Advancing Renal Cell Carcinoma

Transcript:Daniel Heng, MD, MPH, FRCPC: This has been a great discussion and I think we’ve talked a lot about different topics and new therapies, and we’re really excited about them. I want to give the panel an opportunity to have some concluding remarks. Nizar, we’ll start with you, just a two-sentence comment on what you think the state of the art is.

Nizar M. Tannir, MD, FACP: I would like to thank you for moderating this very lively debate.

Daniel Heng, MD, MPH, FRCPC: It was fun.

Nizar M. Tannir, MD, FACP: I’d like to thank my colleagues for their valuable input. I always learn when I go to these activities. I think it’s good news for our patients. I think we are witnessing a revolution in biology, and I think through partnership with industry and academic centers, finally, we are on the brink of really curing some of the cancers that have been tough to cure. So I think the excitement is obviously with immunotherapy, with the immune checkpoint inhibitors. We discussed nivolumab in second place and what other targeted agents can compete in that space. But it is very possible, as Carlos mentioned, some of these combination immune checkpoint inhibitor plus targeted agents [may pan out], such with the avelumab plus axitinib phase III trial that’s about to start or the one that’s already completed, atezolizumab (MPDL3280A) plus bevacizumab. If these two trials or the ipilimumab/nivolumab study are positive, then we are looking at a change in the paradigm of first-line therapy. But I think my view is that in the next three to five years, there’s still a role for targeted agents to be played.

I do not think immune checkpoint inhibitors, whether they’re a combination of two immune checkpoint inhibitors or an immune checkpoint plus a targeted agent, will replace [targeted therapy] or will be the therapies for all patients. I think drugs, such as pazopanib, sunitinib, and other targeted agents, even mTOR inhibitors, will still have their place for our patients. I think the key is, as Carlos mentioned, to try to hopefully understand who are the patients who are best treated with a particular therapy. And I think maybe in the next few years we will finally have biomarkers that can help us select and guide our therapies for our patients.

Daniel Heng, MD, MPH, FRCPC: Paul, what are your concluding comments?

Paul Nathan, MBBS, PhD, FRCP: I think just standing back, we’ve taken a disease that was untreatable for most patients—in other words, most patients did not have benefit from our interventions—and over the last decade or so, we’re now in a situation where most patients do have benefit from our interventions. But the current reality is that, that benefit, is not durable for the vast majority of our patients. And we’re just to the point where we may be able to use immunotherapy, either alone or in combination with other immunotherapies or with targeted therapies, to switch that and take a population of patients and give them durable benefit. And so I’m very excited at the moment. I think there will be a group of patients who are going to have long-term durable benefit, and I think the goal for us is no longer simply palliation. The goal for us is trying to ensure that our patients die from things that are other than their kidney cancer.

Daniel Heng, MD, MPH, FRCPC: Susanne, what about you?

Susanne Osanto, MD, PhD: Well, I do think that these days are really exciting days. I was tremendously excited by the latest trials. At the same time, I realize that we’re still far away from curing our patients and what it comes down to is that we really have to spend an enormous amount of time and money at this moment to try to dissect patients’ host characteristics, the characteristics of the tumors, and also to spend a lot of time on really finding biomarkers that will enable us to dissect the patient population into subgroups that are truly different groups and then try to develop the targeted therapy for those groups and cure them. Of course, I’m afraid that we’re still quite a long way. That’s going to take some time before we will reach that, and I fully agree that we have to put more investigations into material, the circulating tumor cells, the tumor free DNA, cell-free DNA, etcetera. But it’s extremely expensive and it has to be done in a very, very meticulous way in qualified laboratories. It’s not that easy.

Daniel Heng, MD, MPH, FRCPC: Carlos, do you have anything to add?

Carlos H. Barrios, MD: I think that I agree with all the comments. Thank you very much for moderating. Thank you all for all your comments. I think we should consider ourselves very lucky to be witnessing this era in the management of kidney cancer, particularly metastatic kidney cancer. In the sense that we have been able to, over the very last few years, see an enormous array of different alternatives that actually make, like Paul was saying, significant improvements in the outcomes of our patients. However, we need to realize, like you were saying, Susanne, that we’re not curing these patients yet. And in order to change the paradigm and move forward, I think that we need to be both creative and clever. We need to stimulate putting patients in clinical trials, but clinical trials that are not necessarily the same as we have been conducting so far. We need to be more conscious of biology and we should try to stay away from just picking the drugs off the shelf and giving them to the patient. We need to put rational biology into the future development of this area.

Daniel Heng, MD, MPH, FRCPC: That’s excellent. So thank you very much to our panel. We have a very international panel here and it’s been a pleasure to chair it. I’d also like to thank all the patients and all of the investigators around the world who have really dedicated their time to these clinical trials and investigations because without them, we wouldn’t be here talking about all this. And so hopefully the next time we meet again, kidney cancer will have advanced a lot again. Thank you very much.

Trancript Edited for Clarity