In this interview, Oncology Data Advisor Editorial Board member Dr. Rahul Banerjee speaks with Dr. Ben Derman, Assistant Professor of Medicine at the University of Chicago, about his research regarding measurable residual disease (MRD) detection in multiple myeloma and its potential role in guiding treatment decisions.
Rahul Banerjee, MD, FACP: Welcome to Oncology Data Advisor, a digital resource for the multidisciplinary cancer team. My name is Dr. Rahul Banerjee, and I'm one of the Editorial Board members. Today, it's my honor to be joined by Dr. Ben Derman, who is an Assistant Professor of Medicine at the University of Chicago.
What we'll be speaking to him about today is MRD, or measurable residual disease, in multiple myeloma. Dr. Derman is an expert on this topic and is the lead author of a recent study of MRD-guided therapy in myeloma that was published in JAMA Oncology. Dr. Derman, Ben, if I may, it's a pleasure to have you here today.
Ben Derman, MD: Thanks, Rahul. Yes. Thanks for having me.
Dr. Banerjee: Absolutely. So, I think the audience will probably understand or has heard of the concept of MRD, so I don't think we need to go into the broad definition of what it means. But let me start by asking you, when you see MRD negativity on an abstract at the American Society of Hematology (ASH) or as an end point in a publication, what details do you look for? What makes it MRD in your mind and your expert view as you're reviewing published literature about this?
Dr. Derman: Yes, MRD, which many of you may be aware, stands for either minimal residual disease or now the newer term, measurable residual disease. We'll use those interchangeably here. Ultimately, they're signifying the same thing. In myeloma, what we're really trying to understand is, when you get to a very low level of detection of cancer, is it still there? Are we able to detect cancer at this very low level?
When I'm looking at trials and publications, the first thing I want to look at is how deep is the sensitivity and what is the method of measuring or assessing for MRD. Right now, we're blessed with a couple of great different technologies that can get a sensitivity or a depth to one in a million, which we call 10-6. Prior to that—MRD's been around for a long time, this is not a new concept if you go back in myeloma—the difference is that the technology that we have is much better. Before, it was one in 10,000, which is 10-4. Then we have one in 100,000, 10-5. Right now, you really want to look at 10-5 or 10-6, and ideally, something called the limit of detection should be delineated.
For some commercial assays like Adaptive Biotechnologies clonoSEQ®, they have a limit of detection that's been clearly posted and published. That's what the FDA was looking at, as well, when they were reviewing that assay. For flow cytometry, for something called EuroFlow or next-generation flow (NGF), which I'll get into in a second, there's also a limit of detection that we know. You have to have 10 million events looked at, which is essentially the cells that you're looking at, with a cluster of 20 myeloma cells, and that would be the limit of detection. There's also something called the limit of quantitation, which is the limit at which we can actually define how many myeloma cells are left. You can get really into the weeds here.
For the sake of the conversation, what's important to recognize that is if you just start saying, "MRD negativity was assessed," and you don't say, "What was the method? What was the depth? What were the time points that were checked," then it's really a worthless endeavor. Ultimately, what we want is to do the thing that we're not supposed to do, right? Compare across trials. But it serves as a benchmark for us to be able to understand the true MRD negativity.
For me, right now, it should really be no worse than 10-5 when I'm looking at that—otherwise, I don't really think it's telling us much—but ideally, 10-6. The reason is this IFM 2009 trial that was done in France was early versus delayed transplant, but they did assess for MRD at certain time points, sort of after the fact. These were samples that were collected, and then MRD was performed on them later. But what you can see is that patients who achieved MRD negativity at that more sensitive 10-6 level did much better than the patients who were positive at that level but negative at the 10-5 level.
What you really want to know is, at 10-6, what is that level of response? Whether it's next-generation sequencing (NGS) or next-generation flow doesn't matter as much to me. For next-generation sequencing, we're looking at what's called the CDR3 sequence, and there's something called the V(D)J recombination, and these are unique to each myeloma cell. For next-generation flow, you don't need a baseline sample like you do with NGS, but you do require more cells to be input to get the same level of sensitivity. You only need three million cells for NGS, really 1.9 technically, but you can get up to three million. For NGF, you need 10 million, so that's a big difference in the amount of cells that you're getting.
Also, if it's indicated, we should be looking whether it was a first pull, meaning whether it's the first aspirate sample that we take from the bone marrow aspiration send for MRD, because that's going to be your best, most cellular component. That's the one that you really want to see. You'll almost never see that really laid out nicely because it's hard to mandate that, but that is what should be done.
