Public Defence: Marius Lund-Iversen
Cand.med. Marius Lund-Iversen at Institute of Clinical Medicine will be defending the thesis "Prognostic, diagnostic and predictive value of various proteins and mutations in lung carcinomas" for the degree of PhD.
Trial Lecture - time and place
See Trial Lecture.
- 1st opponent: Professor Lars Andreas Akslen, University of Bergen
- 2nd opponent: Dr Eric Santoni Rugiu, Rigshospitalet, København
- Committee Chair: Associate Professor Mona-Elisabeth Rootwelt-Revheim, University of Oslo
Chair of the Defence
Professor Øyvind Bruland
Odd Terje Brustugun
Lund-Iversen and colleagues have studied three different but comparable cohorts with lung cancer. In one cohort (n=236), the significance of the proteins estrogen receptor alpha, thymydylate synthase (TS), folate receptor alpha, folypolyglutamate synthetase and thyroid transctiption factor -1 (TTF-1) was investigated. Protein expressions were examined with immunohistochemistry. The second cohort (n= 436) consisting of surgical treated lung cancer was investigated for the presence of NUT-BRD4, corresponding to t (15; 19) (q13; p13.1) chromosomal rearrangement. The material was examined using the protein expression for
this rearrangement. In the third cohort the significance and occurrence of mutations in exon 20 in the EGFR gene was examined for all EGFR analysis performed over a period of 22 months. During this period, 903 EGFR mutation analyses were performed in non-small cell lung cancer cases. All the analyzes were reviewed and sorted by different mutations. Cases
with mutations in exon 20 was further characterized regard to the type of mutation, histology, smoking habits and response to tyrosine kinase inhibitors. The main findings are that
patients with low expression of thymydylate synthase have better survival and expression of estrogen receptor alpha is an independent prognostic marker. Furthermore, we found that NUT-BRD4 rearrangement is unusual in primary lung cancer, and we confirmed that patients with exon 20 mutations in the EGFR gene have poor response to tyrosine kinase inhibitors.
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