Pancreatic ductal adenocarcinoma (PDAC) is the 3rd leading cause of cancer-related deaths in the United States and has a 5-year survival rate of 9%. This dismal prognosis shows an urgent need for novel therapeutic strategies. A prominent desmoplastic reaction, when the microenvironment surrounding epithelial tumors expands due to infiltration of fibroblasts, pancreatic stellate cells, immune cell populations, and endothelial cells, is one of the hallmarks of PDAC. This dense stromal layer can account for up to 90% of the tumor bulk and is believed to serve as a physical impediment to effective pharmacological treatment and to play an important role in the aggressive nature of the disease. Thus, full understanding of disease development will require experimental assessment of the mechanisms through which the microenvironment can affect the course of disease progression.
The Hill lab uses novel mouse models, human clinical samples, and newly-established assay systems to elucidate how the microenvironment or inflammation contributes to all three stages of tumorigenesis: initiation, progression to metastasis, and therapeutic resistance.
Current Lab Projects
- ER Stress and Chemoresistance
- Early Detection of PDAC
- Exosomal Regulation of Chemoresistance
- Microenvironment-Driven Metastasis
Current Animal Models
Novel therapeutic targets and strategies identified from these projects will have immediate clinical relevance and could potentially change the current treatment strategies for patients with advanced stage pancreatic cancer.