Dr. Banerjee: Totally agree. The idea is that a subsequent pull is to get hemodilution, not as many cells. As you said, the denominated number of cells that are evaluated is super important to this. It makes sense.
Dr. Derman: Exactly. The last thing is, what's the denominator of the patients that you're looking at? We spent a lot of time thinking about this. We talk about an intention-to-treat approach, meaning that any patient who is able to have their MRD assessed, just put quite simply, should have their MRD assessed at a specific time point. If they missed that time point for some reason or something happened and they weren't able to get the test done, that person should be considered to be MRD-positive, even if they actually didn't have evidence of disease or they would've been MRD-negative. It errs on the side of lower rates of MRD negativity.
That's the one thing about that. Some people would say, "Well, why should you penalize, so to speak, a regimen if you weren't able to achieve it?" But that's how we approach intention to treat. As long as we're all universally doing the same thing, that's fine. I like to see what the denominator is clarifying that patients were in a complete response (CR) at the time, not a very good partial response (VGPR) or less. But I think that's really important. Then as time goes on, hopefully, we'll get more data on what's called sustained MRD negativity, which means having MRD checked a year apart and being able to show that patients are able to not only attain MRD negativity, but then sustain it.
Dr. Banerjee: Very, very eloquently stated. I completely agree. Maybe I'll pivot slightly. So far, we've talked about MRD almost as an end point in some ways. We talked about checking on patients who've achieved a CR, and now an MRD-negative CR. In your study that we'll talk a lot more about, that was recently published in JAMA Oncology, you did assess for MRD in that type of end point manner. You also used MRD as a middle point—MRD-guided decision making. Maybe we can talk about that concept. That's another really interesting use of MRD besides just prognostication. Let's start by talking very specifically about your study. Can you tell us a bit more about why you conceptualized it and what the methods and the brief results were?
Dr. Derman: Yes, so this was a phase 2 study, and we built it on sort of a platform of carfilzomib/lenalidomide/dexamethasone (KRd) as induction therapy. This has been studied in a randomized phase 3 fashion in a cooperative group that actually did not show a difference compared with the standard of care of bortezomib/lenalidomide/dexamethasone. We did a phase 2 study that combined it with transplant and followed by KRd post-transplant and found that patients with high-risk disease, as well as standard-risk disease, did very well. The idea was, can we build upon this in the age of new monoclonal antibodies that are available?
Really, the two main ones that have been around are anti-CD38 monoclonal antibodies, such as daratumumab and isatuximab. Then we also have a SLAMF7 monoclonal antibody, also known as a CS1 monoclonal antibody, called elotuzumab. Now, elotuzumab kind of has, I don't know if I would say a checkered past, but it's an interesting story. There's obviously FDA approval for elotuzumab in combination with pomalidomide and dexamethasone in the relapsed/refractory setting. It's been shown to lead to survival benefits in combination with lenalidomide, and it's also been studied with bortezomib. There are some ongoing studies with carfilzomib, so there's some room to suggest that this agent, in combination with other known active anti-myeloma agents, is a worthwhile regimen.
With that said, elotuzumab does not really have single-agent activity. There have also been a few different negative studies including in the frontline, where even elotuzumab with lenalidomide did not outperform lenalidomide and dexamethasone. I think there's definitely been some debate about the role of elotuzumab in the front line. This study was ideally trying to combine something that doesn't add a lot of toxicity, which is one plus for elotuzumab, and using it in an MRD-guided fashion.
This actually bypassed transplant, with the idea that if we extended therapy with elotuzumab plus KRd, we might be able to use MRD to guide us in terms of when to deescalate the carfilzomib. That's the drug that's actually bringing people in for more infusion visits, and what a lot of people will argue, adds probably more of the toxicity of that regimen. Patients who were MRD-negative by next-generation sequencing at a level of 10-6 were able to discontinue their carfilzomib if they were MRD-negative at Cycles 8 and 12. Then we had this graded de-escalation for certain patients based on their level of response.
Dr. Banerjee: Perfect. So then, can you maybe jump to the results then and tell me what you found, what you concluded?
Dr. Derman: Sure, sure. The first thing that we found was that we still were able to achieve very deep and durable responses with high rates of MRD negativity at whatever threshold you really wanted to make a note of. The primary end point was this combined stringent complete response and/or MRD negativity. The idea was that elotuzumab will show up on immunofixation and will therefore make it difficult to determine if some patients have achieved a stringent complete response.
