Gerard Evan, University of Cambridge
The National Cancer Research Instituteís annual conference took place this week, bringing together the whole cancer research community in the UK and beyond, from lab researchers, doctors and nurses to patient groups and research charities. Kat Arney was joined by Professor Gerard Evan from Cambridge University, who opened the conference with a fantastic talk about his work towards developing new approaches for treating cancers by finding common targets across many types of tumour.
Kat - We hear a lot about the term 'cancer' and also its different types - breast cancer, lung cancer. But what is cancer?
Gerard - Well, different cancers are different. But by and large, tissues in our body behave themselves. They stay the same size and if we damage them, they regenerate, and they re-grow, and they go back to the same size. So, they're very tightly controlled. Cancers are cells that have lost control. They donít die when they should. They donít stop when they should. They grow, they spread, they invade, and they kill.
Kat - And what's actually driving these cells to go wrong because they start in our body? You'd think, what's making them go rogue.
Gerard - Yeah, well this is why cancer is so interesting, because for things to go wrong and cancers to have deregulation of their growth and their survival, that implies that normally, these processes are very tightly regulated. And so in a sense, understanding cancer is to understand how normal processes of the normal body is maintained in the beautiful way that it is for so many decades. We know that there are genes which make proteins, and these proteins act as machines that move information around. And they get information from outside and they transfer it to the various places within the cell that then execute that information. And some of that information make cells proliferate, grow; some of it makes cells stay alive; some of it makes cells differentiate into other cell types and move around. And when the genes that make these proteins, these engines that communicate this information, make defective versions, sometimes these engines can work without a signal. And so, they send a go signal all the time or stay alive signal all the time. The cells donít stop and the cells donít die.
Kat - So, weíve got these genes going wrong in our cells and making them grow out of control, but we have lots of different types of cancer. We have breast cancer and lung cancer. How different at this kind of molecular level are these different cancers?
Gerard - Well, we donít have that many genes. We've got about 20,000 genes. So, there's a tool kit that's used again and again and again, but in slightly different variations. So the basic machinery of the cell cycle - how a cell replicates itself is pretty much the same in every cell type. What differs is the signals that trigger that decision of the cell to replicate itself and the various mechanisms that stop that happening. And they will vary from tissue to tissue. Tissues have different architectures, they have different risks of infection, different risks of these mutations arising. And so, it varies from cell type to cell type and tissue type to tissue type in a way that donít really yet understand.
Kat - But we do know a lot of things about how the cell cycle works, how cells multiply, but it still seems that although we have made progress in treating cancer particularly in recent decades, there's still a real challenge here and it does kill hundreds of thousands of people. Why is it so difficult to treat?
Gerard - Part of the problem is, that we know lots of the bits that go wrong, but we donít know how they fit together. Itís a bit like saying, you've got an orchestra and the violins donít work very well, so that doesnít sound very good. But then we would fit all the instruments together and they were all working, and weíd still wonder why it was that we couldnít play a symphony. And that's because weíre missing a bit which is the conductor. So the conductor is a different type of entity to the individual components. Weíre only just beginning to understand how the conductors work in this system. How, if you like, there's oversight over how everything integrates together. Itís a much more complicated problem than looking at the individual bits.
Kat - The work you're doing is actually studying one of these conductors, a gene called Myc, which we know is important in cancer, but trying to understand what it does. How are you trying to use Myc to find better ways of treating cancer?
Gerard - The idea is Ė I mean, we know that cancers, they arise spontaneously within cells in our body and they evolve. So, everybodyís cancer is different to everybody elseís cancer. No two of the same and actually, lots of cells within each cancer are different because they're all evolving in different directions. But there's a great deal of commonality because of this common tool kit that iss used time and time again in different cells and different tissues. So, one of the ideas is, instead of looking at everything that's different from cancer to cancer, you instead focus on what's the same. This protein Myc is like a conductor. It doesnít regulate individual genes and how they're expressed. It seems to coordinate them altogether. And so, it acts as a central regulator. And so, the idea is if you hit that central regulator, maybe you'll hit many different types of cancer, maybe all types of cancer with just one type of drug. It sounds like science fiction, but we certainly think there's evidence to believe itís true.
Kat - And I saw your talk this afternoon and it was really exciting Ė some of the results that you talked about. What is your hope for the future? Do you think this could be a magic bullet?
Gerard - I donít know about magic bullets. I certainly think itís important to demystify cancer. There are lots of ideas that you can't cure cancer because itís endlessly adaptable and there's nothing weíre ever going to be able to do about to really lick it. I donít believe that's true. Cancers at their root are relatively simple types of disease pathology. I just think if we think about them the right way, there's a good chance that we will be able to find therapies that are generally applicable against many different cancers. I'm very, very optimistic.
Kat - Thanks very much. That's Gerard Evan from Cambridge University.