The public defence will be held as a video conference over Zoom.
The 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.
Click here to participate in the digital public defence
Digital Trial Lecture - time and place
Adjudication committee
- First opponent: Professor Pär Stattin, Uppsala University, Sweden
- Second opponent: Chief Physician Ok Målfrid Mangrud, Sykehuset Innlandet HF, Lillehammer
- Third member and chair of the evaluation committee: Associate Professor Viktor Berge
Institute of Clinical Medicine, University of Oslo
Chair of defence
Professor II Åslaug Helland, Institute of Clinical Medicine, University of Oslo
Principal Supervisor
Professor II Håvard E. Danielsen, Department of Informatics, University of Oslo
Summary
Prostate cancer is the most frequently diagnosed cancer among Norwegian men. Currently available risk stratification tools are inadequate for differentiating between men who will develop a life-threatening disease that requires aggressive treatment, and those with a likely indolent disease who can avoid or postpone curative treatment through enrolment in active surveillance.
Identification and application of additional biomarkers that could improve risk stratification is challenging due to tumor heterogeneity, the uneven distribution of a biomarker within a tumor. Tumor heterogeneity in prostate cancer has so far largely been ignored in existing biomarker studies.
One aim of this study was to explore the extent of tumor heterogeneity and its effect on prognostic biomarkers in prostate cancer. We used Gleason score, DNA ploidy and PTEN (phosphatase and tensin homolog) status as representative biomarkers. Gleason score describes the morphology and architecture of tumor glands, DNA ploidy is a measure of cellular DNA content, and PTEN is a tumor suppressor. Furthermore, we studied the prognostic value of DNA ploidy and PTEN expression, separately and collectively, in multiple tumor samples from each patient in one large radical prostatectomy and one large active surveillance cohort.
We demonstrated extensive tumor heterogeneity based on Gleason score, DNA ploidy and PTEN status in the majority of studied patients, suggesting that a single sample does not provide representative information of the tumor as a whole. DNA ploidy was a prognostic marker when multiple samples were analyzed, as opposed to when one randomly selected sample was used. Combined estimates of DNA ploidy and PTEN status provided better prognostic information than each marker independently. Our results suggest that the combined marker of DNA ploidy and PTEN status could be used in addition to Gleason score for earlier identification of patients with aggressive disease in the active surveillance setting.
Additional information
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