Digital public defence: Christian Arstad Christian Arstad at Institute of Clinical Medicine will be defending the thesis Use of somatic mitochondrial mutations as biomarkers in human cancer for the degree of Dr.Philos. (Doctor Philosophiae). 

The public defence will be held as a video conference over Zoom.

The digital defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.

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Adjudication committee

  • First opponent: Professor Per Guldberg, Danish Cancer Society, Copenhagen, Denmark 
  • Second opponent: Professor Aoy Tomita-Mitchell, Medical College of Winsconsin, Milwauke, USA 
  • Third member and chair of the evaluation committee: Professor II Johan Ræder, Institute of Clinical Medicine, University of Oslo 

Chair of defence

Professor Emeritus Torleiv Ole Rognum, Institute of Clinical Medicine, University of Oslo


When characterizing cancer biology, the studies of differences between normal cells and cancer cells are prerequisite. Alterations in nuclear cell DNA are considered imperative in cancer cell transformation. These alterations are named mutations.  A separate cell compartment is called the mitochondrion. It is the powerhouse of the cell and the mitochondrion contains a unique DNA. The mitochondrial DNA also acquires mutations in cancer cell conversion.  In this thesis mitochondrial DNA was separated from nuclear DNA in tumor cells.  When analyzing numbers of tumors from different origin, repeated regions of corresponding mutations in mitochondrial-DNA were isolated.  It was hypothesized that this spectrum of mutations in mitochondrial DNA were possible biomarkers. This was examined in a survival study of patients treated for rectal cancer where the mitochondrial-DNA mutations were demonstrated in the pelvis post-surgery.  Various pathological examinations of tumor-tissue stipulate the severity of the disease.  By microscopic inspection, visible changes and borders to normal tissue are included in the assembled analysis. The pathology-report supports the level of therapy to be chosen. The mitochondrial DNA mutations were hypothesized to represent a clonal relationship and examined in a lineage tracing model. In two studies, the biomarkers were identified in primary tumor tissue but also in the surrounding tissue pathologically characterized to be normal. The information from this thesis is as follows:  The mitochondrion is a potential vital player in the initiation and progress of cancer. Mutations in mitochondrial DNA can be traced in tumor tissue. Mutations in mitochondrial DNA are likely preconditions for cancer initiation and progress. Mutations in mitochondrial DNA possibly represent early stages in the process of cancer initiation and progress.

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Published June 12, 2020 10:15 AM - Last modified July 20, 2020 1:02 PM