The other thing that we found was that MRD negativity actually deepened over time. We have this idea that eight cycles is something magical, but it's really arbitrary, right? This is how studies were done. The SWOG S0777 study with VRd used eight cycles. I don't think that's true that there's just something magical. What we found is that, sure, there was a certain number of patients who were able to achieve these deep responses at Cycle 8, but those responses actually deepened over time for those who did not make it to that point. I think that's a key point, because if we're going the way of bypassing transplant for many patients based on their preference, comorbid conditions, or other reasons, we have to take into account the fact that we probably need to be giving more than eight cycles for patients. Going on to maintenance therapy simply after eight cycles may not be the right move for everybody, and I think using MRD to be able to guide patients on that route is really important.
Dr. Banerjee: Absolutely. So, I will ask—and I have to go back and look for patients who did achieve MRD negativity early versus those who took eight to 12 cycles to get there—did the kinetics of time to MRD negativity seem to make a difference here?
Dr. Derman: The majority of patients who ultimately achieved MRD negativity did so by the end of 12 cycles, which tells us that maybe eight cycles are not enough. But certainly, there is probably a number that is appropriate for many patients to be able to look and see. I think the challenge right now is that for many patients who are wanting or debating whether to pursue a stem cell transplant, everybody wants to be able to say, "Let's do four cycles of induction therapy and let's do a bone marrow biopsy and check for MRD. If we see that a patient is MRD-negative, then we will bypass transplant and continue on this regimen, because clearly, it's worked well."
The problem is twofold. One is that four cycles is too early. You're probably going to catch some people who are very lucky who are MRD-negative, but the vast majority of people are not going to be. The flip side is if you say, "Well, let's do eight cycles instead, and if you're MRD-negative at eight cycles, then we'll do a transplant." But now you're making it harder to do stem cell collection unless you did it earlier. It's not as clean. I think that's going to be the challenge—finding out that right point at which we might be able to use this to really guide decision making. I think MRD is probably more helpful at later time points to help guide decision making than it is right now at these very early time points.
Dr. Banerjee: Very helpful. In this study, did you end up collecting everyone's cells for transplantation, or was it kind of up to the provider and patient preference?
Dr. Derman: We didn't mandate it, but for the vast majority of the patients on this study, anyone who was transplant-eligible did have their stem cells collected. They took a break after four cycles for stem cell collection. We did express that if they wanted to, they could go off protocol and get a transplant. If they did, then we obviously were not including them as far as analysis moving on, except for following for progression and overall survival. But the vast majority of patients stayed on study and continued the regimen, and you can see that these long-term durable responses are pretty impressive. In fact, we have a companion study that looks at whether we can discontinue therapy, and we can get into that a little bit later. But many of those patients had such deep responses that they were able to eventually discontinue all treatment down the line.
Dr. Banerjee: Including lenalidomide maintenance, for example.
Dr. Derman: Including lenalidomide maintenance.
Dr. Banerjee: Perfect. Maybe we can pivot; I do want to also talk about another interesting part of the study, which was not just bone marrow assessments, but peripheral blood assessments. I'm presuming the study you're referring to, though, is the MRD2STOP study?
Dr. Derman: Correct.
Dr. Banerjee: So, maybe we'll start by talking about that, because that is the holy grail of any type of myeloma treatment—to be able to stop therapy entirely. There are obviously some sequelae survivorship-wise from therapies that they've received, but they're not having the ongoing cytopenias, deep vein thrombosis (DVT) risk, and financial toxicity of maintenance lenalidomide. I'd love to hear a bit more about the MRD2STOP trial, what that entails, what you've seen so far, and what you're hoping to get out of it.
Dr. Derman: Yes, this was a study that really came out of visits with patients. I was a fellow at the time, and I was seeing so many patients who had gone through many of our trials and were five, six, seven years out and on indefinite maintenance therapy. Everyone would say, "I have diarrhea. I'm always holding medication because of intermittent low blood counts, cytopenias. I have cognitive issues. Sometimes it's neuropathy." And you always said, "Well, in America, we just do lenalidomide maintenance until it stops working."
But what if the patient's never going to have their disease come back? What if maybe we actually are curing some myeloma patients? I mean, if you look at the IFM 2009 data, eight-year progression-free survival for patients who got a transplant in just one year of maintenance and then stopped was 35%.
