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Transcript:Keith Stewart, MB, ChB: Let’s wrap up this discussion. I’d just like to thank you all for a stimulating discussion. I’d also like to get your closing thoughts. Gareth, what are your messages for the community out there?
Gareth Morgan, MD, PhD: I think it’s really an exciting time. The strategies have changed—maximizing response, minimizing toxicity, segmenting patients into different subgroups. It really is something that’s going to come into general activity over the next couple of years. Really, it’s an exciting time.
Keith Stewart, MB, ChB: It is still a very fluid situation. Sagar?
Sagar Lonial, MD: The recommendation I would have is, have a plan. Know what your goals are early on. Know who your go-to center is, so that you can get guidance from them. And know what the trials are that you have in your area, because patients are coming and are looking up trials ahead of time. They want access to these drugs.
Keith Stewart, MB, ChB: Tom, is this a curable disease?
Thomas G. Martin, MD: I think we can cure probably 10% of the patients now. And perhaps with the new drugs—with monoclonal antibodies together with IMiDs and proteasome inhibitors—maybe we’ll increase that cure fraction to 20%. But we need to do better than that. Maybe it is genomics that will help us do better than that? Maybe it is monitoring MRD Maybe it is with some of these new drugs?
I’m really excited about immunotherapies. I’m like Ivan. I think immunotherapies are the future in myeloma—especially the checkpoint inhibitors, the bispecific T-cell engagers. If we can figure out the best way to use CAR T cells, and if it can clear up MRD and cure patients, it would really be dramatic.
Keith Stewart, MB, ChB: Immunotherapy. Ivan, the future?
Ivan M. Borrello, MD: The time has come. All joking aside, this is enthusiasm based on clinical data—it’s not theoretical enthusiasm. But I would also caution to not be overoptimistic in delivering something. What we need to understand is how to position immunotherapy at the various stages—from induction, transplant, relapse, maintenance, etc—in the context of the plethora of the other drugs that are coming out. This is an incredibly exciting time in myeloma, illustrated by, I think, many of the complexities that we’ve highlighted here today.
Keith Stewart, MB, ChB: Saad, we’ve talked about a lot of very expensive agents and how we’re piling on with new immunotherapies. How are we going to address the economics of this? Do you think there’s a solution?
Saad Z. Usmani, MD: I think we probably need to have another 90-minute session to have that discussion, but I think some of the health economic issues will be mitigated by some of the drugs becoming generic in a few years. But you’re right. I think that’s the big elephant in the room: how can we address the cost?
Keith Stewart, MB, ChB: Do you think we can develop regimens which are explosively active enough that we may not need to treat forever?
Saad Z. Usmani, MD: I think that that would be the key. We have been talking about continuous therapy—keeping the disease under check. But if we have a phenomenal R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) for myeloma that we can use for a finite amount of time and get patients to very good depths of response, and we get 5 or 6 years of progression-free survival out of that, that will be worth it.
Keith Stewart, MB, ChB: Well, thank you everybody. This was a great discussion. On behalf of our panel, we’d like to thank you, the audience, for joining us. Thank you, everybody.
Transcript Edited for Clarity