|R e s e a r c h I n t e r e s t
|To examine the cellular and molecular mechanisms underlying the development of pancreatic diseases, we are focused on understanding how specialized cell types of the pancreas are formed and how they contribute to diseases. To do this, we utilize mice to study pancreatic development and model aspects of pancreatic disease.
Studies in mice have shown that acinar cells can give rise to ductal adenocarcinoma, but it is unclear what role ductal cells have in the initiation of the disease. Thus far, it has not been possible to address this issue, but we have developed mouse models that induce cancer initiating mutations in each cell type to address this open question and examine how each cell type affects the biology of pancreatic ductal adenocarcinoma.
Three different precancerous, or precursor, lesions are thought to precede the formation of pancreatic cancer. Whole genome sequencing of these lesions have provided insights into the mutations that are associated with the disease, but it is unclear what role these mutations have in that initiation and progression of each lesion, particularly the large cystic intraductal papillary mucinous neoplasia lesions (IPMN). We recently developed a mouse model of IPMN and we will utilize this unique model to examine the impact of these human gene mutations on IPMN development.
Pancreatic ductal cells not only provide a conduit for acinar-cell-derived digestive enzymes, but they also create the structural foundation of the entire pancreas. However, it is unclear how proliferation of normal ductal cells are controlled during development to create the proper sized organ. Our initial studies examining the mechanisms regulating proliferation and differentiation in the pancreas will focus on several candidate genes identified by gene expression microarray analysis that may be involved in regulating proliferation and differentiation of ductal cells.
|P u b l i c a t i o n s
Further publications can be found here.