Prof Kaye: CRUK lifetime achievement award winner

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Published: 23 Nov 2016
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Prof Stan Kaye - The Institute of Cancer Research, London, UK

Prof Kaye speaks with ecancertv at NCRI 2016 about the CRUK lifetime achievement award and work on ovarian cancer therapy.

He also discusses the future of drug development and the impact of Brexit on collaboration.

I was delighted and honoured to be given the CRUK lifetime achievement award which was really an honour bearing in mind the illustrious list of people who have been awarded it in previous years. I guess it was an opportunity to look back over my own experiences in drug development and in ovarian cancer therapy, which has been a particular focus, based on my time initially when I trained at Charing Cross Hospital in London, then moved to Glasgow where I was for twenty years and then back at the Royal Marsden Hospital heading up the drug development unit and getting increasingly involved in some exciting steps forward in ovarian cancer.

What I did, actually, was to go through various lessons which I thought might be quite useful for some of the youngsters in the audience and they were to do largely with emphasising the critical role of team science. I illustrated that with my own partnership with Paul Workman that goes back many years, now Chief Executive of our institute. The critical thing is that for successful cancer research nobody can do it by themselves and the interaction between clinical people and laboratory people is crucial. So I tried to emphasise how people are what it’s all about and hopefully that came over.

Presumably Brexit is not particularly good for team working?

It’s not, no. I’m fairly relaxed about it because common sense is bound to prevail. There are so many outstanding scientists that come from different parts of the world, to limit their ability to work together is just nonsense and you hope that that will prevail but you never know.

What is exciting for ovarian cancer at the moment?

What I talked about, and it still excites me, is the notion of targeted therapy, that we now recognise that ovarian cancer is a mixture of different types of disease and the most important and the most likely to be taken forward as a target is that disease based on BRCA mutations, BRCA1 and 2 mutations, which carries this thing called homologous recombination deficiency. It’s a long word but essentially it renders them sensitive to a new class of drug called PARP inhibitors which you may have heard of, polyamine ribose polymerase. Now, what we’ve shown is that potentially up to half of women with the commonest kind of ovarian cancer may respond to this very well tolerated form of treatment which is just nothing like chemotherapy. In fact, I quoted that phrase from some of the patients we used to treat in the early days, that’s what they told us – this is nothing like chemotherapy. What it has now taken forward from the early phase I studies that we did, actually started in 2005, eleven years ago, is a drug that has now actually been approved and is now available as a maintenance treatment to try to prevent the disease recurring or delay the recurrences. There are now other PARP inhibitors coming along that we did the early trials on as well. So it’s the demonstration that it is possible to start to target the disease, ovarian cancer, in this way. Of course other cancers, lung cancer is a good example, where targeted treatment is already making an impact. So ovarian cancer has been a bit behind that but we’re getting there.

Any further thoughts?

The only other thing is that, of course, the truth is that chemotherapy is still the lynchpin. Drugs like carboplatin and Taxol and the limitation there is still as it was – drug resistance. The cancer cells eventually become resistant to chemotherapy. The good news is that I think we’re going to understand more about why that happens because we’re getting better at sampling cancer cells from women who have had chemotherapy where the disease has come back, either biopsies from ascites, which I talked about, or from the blood. The powerful techniques we’ve got to actually dissect the molecular mechanisms out that have caused resistance are starting to help us understand how to begin to deal with it.

So I talked about that and that is looking better and just finally in terms of other targets I did just mention something called the alpha folate receptor which is not to do with PARP inhibitors but actually is highly expressed in ovarian cancer. A very good target, it’s been used in different ways. We’ve used it to develop a specific drug which is now looking really pretty effective and is now in a three centre study in the UK. That was another example of how with people in our cancer therapeutics laboratory, Ann Jackman, and in our drug development unit, Udai Banerji and obviously Johann de Bono we’ve got the right people working together.

What phase is this study in?

It’s now in a phase Ib study so that’s going to be an expansion in twenty patients. Obviously a lot of people have been involved in that and because that went through our drug development unit that unit actually has got over a hundred people in the staff; it’s a very focussed unit with dedicated medical and nursing staff. So we hope to be able to say more about that next year.