Anti-CD47 treatment)have been incorporated into the model and simulation results have been compared with the clinical data.Then, optimal drug protocols have been investigated with different immune strengths and initial conditions.Based on our numerical findings, it is revealed that the most successful treatment strategy is the combinationtreatment and drug dose is more critical than drug scheduling [3]. However, high drug dose may not bepreferable due to side effects. Therefore, we believe that this study will encourage new drug studies not onlyto reduce side effects of therapy, but also to stop cancer progression.References[1] M. Cioffi, S. Trabulo, M. Hidalgo, E. Costello, W. Greenhalf, M. Erkan, J. Kleeff, B. Sainz, C. Heeschen,Inhibition of CD47 effectively targets pancreatic cancer stem cells via dual mechanisms, Clinical cancerresearch, 21 (10) (2015) 2325–2337.[2] D.H. He, J.X. Xu, A mathematical model of pancreatic cancer with two kinds of treatments, Journal ofBiological Systems, 25 (01) (2017) 83–104.[3] T. Akman Yıldız, E. Köse, S.L. Elliott, Mathematical Modeling of Pancreatic Cancer Treatment withCancer Stem Cells, Manuscript submitted for publication (2020).

Mathematical Modeling of Pancreatic Cancer with Clinical Data

https://ir.library.illinoisstate.edu/cgi/viewcontent.cgi?filename=0&article=1457&context=beer&type=additional

Mathematical Modeling of Pancreatic Cancer with Clinical Data

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ISU ReD: Research and eData