Janel Kopp

Prospective Graduate Students / Postdocs

This faculty member is currently not looking for graduate students or Postdoctoral Fellows. Please do not contact the faculty member with any such requests.

Assistant Professor

Research Classification

Research Interests

Modeling cancer
Pancreatic cancer
Pancreatic development

Relevant Degree Programs

Affiliations to Research Centres, Institutes & Clusters


Graduate Student Supervision

Master's Student Supervision

Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.

Cell of origin can change the transcriptome profile of tumors arising from distinct pancreatic cell types (2019)

Both acinar and ductal cells can give rise to PDAC in murine models. However, the gene expression profiles of these tumors, as well as their role in tumor heterogeneity remain unknown. The objective of this study was to understand whether the cellular origin of PDAC could cause functional or molecular heterogeneity. We created PDAC cell lines from mouse models (Sox9CreER;KrasLSL-G12D;Trp53f/f mice a.k.a. Duct:Kras-p53 mice and Ptf1aCreER;KrasLSL-G12D;Trp53f/f a.k.a. Acinar:Kras-p53 mice), which developed tumors originating from ductal or acinar cells, respectively. Duct:Kras-p53 mice formed high grade PanINs, developed PDAC much faster, and had a shorter lifespan compared to Acinar:Kras-p53 mice. In contrast, Acinar:Kras-p53 mice formed abundant of low grade PanINs with mucinous characteristics and PDAC initiation was delayed. I performed differential gene expression analysis between 12 acinar- and 13 ductal-cell-derived tumors using a specific R programming language package called DESeq2. I found 827 differentially expressed genes between tumors of different cellular origin (p-value
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Cell of origin in pancreatic ductal adenocarcinoma (2017)

Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a ductal morphology. Prior research has identified both pancreatic acinar and ductal cells as possible cells of origin for histologically similar PDAC. However, because different mutations were induced in acinar and ductal cells, apt comparisons could not be made to address whether the tumor cell of origin influences PDAC initiation, development, and other tumor differences. To address this open question, I induced oncogenic Ras expression (KrasG¹²D) with concomitant homozgyous Trp53 deletion at 4 weeks of age in a ductal cell specific (Sox9CreER; KrasLSL-G12D; Trp53flox/flox (“Duct:KPcKO”)) and an acinar cell specific (Ptf1aCreER; KrasLSL-G12D; Trp53flox/flox (“Acinar:KPcKO”)) mouse model. I found that Duct:KPcKO mice met their humane endpoints earlier (82 days post injection, p.i.) than the Acinar:KPcKO mice (128 days p.i.), for reasons associated with differences in the timing of PDAC onset. While tumors from both cells of origin were similarly proliferative and shared many physical characteristics, Duct:KPcKO mice developed tumors much earlier than Acinar:KPcKO mice and this was further associated with a difference in precursor lesion initiation. Specifically, ductal cells only formed high-grade lesions while acinar cells formed precursor lesions of all grades. These findings suggest that cell type intrinsic differences may allow ductal cells to rapidly form PDAC under genetically favorable conditions. In comparison, acinar cells likely require additional steps to alter cell identity and become duct-like – thus delaying PDAC initiation and extending survival. Taken together, I have demonstrated, by using cell type specific mouse models, that cell of origin can alter disease initiation, progression and impact PDAC phenotype.

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