Science Interviews


Sun, 8th Oct 2006

Treating Cancer in The Clinic

Professor Fran Balkwill, Queen Mary's School of Medicine and Dentistry, University of London

Part of the show How Cancers Form, Cancer Biology and Future Therapies

Chris - Fran's from Queen Mary's School of Medicine and Dentistry at the University of London, and she's at this conference too. Fran's normal work is on what causes cancer and perhaps what we might be able to do about it. But we've heard from Gerard some of the mechanisms of where cancer comes from. Are we in the position to start unleashing some of our killer weapons against cancer?

Fran - The two big things that have happened to me over the last twenty years of cancer research is first understanding what cancer really is. We know that cancer is a disease of genetic damage. It's damage to DNA. When you know that and know there are certain types of genes, not all bits of DNA damage cause cancer, we know what kinds of proteins are altered when there is a problem and the cancer occurs, it gives us new targets. It gives us much more specific treatments and I think that if you understand the disease, that's the first step towards curing people or at least making a big difference to patients.

Chris - I want to just throw the cat among the pigeons for a minute Fran. For the last fifty years we've known about the structure of DNA, we've known about the genetic code and we know that cancer is a genetic disease. We even know of some viruses that trigger cancer. But we've still got record numbers of people who succumb to it. We're very good at diagnosing it but not terribly good at getting rid of it yet. Or are we?

Fran - I think that there are a whole load, and we're hearing about them at this conference, of new targeted treatments that will target much more specifically. The old treatments we have for cancer have been 'sledgehammer to crack a nut' kind of treatments. There are new treatments coming out, but it takes a long while. Each treatment has to be carefully tested in clinical trials, and we all know the kinds of problems that can arise during clinical trials. They have to be tested very carefully in clinical trials. In phase one with a few patients for whom there is no other treatment. In phase two you look for an effect in patients in a slightly better state and in phase three when you compare them with an existing treatment. This all takes a great deal of time. And remember, to develop any anti-cancer drug costs about a billion dollars. We heard just now about the amount of funding Cancer Research UK is putting into basic academic and clinical cancer research, but this wouldn't fund a single new drug a year. There are many many reasons and there is a long lead time between finding a disease and what would have to be a whole load of cures because cancer is a whole load of different diseases.

Chris - And a very varied condition. But what are the drugs people are trying to develop to get more targeted therapies?

Fran - What I was talking about today was slightly different and not hitting the cancer cell at all. One of the things I was talking about that has become more important recently is that cancers are not just made of cancer cells. They're not just made of those malignant, out of control evolved cells that take on a separate life form. What cancers do is corrupt other cells in the body that normally do a good job and help us fight infection, heal wounds and repair damage. They corrupt those cells and take them over to help themselves grow and spread. The way that happens is a process very akin to a very mild form of inflammation. So another way of adding to the existing cancer treatments and maybe improving their action is to maybe look at some of the ways that we target chronic inflammation and see if that has an impact on cancer. Many of the cells that you find in chronic inflammation and many of the chemical messages that pass between cells during chronic inflammation are also found in cancer. That's a sort of additional approach, and some of us think that it's quite an exciting one.


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