|Start Date / Time||October 5, 2022 at 9:00 AM|
|End Date / Time||October 5, 2022 at 10:00 AM|
|Presenter Name||Amanda Ruelas, Amelia Cephas (grad students)|
|Presentation Title||See Below|
|Status||This meeting is currently scheduled|
Students and Postdocs
“Pancreatic Ductal-Derived Metaplasia and Neoplasia”
Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer-related deaths in the United States and will likely become the second by 2030. While ductal cells are known as the dominant cell of origin in humans, current mouse models show that ducts are refractory to transformation. Using a combination of genetically engineered mouse models, immunohistology and bioinformatic analyses, I will describe our current efforts to investigate the pathological and genetic changes to pancreatic ducts in response to oncogenic mutations in chronic injury, which enhances their susceptibility to transformation.
"Tuft Cells Inhibit
Pancreatic Injury Through the
Synthesis and Secretion of IL-25"
Tuft cells are solitary chemosensory cells that are normally absent from the murine pancreas but transdifferentiate from acinar cells in response to chronic injury or oncogenic mutation. We have found that tuft cell ablation enhances pancreatitis and alters the immune infiltrate. Preliminary data show that tuft cells are the solitary source of anti-inflammatory cytokine IL-25 in pancreatitis and pancreas specific ablation of IL25 enhances pancreatic injury. We are using genetically engineered mouse models to test the hypothesis that tuft cells inhibit inflammation and preserve organ function through the synthesis and secretion of IL-25.