Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Sonja Eriksson Steigen, UiT Norges arktiske universitet,
- Second opponent: Professor Julia Sidenius Johansen, København universitet,
- Third member and chair of the evaluation committee: Professor Kristian Bjøro, Universitetet i Oslo
Chair of the Defence
Professor Kjersti Flatmark, University of Oslo
Principal Supervisor
Group Leader Elin H. Kure, Oslo University Hospital
Summary
Pancreatic and periampullary adenocarcinomas – the significance of tumor origin and histological subtype for clinical outcome
Pancreatic and periampullary adenocarcinomas arise from four nearby anatomical locations in the pancreatic head all associated with high mortality. The most frequent, with the worst overall survival, is pancreatic adenocarcinoma. The only curative treatment is surgery, and efficient treatment options are lacking.
The aims of the thesis were to analyze the pattern and management of recurrence and survival of ampullary and duodenal adenocarcinomas. Further, to explore the clinical relevance of the histological subtypes pancreatobiliary and intestinal, by identifying potential prognostic molecular biomarkers linked to histological subtypes and site of origin, In addition, facilitate biological and preclinical studies by generating primary patient derived xenograft cell models from pancreatic adenocarcinomas.
The identified prognostic molecular markers emphasize that these tumors are distinct at the level of histopathology and subtype could be included when treating these patients. Patient derived xenografts and corresponding cell lines were successfully established. The cell lines had the capacity to form new cancerous tumors with the same molecular expression pattern as the chemotherapy naïve primary tumors.
Additional information
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