Janel Kopp, Assistant Professor

Postdoc: University of California San Diego (2007-2014)
PhD: University of Nebraska Medical Center (2002-2007)
BSc: South Dakota State University (1998-2002)

Office:  604-827-0626, Lab: 604-827-0635
E-mail:  janelk@mail.ubc.ca, Website: http:janelkopp.com

 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
  1. Zhang, A.M.Y.*, de Winter, T.J.J., Wang, S., Flibotte, S., Zhao, Y.B., Hu, X, Li, H., Schaeffer, D.F., Johnson, J.D.&, and Kopp, J.L.& Effects of hyperinsulinemia on pancreatic cancer development and the immune microenvironment revealed through single-cell transcriptomics. Cancer & Metabolism 2022 Feb 21;10(1):5. doi: 10.1186/s40170-022-00282-z
  2. Espinet E., Gu Z., Imbusch C.D., Giese N.A., Buscher M., Safavi M., Weisenburger S., Klein C., Vogel V., Falcone M., Insua-Rodriguez J., Reitberger M., Thiel V., Kossi S.O., Muckenhuber A., Sarai K.*, Lee A.Y.*, Backx E., Zarei S.*, Gaida M.M., Rodriguez-Paredes M., Donato E., Yen H.Y., Eils R., Schlesner M., Pfarr N., Hackert T., Plass C., Brors B., Steiger K., Weichenhan D., Arda H.E., Rooman I., Kopp J.L., Strobel O., Weichert W., Sprick M.R., Trumpp A. Aggressive PDACs show hypomethylation of repetitive elements and the execution of an intrinsic IFN program linked to a ductal cell-of-origin. Cancer Discov. 2021 Mar;11(3):638-659. doi: 10.1158/2159-8290.CD-20-1202
  3. Zhang A.M.Y.*, Magrill J., de Winter T.J.J., Hu X., Skovsø S., Schaeffer D.F., Kopp J.L. &, Johnson J.D. & Endogenous Hyperinsulinemia Contributes to Pancreatic Cancer Development. Cell Metab. 2019 Sep 3;30(3):403-404. doi: 10.1016/j.cmet.2019.07.003.
  4. Lee A.Y.L.*, Dubois C.L., Sarai K.*, Zarei S.*, Schaeffer D.F., Sander M., Kopp J.L. & Cell of origin affects tumour development and phenotype in pancreatic ductal adenocarcinoma. Gut. 2018 Jan 23. pii: gutjnl-2017-314426. doi: 10.1136/gutjnl-2017-314426.
  5. Kopp J.L., Dubois C.L., Schaeffer D.F., Samani A.*, Taghizadeh F.*, Cowan R.W., Rhim A.D., Stiles B.L., Valasek M., Sander M. Loss of PTEN and Activation of Kras Synergistically Induce Formation of Intraductal Papillary Mucinous Neoplasia From Pancreatic Ductal Cells in Mice. Gastroenterology. 2018 Apr;154(5):1509-1523.e5. doi: 10.1053/j.gastro.2017.12.007.
Further publications can be found here.