Research Interests
Pancreatic Disease
Research Focus Teams
Diabetes
Departments
Cellular & Physiological Sciences
Contact
Email: janel.kopp@ubc.ca
Office Phone: phone: 604–827–0626
Publications
Lab Website
Dr. Janel Kopp is an assistant professor in the Department of Cellular & Physiological Sciences in the Life Sciences Centre at the University of British Columbia. She is also a research scientist in the Pancreas Centre BC and an associate member of the Department of Pathology and Laboratory Medicine. She obtained her Bachelor’s degrees in Chemistry and Microbiology from South Dakota State University and her Doctorate from the University of Nebraska Medical Center.
Dr. Kopp’s postdoctoral fellowship at the University of California San Diego with Dr. Maike Sander focused pancreatic development, regeneration, and tumorigenesis. Her current research focuses on understanding how different cell types in the pancreas can give rise to pancreatic ductal adenocarcinoma.
Kopp was awarded a F32 Postdoctoral Fellowship from the NIH National Cancer Institute in 2008, a JDRF Advanced Postdoctoral Fellowship in 2012, the Canadian Institutes for Health Research New Investigator Award in 2016, the UBC Faculty of Medicine Distinguished Achievement Award- Early Career in 2018, and the MSFHR Scholar Award in 2019.
Our laboratory is interested in understanding the molecular mechanisms involved in the development and regeneration of the pancreas. In addition, a major focus of our laboratory is understanding how normal pancreatic cell types initiate pancreatic ductal adenocarcinoma. 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.
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.