Recorded: 06 Jun 2006
Well, the question how do viruses cause cancer. That was the main question in those days and there were just several viruses and I stayed with the virus which I now new something about and that viruses have a number of oncogenes, they have many oncogenes, they have very different kind and they were just discovered. So I pulled out the special technique by the monoclonal antibody I cloned several oncogenes out of retroviruses. One of them was the Myc Oncogene, which was then published as the first DNA tumor, DNA binding oncogene, a nuclear protein, which published in Nature and then the second oncogene over the same probe. That was just like in the fairytales killing six flies with one slap or something, how do you say it? So the next oncogene was a A-kinase, that was another kind of kinase in the chicken system Gag-Mil and in the UN system that’s Gag-Raf and we published that one as the first new kinase and that’s been around since then. It’s one, and it was never really been identified to cause cancer until the human genome came from the Singer Laboratory in England after having finished the genome the sequencing now, they’re sequencing all of the cancer cells…
First of all, this enzyme the Raf kinase is one of the most conserved signal transduction pathways in a normal cell and then the human genome analysis followed by cancer cell analysis showed this is a very relevant molecule in cancer. And even in the States companies like Merck and other ones develop inhibitors and they are in very good clinical phase trials, so this is a very good target to hit cancer. It is much better than gene product upstairs and the sequence the Ras kinase have so many, downstream, downstream effects, Raf is a bottleneck so it really if you find a drug again the Raf kinase you really do something to the tumor cell that’s why this is a very relevant target. I’m only testing it in a few experiments. We are still using, studying, and characterizing the enzyme.
The biggest surprise came, referring to my work, when they sequenced tumor cells and it kind of a very broad screening of tumor cells in tissue culture and even in cancers and everybody expected tissue culture cells to be so artificial and having lost all of their very important functions; this is not the case. So the tissue culture cells we are using in several aspects are pretty useful to understand what the cancer cell is doing. So, for me it was a surprise that the Human Genomic Project on cancer cells, which kind of oncogenes showed up, what they did, which cancer they correlated with and that you could use it, in cells, even in tissue cartilage cells to study it.
Karin Moelling currently retired professor, still affiliated with the University of Zurich and the Max-Planck-Institute for Molecular Genetics in Berlin. She studied molecular biology at the University of Berkely, Califonia. She received her PhD at the Max-Planck-Institute for Virology at Tübingen in Germany. She did two post-doctoral research at the Robert Koch Institute in Berlin (1973-1975), and at the Institute of Virology, University Giessen. In 1977 she received her Habilitation at the University of Giessen in Biophysics on "Replication of retroviruses".
From 1976 till 1981 she was the Head of Independent Research Group at Max-Planck-Institute for Molecular Genetics in Berlin, Germany, on oncogenes, proto-oncogenes, cancer and HIV. In 1993 she became the Director of Institute of Medical Virology (IMV) and Full Professor at University of Zurich in Switzerland, she held this position till 2008. Between 2008-2009 she was Fellow of Institute of Advanced Study in Berlin and between 2008-2011 she became a Group Leader, Viruses and Cancer at University of Zurich.
Her research focus on retroviruses and cancer from molecular mechanisms to drug design. She is a Member of the European Molecular Biology Organization. She received several awards e.g. SwissAward in 2007, 4 prices: Czerny Price, Richtzenhain Price, Meyenburg Price and Ansman Price. She was Selected as Heisenberg Fellow in German Science Foundation.