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 Bernhard Lüscher, University Hospital RWTH Aachen, Germany
- Second opponent: Associate Professor Gerd Berge, UiT - The Arctic University of Norway, Norway
- Third member and chair of the evaluation committee: Professor Marit Inngjerdingen, Faculty of Medicine, University of Oslo
Chair of the Defence
Associate Professor Thomas Sæther, University of Oslo
Principal Supervisor
Professor Jason Matthews, University of Oslo
Summary
Cancer is one of the deadliest non-communicable diseases affecting humans worldwide. Massive research efforts are currently underway to understand the complexity of the disease, and to find new therapeutic strategies to meet clinical needs. It is well established that the immune system plays an important role in tumorigenesis, and this has led to recent breakthroughs in targeted immunotherapy. Despite this, several forms of cancer remain nonresponsive to treatment, and many patients develop resistance to therapy.
In her doctoral thesis within the field of cancer research, Marit Rasmussen and colleagues further elucidate the role of the mono-ADP-ribosyltransferase PARP7 in cancer development and in antitumor immunity. PARP7 is known to be involved in a variety of cellular mechanisms including stress responses, metabolism and gene regulation. However, the role of PARP7 in cancer development and progression is not yet fully understood.
The doctoral project aimed to identify novel PARP7 targets and mechanisms involved in breast and pancreas tumorigenesis and cancer immunity. Rasmussen and colleagues show that PARP7 modifies and negatively regulates estrogen receptor alpha in vitro, a known driver of tumorigenesis in several subtypes of human breast cancer.
However, primary cancer cells do not develop nor grow in isolation, and they are heavily influenced by the tumor microenvironment, particularly by the immune system. PARP7 negatively regulates the type I interferon pathway, which is involved in cancer immunity. By abolishing PARP7 function in vitro, either pharmacologically or by gene editing, type I interferon signaling was restored. Furthermore, by utilizing syngeneic mouse models in vivo with either cancer cells devoid of PARP7 or mice lacking PARP7 activity, Rasmussen and colleagues further demonstrate that inhibiting PARP7 may hold promise as a therapeutic strategy for several types of solid cancers.
Additional information
Contact the research support staff.