Dr. Banerjee: Again, a European study, not the American practice.
Dr. Derman: Correct, right. That was 35%. We don't have that long-term follow-up yet with the DETERMINATION trial. But that means that 35% of patients have not had their disease progress at eight years, following five cycles of therapy, a transplant, and one year of lenalidomide maintenance. That's pretty impressive when you think about it. So, might that number be higher with people who are on longer courses of lenalidomide maintenance or receiving quadruple therapies now? That was really the question.
What we designed was a single-arm study for patients who have sustained MRD negativity, meaning they've been on maintenance for at least a year. They have one prior bone marrow that showed at least MRD negativity at 10-5. What we are doing right now is performing clonoSEQ and NGS testing for all of these patients with a 10-6 depth. If they're negative for disease or have undetectable disease at that 10-6 threshold, their positron emission tomography (PET) scan is negative for disease, and blood counts of all their myeloma parameters suggest no evidence of disease, then we are offering them to be able to stop their maintenance therapy and undergo MRD surveillance with us.
This means blood counts and myeloma parameters in the peripheral blood every three months and then a bone marrow biopsy and aspiration with a PET scan every year, which has kind of been our standard for monitoring patients anyhow.
Dr. Banerjee: It's almost like they're smoldering again—high-risk smoldering myeloma, just on this side of the myeloma treatment.
Dr. Derman: Exactly. I mean, that's a good way to put it. So, the goal is ultimately to see two things. One is, does this work, right? I mean, can you do this? Are we actually identifying patients that might be cured of their disease, who have no evidence of disease? They're not on treatment, and we're hopefully sparing them of the comorbid conditions that might arise from being on indefinite lenalidomide maintenance therapy. But it's not just lenalidomide; it could be any maintenance therapy there is. We're hoping to be able to share some interim data soon, but we're going to be following patients for three years on the study. Ultimately, we really probably need longer than that to be able to see what's actually happening. There are some prospective randomized studies that are actually ongoing right now, looking at similar concepts as well.
Dr. Banerjee: For example, the DRAMMATIC study. Absolutely. I mean, we could talk about this all day. With the MASTER study, I know that the risk of MRD resurgence was dependent on the high-risk cytogenetics or the features of the myeloma. Some people will probably be cured with a transplant alone or KRd alone, and we just don't know who those patients are. To your point, MRD assessment might help us figure out retrospectively, these are the people for whom we can stop therapy.
Dr. Derman: That's a perfect way to put it. Instead of waiting 10 years on lenalidomide maintenance therapy to see if the disease is going to come back, is there a way that we can rewind and go back to maybe two years post-therapy to be able to say, "Hey, you're somebody who we think can stop"?
It poses an interesting question. If you have a really young myeloma patient—I just saw one yesterday in clinic, somebody who's 50 years old—let's say that maybe their disease really is cured, and let's say they have a normal life expectancy now. That's the hope, if you're being optimistic. Let's say they're going to live to 75 or 80. Are you telling me they're going to be on lenalidomide for 25 years? No way, right? We can all agree that's not going to happen. Wouldn't it be nice to be able to intercept our administration of a drug that actually causes second blood cancers in a small number of patients? If we can actually decrease that risk substantially, that would be hugely important.
The DETERMINATION trial showed that 3.5% of patients got a second blood cancer. If you look at the IFM data, which was a similar study but with only one year of maintenance, it was about 0.5%. Now, assuming that we have accurate data collection, that's actually a pretty substantial difference. That means that for every 30 to 35 patients that we put on indefinite maintenance therapy, one of those people is going to get a second blood cancer in their lifetime.
Dr. Banerjee: Completely agree. The final thing I'll add is the benefit of the way you're doing this in a clinical, scientific manner. I'm sure there are many physicians out there who are using MRD assays and saying it's negative. For the young patient, saying "Let's just stop and see what happens," I see the rationale for that; but I think that through studies like this, we'll actually understand, "Well, who is it that's going to remain MRD-negative? How many years of therapy do you need? What assays do you use?" and so forth. I'm excited to see results.
Dr. Derman: The other thing that we're doing with it is assessing the bone marrow. We're actually trying to use CD138 enrichment to be able to analyze a larger sample of the bone marrow than what we've previously been able to do. That's going to be another really interesting piece, because you might have patients that were negative at 10-6 and ultimately have disease relapse, and then you find out, "Well, actually, if we had gone deeper, we would've found some disease." We're really trying to distinguish between who are the ones that are destined to have progression if we stop their treatment versus those who are not. The other thing is looking in the peripheral blood at mass spectrometry to see if we can actually detect disease in those patients as well.
