Mentor(s): Payton Stevens and Mohamed Dawood

Macrophages, immune cells derived from white blood cells, are essential for combating disease. Pancreatic cancer manipulates the functions of these cells, diminishing their collective immune response. Dr. Payton Stevens’ lab at Miami University aims to investigate this phenomenon in the very near future. In the pancreatic tumor microenvironment, anti-cancer M1 macrophage phenotypes are altered to pro-cancer M2 phenotypes. This research will analyze M1 and M2 macrophage levels via immunohistochemical (IHC) staining of tissues in a mouse pancreatic cancer model (the KPC model), which have pancreatic-specific oncogenic mutations. The study will compare typical KPC tumors and tumors of KPC mice lacking Frizzled 6 (Fzd6). Fzd6 is a Wnt pathway receptor linked to cell development and tissue organization that Dr. Stevens found promotes pancreatic cancer progression. It is hypothesized that the absence of Fzd6 will reduce pro-cancer macrophage alterations, potentially mitigating immune suppression in the tumor microenvironment. IHC techniques involve embedding tissues in paraffin wax, sectioning, deparaffinizing, rehydrating, and staining to visualize immune components. By examining the connection between Fzd6 and macrophage behavior, the lab aims to uncover its role in macrophage transformation. The findings of this study have the potential to provide valuable insights for developing enhanced immunotherapies for pancreatic cancer.

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