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: Researcher Andreas Hallqvist, University of Gothenburg, Sweden
- Second opponent: Dean Per Sigvald Bakke, University of Bergen, Norway
- Third member and chair of the evaluation committee: Associate Professor Kristina Yvonne Kathe Lindemann, Faculty of Medicine, University of Oslo
Chair of the Defence
Professor Øyvind Sverre Bruland, University of Oslo
Principal Supervisor
Professor II Åslaug Helland, Faculty of Medicine, University of Oslo
Summary
Lung cancer is the 3rd most common cancer in Norway and is the leading cause of death among cancers.
Underlying chronic inflammation contributes to cancer development. Many lung cancer patients also have chronic obstructive pulmonary disease (COPD), which is both a local and systemic inflammatory disease. The first aim of the thesis was to better understand how chronic inflammation is mirrored by serum markers in COPD and early-stage lung cancer patients with and without COPD. In the COPD patients versus the lung cancer patients groups, we found increased levels in 9 of 18 serum markers reflecting inflammation, endothelial activation, and extracellular matrix (ECM) remodelling. Some of these markers are also associated with prognosis.
Stereotactic body radiotherapy (SBRT) is an effective, curatively intended treatment for early-stage lung cancer patients. Radiation pneumonitis is a common side effect after radiation. The second aim of the thesis was to identify clinical biomarkers for predicting the development of radiation pneumonitis. We found that a decrease in lung function of 7-8% at 1-1.5 months after SBRT might indicate the development of symptomatic radiation pneumonitis since it appears before imaging changes and symptoms. Smokers and patients with emphysema were less inclined to develop symptomatic radiation pneumonitis, which occurred in 18% of all patients.
The third aim of the thesis was to determine how radiation pneumonitis affects markers of chronic inflammation, such as leukocyte and lymphocyte activation markers in serum. Using a microarray technique, we found that T cell dysfunction in serum was associated with the development of radiation pneumonitis and poor survival. These observations suggest new pathogenetic mechanisms and new possible targets in radiation pneumonitis.
Additional information
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