Dr. Banerjee: Perfect. So, just to the audience, CD138 is found on plasma cells. Ben, correct me if I'm wrong, but the idea is that you're able to enrich, you can make both the numerator and denominator more packed, more likely to detect MRD at a more sensitive level if you're looking at myeloma cells and not only created cells.
Dr. Derman: Right. It's exactly right. We look at two to three million cells normally when we do this test. It's unselected, and there are probably only a few tens to hundreds of thousands of plasma cells in that sample. Especially if you're on therapy, it's probably even less. You're looking at one in a million, but it's probably only one in 10,000 to 50,000 of plasma cells that you're looking at.
But what if you could take a larger sample that has maybe 50 to 100 million cells and narrow it down to just the fraction that you care about, which is those plasma cells, the CD138 cells? If you can actually analyze that sample, it's representative of a much larger sample. Now, we don't know if this works; that's part of what we're analyzing. But that's the science. That's the cool science that is behind it. Hopefully, we'll be able to show that it might give additional information.
Dr. Banerjee: Agreed. The biggest barrier, too, is the development. The science is obviously that we're still asking our patients to get bone marrow biopsies—taking the first pull, a lot of pain and discomfort that comes with it, no matter how much lidocaine we use.
You briefly mentioned the idea of peripheral blood mass spectrometry (mass spec). I'll let you go into the details. It's made some press recently. There was a paper out of Boston from Dr. Ghobrial's group that talked about using mass spec to identify MGIP, monoclonal gammopathy of indeterminate potential. There's a lot of buzz about this topic right now. Can you fill us in on what you used for your peripheral blood assays in your study and where you see the peripheral blood MRD world going?
Dr. Derman: I think it's here to stay for sure, and it's going to increase in its use. But I do give some caution about where I think appropriate uses are. So, mass spectrometry is based on this idea. Each myeloma cell in each patient is essentially coming from a clone that makes all the exact same protein with the exact same molecular weight or molecular mass. If you take a sample for a patient who has enough of that protein to capture the signature or that molecular mass, you can trace that protein in a very sensitive level over time using mass spectrometry, because we know the exact molecular mass that we're looking for.
Dr. Banerjee: To be clear for the audience, this is the paraprotein, the actual antibody being produced by the cell, not the cell itself.
Dr. Derman: Right, this has nothing to do with the cells in the bone marrow that might be making it. It's actually just the protein product that's being made. It's measuring, in some respects, the same type of thing that we look at with a serum protein electrophoresis. But this is much more sensitive, 10 to 100 times more sensitive than that.
There are a couple of different methods that can be used. One is called MALDI-TOF, which is a standard method that's been validated now, and it's actually available commercially at Mayo Clinic and some other places. Then there is liquid chromatography mass spec, which is does appear to be more sensitive, but it's also more laborious. Basically, it's additional technology to help separate out the proteins using liquid chromatography, so you get a better resolution, essentially, a deeper sensitivity.
We showed previously that MALDI-TOF can estimate MRD at maybe 10-5 level, one in 100,000 in the bone marrow, and LC-MS or liquid chromatography mass spec approaches 10-6 or maybe even better than that. It's exquisitely sensitive, which makes it a great MRD test. I could see a world where we do this test in the blood, and if you're negative, we confirm it with a bone marrow. But if that test is positive, well, it probably doesn't make sense to be doing a bone marrow. We know that there is some disease left. That's maybe a long way in the future, but it certainly could spare a lot of patients of a bone marrow biopsy.
But you brought up a good point about screening with this MGIP. It's interesting because when we've done this work, and you talk to people who are expert mass spectometrists, if that's what we call them. what you see is that normal individuals also have lots of little spikes because that's how our immune system works. We generate a cluster of antibodies depending on infections that we're exposed to, inflammation, etc. So, it's not surprising when you look at patients who seemingly are asymptomatic and don't have myeloma, and you look for these abnormal proteins, these paraproteins as we call them. Now, when you use mass spectrometry, you almost double the rates of what you're detecting. But we might just be pathologizing normal human physiology, meaning we're calling things abnormal that are not abnormal.
