Recorded: 23 Feb 2012
After Berkeley I took a faculty position at Colorado and started my own lab. And that was a very interesting time, because that time we decided to look at the properties of the viruses more closely, tumor cell biology, including some viruses that cause leukemia in animals. And I stayed in Colorado five years and then left for Seattle. And it was in Seattle that I was joined by a very gifted Japanese
Kumarato Yashima. We worked together to do more biology, but then we decided, well actually we should do genetics of the virus. And we mutated the virus, and then looked for virus mutation's phenotype, and found the first temperature sensitive mutant that was temperature sensitive for transmission.
Well we were really not all that focused, we felt that we wanted to look at the genetic make up of the virus, and the best way to do that would be to induce mutations and look what happens. And since the best phenotype that we measure was transformation, that also gave us the first mutants that we could work with. I must say at that time we probably didn't completely realize the significance of the discovery. Because I was also interested in other strains of Rous sarcoma virus, there was this puzzling defectiveness of the Rous sarcoma virus that was used in Rubin's lab. The virus could cause cancer, but it could not reproduce itself. And that was pretty much cleared up in a couple of years, but I looked then at other Rous sarcoma virus strains and they were not defective. And it was really the isolation, or rather reactivation, of these strains that made it possible to do more genetics. And it made actually the whole genetics of retroviruses is possible because we had a unique virus that could both reproduce itself and induce oncogenic transformation. That is very uncommon for highly oncogenic retroviruses. Most of them are defective and are much harder to deal with genetically.
It was sort of a random search, and whatever we found, it turned out to be very interesting. And we weren't always sure when we found it, whether it interesting or not interesting. It all-- it was a process over months or years that we realized what it really, really meant.
Well there were really two big questions. One was: how do these viruses cause cancer? And the other question, that was sometimes confused with it, with the cancer question, was the question: how do they reproduce molecularly? And there was this puzzling finding that these RNA viruses required DNA synthesis to reproduce. And a lot of people were attracted to this problem, and were working on this. And actually ignoring the cancer question. So there was almost a dichotomy in the field. On the one hand, the fascination with the requirement of DNA synthesis. On the other, why do these viruses cause cancer?
Dr. Peter Vogt, M.D., Ph.D., serves as Member of Scientific Advisory Board of Onconova Therapeutics, Inc. Dr. Vogt is at the Scripps Institute in La Jolla, CA. He is a member of the National Academy of Sciences and a Lasker Award winner. His fundamental studies on oncogenic avian retroviruses led to the identification of oncogenes in human cells. Dr. Vogt is the editor-in-chief of Virology, a scientific journal.
Dr. Peter Vogt intends to continue his work at the Scripps Research Institute. He is currently working to generate small molecule inhibitors that interfere with the spread of cancer as a new therapeutic approach.