| Abstract: |
| Glioblastoma multiforme (GBM) is an aggressive brain tumor that is extremely fatal. Gliomas are characterized by excessive amounts of cell proliferation and migration, which makes them impossible to remove with surgery alone. While immunotherapy has proven to be an effective treatment in many cancers, phase III clinical trials with GBM have failed to show promise possibly due to the characteristically high immune-suppressive glioma microenvironment. Experimental evidence suggests that a combination treatment of immune-checkpoint inhibition and chemokine receptor 2 (CCR2) inhibition extends survival in murine models. We develop and analyze an ordinary differential equation model of glioma-immune system dynamics to investigate how disruption of the CCL2/CCR2 chemokine ligand/receptor axis can weaken the immunosuppressive behavior of the tumor microenvironment and thus allow for more successful treatment via immune-checkpoint inhibition. |
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