I guess my point is, for a screening process, I think we have to find out if there is any benefit to identifying more people who have a very teeny tiny, potentially inconsequential, likely inconsequential spike on mass spec and subjecting them to lifelong monitoring when it will never become anything, not to mention the psychological aspects of that. Why not just wait until it shows up on a less sensitive test because that alone is also, in some cases, too sensitive, right? We have lots of people that have very small numbers on their serum protein electrophoresis (SPEP) who never develop myeloma. I'm not sure where mass spec will fit in on that aspect.
Dr. Banerjee: This is super helpful. I think the two great points you brought up are: one, how to position these mass spec assays—I agree with you on this side for someone who we know has pathological entity of myeloma, using it as a bridge to MRD assessments in the marrow or so forth might be helpful—and the other point will obviously be the cost of all of this. I'm sure if MRD costs two cents to do, everyone would be testing for it all the time. But I know researchers across the world, including Dr. Mehra in India, are working on this. In the future, you would envision, as you said, this kind of being a bridge towards marrow assessments. Do you possibly see a world where we don't need to build marrow biopsies at all anymore for surveillance in myeloma?
Dr. Derman: I'll never say no. I'll never say no. But the thing about myeloma is that if you really want to understand the DNA aspects of myeloma, when you want to understand the genetic components, it's going to be very hard to be able to use peripheral blood to assess that. The reason is that myeloma just doesn't really go into the peripheral blood. There is work going on with circulating tumor DNA in the blood. There's work going on with cell-free DNA in the blood. The truth is that most of these do not approach the sensitivity of what we can get from a bone marrow biopsy. While I would love that world, I do think that it's still a ways away, if ever, that we're going to completely get rid of bone marrow biopsies.
Dr. Banerjee: Agreed. It's tough because, as you know, myeloma infiltration can be patchy, so bone marrow biopsy is also not perfect. But you're exactly right. At least the odds of running into a myeloma cell are higher with a marrow than they are in the blood.
Dr. Derman: Right. I mean, everything points to this complimentary aspect of things. That's what we showed in our Elo-KRd study. We looked at mass spec in an older phase 2 study of ours with KRd and transplant. Mass spec definitely adds information, but it often has to be put together with what we see in the bone marrow. I think that's the important piece of this, that you have to piece together the story for each patient uniquely. Some people are going to have more PET-positive presentations of disease where imaging is going to be the way to diagnose them or monitor them. Those three pieces, putting them together in a cost-rational way, is going to be important.
Dr. Banerjee: Absolutely. Very, very eloquently stated. Well, thank you, Dr. Derman. This has been super illuminating, I'm sure, for our audience and for me as well, being a myeloma doc myself. Any parting words about MRD and where you see it going?
Dr. Derman: As time goes on, we'll probably be able to get deeper and deeper in our ability to assess for disease. Maybe we'll have a 10-7 or 10-8. Who knows, eventually? But ultimately, what really matters to me is, can we use it to actually guide our decision making? I think that's what we should really be looking at right now. We need more studies that use MRD in the algorithm for de-escalation or potentially escalation of treatment. So keep looking out for that.
Dr. Banerjee: I'm excited to see much more of this in the years and probably decades to come, to be honest. Thank you again for your time, Ben. This was a great talk, and thanks to the audience for listening. Again, my name is Dr. Banerjee. This is Dr. Derman, who we're speaking with. And this was an episode of Oncology Data Advisor. Thanks again.
About Dr. Banerjee and Dr. Derman
Rahul Banerjee, MD, FACP, is an Assistant Professor in the Division of Medical Oncology at the University of Washington, and he also holds a faculty appointment at the Fred Hutchinson Cancer Center. He previously completed his Hematology/Oncology Fellowship and Advanced BMT/CAR-T Fellowship at the University of California, San Francisco. His clinical interests are in multiple myeloma, amyloid light-chain (AL) amyloidosis, and chimeric antigen receptor (CAR) T-cell therapy. His research interests are in toxicity management, digital health, and the patient experience.
Ben Derman, MD, is an Assistant Professor of Medicine at the University of Chicago Medicine, where he specializes in the treatment of multiple myeloma and other plasma cell disorders. His primary research interest in the development of sensitive tests using MRD to guide decision making. In addition, he is investigating strategies to include quality of life and outcomes for patients with multiple myeloma, as well as ways to address racial disparities to improve patient care. Dr. Derman's work has been published in numerous peer-reviewed journals.
For More Information
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Transcript edited for clarity. Any views expressed above are the speakers' own and do not necessarily reflect those of Oncology Data Advisor.
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