Expanding Myeloma Treatment Options Through Expert Collaboration: A Roundtable Discussion

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Topics include: Treatment

As part of Patient Power’s coverage of Myeloma 2016, several renowned experts joined together to discuss what they learned at the meeting.  Drs. Ken Anderson, Keith Stewart, Noopur Raje and Sagar Lonial, discuss how the Myeloma 2016 meeting fosters collaboration among myeloma researchers, from all over the world. The experts discuss new discoveries, genetics, combination therapies, as well as how technological changes are allowing increasing the pace of advances in the field.

Clinical Trials Mentioned in This Video

pembrolizumab (Keytruda)
Monoclonal Antibodies
trametinib (Mekinist)
Immunomodulatory Drugs (IMIDs)

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Transcript

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

Dr. Anderson:

Hi. I'm Dr. Ken Anderson from the Dana-Farber Cancer Institute, and I'm here at Myeloma 2016 in Boston where one more time this year we had extraordinary progress reported. Important not only for caregivers but especially for patients, and we're going to try to highlight the features here. With me, I'm honored to have Professor Keith Stewart from the Mayo Clinic in Arizona, Professor Noopur Raje from Mass General Hospital in Boston, and Professor Sagar Lonial from the Emory Winship Cancer Center in Atlanta, Georgia. 

So I guess I'll start off and say how gratifying it is and how blessed we are in myeloma to continue to have advances year after year after year. I'll just mention for all the patients that are here that we've had about 16 new approved medicines over the last dozen years, and we had seven in 2015 alone. So this meeting highlights not only how we're going to use those medicines, but what is the prospect for the future. So maybe I can ask Sagar first to talk a little bit about some of the promise of the monoclonal antibodies that was really exciting here at this meeting.

Dr. Lonial:            

Yeah, I think the antibodies story and the whole concept of trying to modulate immune function with the PD1 inhibitors, that's really an amazing story, and I sort of think that in many ways the clinical data is outstripping the laboratory data, which is okay, because that means we're not waiting for data to be able to test and do things. I think between PD1, PDL1, CD38, SLAMF7 and other potential targets, we've got a whole host of antibodies now, and I think how to put them together with our current treatment is going to give us work to do in the next few years. 

Dr. Anderson:    

Very nice, and in terms of other areas of promise besides the immunology, we had a lot of information presented at this meeting about genetics and multiple myeloma, the CoMMpass trial has talked about new ways of identifying circuits that convey gross or our own drug resistance or trigger death of myeloma. But are there any promising features that really patients should know about in terms of the ability now to target myeloma? 

Dr. Stewart:         

Well, I think what we saw in this meeting was that the amount of information in this base of genocide myeloma is just exploding. The CoMMpass Study, which is a study funded by the Multiple Myeloma Research Foundation, which has studied a thousand patients and followed it for eight years is beginning to generate a large amount of data on which patients we can target, what the different genetic mutations mean in terms of prognosis. And I think for patients they're watching, one of the really existing things we heard about today was the fact that maybe you don't need to do a bone marrow to find these things out but you can actually begin to use technology to detect from the peripheral blood and perhaps select patients for clinical trials based on a blood test rather than a bone marrow test, which I thought was—I wouldn't say a glimpse into the future but something that would be revolutionary.

Dr. Anderson:    

Yeah, I hear you very much so and I think, you know, that the technology advances is what you're talking about and the ability to share data in all of the gene data that's existent around the world in order to better understand the disease… 

Dr. Stewart:         

…and that issue, say there's the precision therapies, which we can glean from that and we heard some very interesting data on targeting with a drug called trametinib (Mekinist). We've heard of using drugs to target BRAF and if you've heard a lot about the mechanisms of action of how thalidomide (Thalomid) and lenalidomide (Revlimid) and pomalidomide (Pomalyst) work, which follows our understanding of how to use those drugs and what patients to use them and how to improve on them really. 

Dr. Lonial:            

I thought your group had given us the answer on that, and I see today that there are even more mechanisms than we thought of before.

Dr. Stewart:      

Possibly.  

Dr. Anderson:    

In order to interrupt this little banter over here, I would just mention that one of the neat things of this meeting is learning how the immunomodulatory drugs work but then trying to capitalize on that mechanism and one of the neatest things I learned here today is that the IMiDs—lenalidomide, thalidomide, and pomalidomide work by binding to something called cereblon, which turns on a degradation of downstream proteins—proteins that are really important and essential for myeloma to grow.

