Dr Neal Shore - Carolina Urologic Research Center, South Carolina, USA
Prof Karim Fizazi - Department of Cancer Medicine, Institut Gustave Roussey, France
Prof Kurt Miller - Benjamin Franklin Medical Centre, Berlin, Germany
Prof Nicholas James - Institute of Cancer and Genomic Sciences, Queen Elizabeth Hospital, Birmingham, UK
NS: Just closing in on time. We have the audience poll response and based on our polling question, here is our polling question, and here is the response by percentages.
NJ: Drumroll.
NS: Yes, a drumroll please. How would you now look to diagnose this patient who has high risk androgen sensitive metastatic disease with a good performance status? ADT only – 3%; ADT plus abiraterone acetate and prednisone – 79%; ADT and docetaxel – 3%; ADT, docetaxel, abiraterone and prednisone – 14%. Are those results surprising to you or is it…?
KM: That’s what you would expect. We just presented very convincing data so that’s how the mind works. What you heard last, that gets stuck in your brain.
NS: But didn’t you say in your session you thought it was still… did the audience get polled and it was about almost an even split?
KF: The question was more would you use just one treatment or would you combine? So more people were keen to combine already while probably we have a half or two-thirds, I can’t remember, were more keen to wait for data before combining. I’m not that surprised either, remember when you asked the question you told people this is assuming the drugs are available in your country, there’s no restriction. So basically if you try to compare the various trials the feeling is that docetaxel and abiraterone have quite similar efficacy or overall survival benefit, even if it’s not that easy to compare and people will obviously choose the less toxic compound. My answer would have been randomise C and D and this is actually what we are doing because at the end of the day we really want to know whether three drugs is really better. Hopefully we will have the answer in a couple of years from now.
NS: That’s very well said. I would like to give the panel an opportunity just to have some concluding statements, your thoughts on what we’ve discussed today, ASCO, the ground-breaking trials that you’ve both been championing. Let’s start with you Karim.
KF: Maybe I will come back to what Eric Small said during his discussion of my paper which was at the end of his talk he reminded people that basically we’ve been using castration alone for seventy years for these men with de novo metastatic prostate cancer with a long series of negative phase III trials. This changed back in 2015, so just two years ago, with a demonstration that docetaxel should be used at least in fit patients with a debate about how many metastases, all these things. But clearly practice changed two years ago and now in 2017 we’re changing again the field and the standard of care with abiraterone. So we’ve just continued changing the field like that and accelerating research that’s going to be fantastic for all the patients.
NJ: Absolutely, I can only agree with that. As always when you make an advance you create new questions and new problems. I think practice will change, clinicians and patients are mostly going to prefer abiraterone over docetaxel. There may well turn out to be a role for docetaxel and abiraterone and Karim’s PEACE1 study is going to be extremely important in answering that question. We will then be faced with quite difficult problems as to what you do if you’ve had docetaxel, abiraterone and then you’re castrate refractory, you’re kind of running out of options. So we will have a whole raft of new problems to deal with and, as always, you answer one question you create another one.
NS: Well said. We’re just trying to keep these folks, if not cured, alive as long as possible, out of the emergency departments, out of the hospital, quality of life.
NJ: If you did indeed prolong survival by 25% by bolting docetaxel on top of abiraterone you’re already at seven years or so for median survival with metastatic, another 25% you’re out at ten. So that’s starting to look pretty good.
NS: Thank you. Kurt?
KM: Yes, it’s kind of disruptive innovation, I would say. It’s like the iPhone but it’s a little bit easier to use. The good thing is really it took some time until the docetaxel thing was adopted, also for the urological community, this is much easier. So it’s a low threshold thing to get this in your daily practice and I think that’s what’s going to happen. As Karim said, it’s good for all patients.
NS: Great final comments, I don’t have anything to add other than to say thank you so much for your presentations, your participation, the leadership you’ve shown. These are not easy things to accomplish these large trials and getting the patients in. You have huge numbers of collaborators that I know you’re both incredibly grateful for and all the patients and the families. We’re doing so much better in prostate cancer, it’s really remarkable. You said earlier, Nick, what’s happened and the median overall survivals have changed significantly in the last few years, thanks to all this research.
I want to thank the folks from ecancer. If you want to watch the programme again you can go to ecancer.org and if you’ve got other colleagues who want to see this you can get to that as well, it will be on and archived for some time to come. So, again, gentlemen thank you so much. It’s been great to share this time with you at ASCO and thank the audience for listening.
