Carinna Solano-Vargas
Research Mentor(s): Yaqing Zhang
Research Mentor School/College/Department: Surgery
Presentation Date: 08/03/2022
Presentation Type: Poster
Poster Number: 24
Session: Session II: 1:30 – 2:20pm
Room: League Ballroom
Authors: Carinna Solano-Vargas, Padma Kadiyala, Wenting Du, Yaqing Zhang, Marina Pasca di Magliano
Abstract
Pancreatic cancer makes up three percent of all cancer diagnoses and seven percent of cancer deaths in the US. The five-year survival rate is low and the tumors often reoccur after surgery due to most diagnoses made at late stage of tumor progression. Research on pancreatic cancer is extremely important for us to gain an understanding about tumor progression and be able to diagnose it earlier. One of the hallmark characteristics of pancreas cancer is the presence of stroma and immunosuppressive cells. Among the stromal cells, cancer associated fibroblasts secrete factors that support tumor growth through the recruitment of immunosuppressive cells. Our preliminary data show that the signal transducer and activator of transcription 3 (STAT3) is activated in cancer associated fibroblast in pancreas cancer. STAT3 is a transcription factor that plays a role in signaling pathways related to tumor progression and its evasion of the immune system. When it becomes activated by phosphorylation, it signals cells to stop apoptosis and continue proliferation. We hypothesize that STAT3 signaling drives cancer associated fibroblast reprogramming, which in turn promotes recruitment of immunosuppressive cells to pancreas cancer. For our study, we are using a genetically engineered mouse model in which we knocked out STAT3 specifically in fibroblasts. Using techniques like immunofluorescence, we were able to visualize the consequence of STAT3 deletion on pancreas cancer tumor microenvironment. Our long term goal is to further evaluate the role of STAT3 in fibroblasts which would allow us to design better treatment strategies to target pancreas cancer.