Well, a new class of medicines now called degronfor degrade and IMiDs for IMiDs we heard about here very exciting; never done before but the ability to turn on with a medicine this ubiquitin E3 ligase, or this garbage degradation system but now to link it to proteins that we want to degrade selectively. And you know that opportunity to degrade a protein that actually causes a disease, I think, has implications not only for myeloma and other cancers but many diseases. 

Dr. Stewart:         

Yes, that was very exciting—clearly one of the major advances of the meeting. You mentioned, you know, learning how to combine immune-modulated drugs with other different types of monoclonal antibodies or proteasome inhibitors, and you’re fond of talking about using a team. And maybe it'll bring Dr. Raje in to tell about what did you learn about combination therapies here?

Dr. Raje:                

I think to me what was striking about this meeting is like all of you have pointed out here, is not just advances in all the drugs that we have today but the technology. We learned about interesting technology. We learned about the genetics. We learned about tools of monitoring the disease, not by just using blood tests like you just pointed out, Keith, but also by imaging techniques, which we heard about and then correlating it with minimal residual disease and then learning the drugs, which we've been using now for the last 10 years.

We learned completely different mechanisms, as you just pointed out. So that really is empowering and empowering in a way that we can now begin to understand how to combine all of these drugs and really utilize them to their maximum potential. So that to me was absolutely fascinating. We have all of these wonderful drugs. Now we're going to begin to learn as to how to combine these—combining the IMiDs with some of the checkpoint blockade monoclonal antibodies to me seems to be a very exciting advance. 

So we heard data with pembrolizumab with both pomalidomide and lenalidomide, and we heard that people who are actually refractory to these IMiDs when you combine the checkpoint blockade, you restore sensitivity and they start responding to these drugs. So I think we are in an exciting time with all of these advances both technologically as well as with drugs.

Dr. Anderson:    

Very nice and just one other thing for Noopur, you’re specialized on management of bone disease over many, many years. Anything new that you can report from this meeting? 

Dr. Raje:                

So there was data where we talked about an enzyme, which works on the osteoclast. Suzanne Lentzsch presented that data this morning. It's still not a targetable enzyme. It's not a druggable target, but hopefully in the very near future we will have drugs outside of what we are typically used to using like zoledronic acid (Zometa) and like pamidronate (Aredia). You know, we also are focusing on a whole bunch of other drugs, which are the bone anabolics, and I think those are in early phase clinical trials with a DKK1 antibody. Now we have a sclerostin antibody. We also have an ACE antibody, and all of those are in Clinic 4 patients with myeloma. 

Dr. Anderson:    

So I think the message is an overwhelmingly positive one. We have genetically targeted therapies. We have immune therapies, and what you are saying for us, Noopur, is we have ways once we prolonged life without myeloma, we want this to be a quality life. And we have advances that are parallel in improving on the complications.

Dr. Lonial:            

I think what really struck me over the day-and-a-half or so was the real collaborative nature of the meeting. I mean, I think it was a very—it was a relatively small meeting as far as myeloma meetings go, but you had people from all over the world that were really showing their science, not to one-up each other but to say how can we do this to make things better? That collaborative feeling I think is somewhat unique in our field, but I think it's why we have been able to do so much in such a short time. 

Dr. Stewart:         

I think this meeting brings together not just the clinicians, but it brings together the charitable organizations, the pharmaceutical companies, and the scientists all in one room. I heard somebody saying it's a forum in which people aren't afraid to express and be criticized and make progress in that fashion.

 

Dr. Anderson:    

Yeah, I think the other thing is it's really a think tank, a real strategy session for the future and not only are there leaders in myeloma here, but the next generation of really very bright and enthusiastic investigators are here, so the promise for progress is even brighter still. 

Dr. Stewart:         

I would say what one would take away from me? And it was an almost unanimous consensus on where people think treatment of myeloma is going, which is multiple drugs, proteasome inhibitor, immune modular, monoclonal antibody at diagnosis aiming for complete responses and longer duration of life and better quality of life.

Dr. Anderson:    

Yes. I think it's fair to say that, you know, over the last 10 to 15 years, the management has been transformed. Minimal residual disease is a reality and as you've said, Keith, long-term disease-free survival is real. And with immune therapies and others coming, it's never been a more promising or optimistic time for patients with myeloma.

Please remember the opinions expressed on Patient Power are not necessarily the views of our sponsors, contributors, partners or Patient Power. Our discussions are not a substitute for seeking medical advice or care from your own doctor. That’s how you’ll get care that’s most appropriate for you. 

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Page last updated on May 4, 2016