Welcome to the home page of Tor Erik Rusten's group
Our group aims at understanding the cell biological basis of epithelial-derived cancer at the cellular, organ and organismal level. Epithelial-derived cancers (carcinomas) develop in a stepwise manner with complex interactions between cancer-initiating cells, nearby normal cells, the immune system, extracellular matrix and the overall animal physiology. Moreover, cells from the original tumor evade its original location, invade neighboring tissues and disseminate, finally killing the host. Current dogma holds that several protective control mechanisms both at the cellular and organ level must degenerate by mutations or gene expression changes of tumor suppressors and proto-oncogenes to drive these changes that are not easily addressed in simple cell culture systems. To overcome these limitations and to capture a wider array of the complexities of the mechanisms of carcinogensis we are using a combination of the genetically amendable animal model system, Drosophila melanogaster and a human organoid model system that approximates real organ architecture in vivo. Drosophila is very powerful to study the biological function(s) of unknown and identified tumour suppressor genes and oncogenes and place them into pathways and context. Drosophila conveniently lends itself to analyse tumor suppressors as genetically labelled homozygous mutant cells can easily be made in an otherwise heterozygous mutant background, emulating loss of heterozygosity of tumor suppressors in cancer, representing an in vivo cancer model under physiological conditions. Additionally, proto-oncogenes can easily be expressed and analysed in a controlled manner in any organ. Finally, cooperation of oncogenes and tumor suppressors in carcinogenesis can be studied in vivo under different physiological conditions. Human organoid cell culture is another powerful system to model epithelial-derived cancer development in their 3D environment approximating an in vivo situation. In particular, the loss of organized epithelial structure, contact inhibition restricting tumor growth, breakdown of extracellular matrix and cell evasion can be studied.
Fergal O’Farrell, Ashish Jain, Rojyar Khezri, Tor Erik Rusten, Nadja Katheder, Mahidur M. Rahman.
We collaborate with the research groups of:
- David Bilder, University of California, Berkeley, US
- Christos Samakovlis, University of Stockholm, Sweden
- Terje Johansen, University of Tromsø, Norway
- Heinrich Jasper, Buck Institute for Research on Aging, Novato, US
- Thomas Vaccari, IFOM, Milan, Italy
Post Docs and PhD students
We are always looking for talented and motivated Post Docs and PhD students that wants to join the lab.
If you are interested please contact Tor Erik Rusten by email well in advance to be able to secure funding.
Post Doctoral fellowship:
Norwegian Research Council (2 years, June-start January)
The Norwegian Cancer Society (2years, June-start January)
Helse Sør-Øst (2 years, September-start January)
EMBO (2years, August-Start January)
HFSP (2 years, August-Start January)
FEBS (up to 3 years, bianually)
Growth coordination during development
Mar 27, 2017
Jørgen Wesche appointed group leader for the Mesenchymal Cancer Biology Group at the Department of Tumor Biology
Mar 15, 2017
Prestigious research prize from the Norwegian Cancer Society to pioneer in autophagy research
Mar 7, 2017
Tor Erik Rusten
Microenvironmental autophagy promotes tumour growth
Nature, 541 (7637), 417-420
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
Autophagy, 12 (1), 1-222