Key Summary Points
Real-world studies show that patients with multiple myeloma are becoming triple-class exposed in earlier (≤ 3) lines of therapy |
Heavily pretreated patients with multiple myeloma, including those who are triple-class and B cell maturation antigen (BCMA)-directed therapy exposed, have limited treatment options and poor clinical outcomes; effective treatment strategies in this population are needed |
Patient-reported outcomes collected from patients in the clinic generally aligned with those of clinical trial findings; however, patients seen in the clinic were more likely to have high-risk features (e.g., penta-drug refractory disease, high-risk cytogenetics, extramedullary disease) and experience adverse events (e.g., cytopenias) compared with patients enrolled in clinical studies |
Patients with a delayed diagnosis of multiple myeloma had significantly more symptoms, including pain, and were more likely to experience mobility issues than those patients who received a timely diagnosis |
Patients with newly diagnosed multiple myeloma who received quadruplet therapy and experienced early treatment failure (< 1 year to progression) frequently received chemotherapy, while patients whose disease progressed later (> 1 year) were treated with an anti-CD38 monoclonal antibody-containing regimen. Early progressors had poor treatment response and survival outcomes |
Digital Features
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Introduction
Paula Rodriguez-Otero (PR-O): Hello! My name is Paula Rodriguez-Otero. I am a hematologist working at the University of Navarro in Pamplona, Spain.
Luciano Costa (LC): Hi! I’m Luciano Costa. I’m a hematologist and a multiple myeloma physician at the University of Alabama at Birmingham. Well, thanks for joining us for this podcast. Of course, I have the pleasure to share the virtual stage with Dr Rodriguez-Otero. I think, Paula, this meeting was quite intriguing in many ways. We saw this blossoming of real-world evidence and patient-reported outcomes, which is always something interesting to see, and I think, is really a change from prior meetings. We’re going to tackle some of those [abstracts] that are the most relevant for myeloma care today.
Patient-Reported Outcomes Among Patients with Triple-Class Refractory Multiple Myeloma in Real-World Clinical Practice: A Prospective, Multi-site Observational Study—Charalampous et al. Abstract 6727 [1]
LC: Paula, I’d like to start with discussing with you this very interesting abstract from Dr Charalampous from the Mayo Clinic. They had 55 patients with triple-class refractory multiple myeloma who they followed longitudinally and collected patient-reported outcomes. What they saw was, the patients who received [chimeric antigen receptor] CAR-T cell therapy—something that, of course, you are very familiar with and really a global leader on—those patients had a worsening quality of life through months 2 and 3, but they improved back to or above the baseline levels. But for the patients who had no CAR-T therapies, the quality of life largely plateaued. And when asked about how patients felt, almost 78% on CAR-T vs 35% on non-CAR-T described themselves as being “a little bit better” or “much better” as early as month 1 in CAR-T vs non-CAR-T cell therapy. So, Paula, I think we haven’t seen much of that comparison with patient-reported outcomes. Does this match your experience? Does that resonate with what you see with your patients?
PR-O: Yeah, definitely. And I think that this is also in line with previous publications from other clinical trials, in which patient-reported outcomes were captured. With this acute toxicity related to CAR-T cell therapy, there is this deterioration of the quality of life that happens early on after the infusion. But then, due to the depth of response and improved survival, patients recover or even improve regarding the baseline levels. So definitely, this is in line with previous reports, and also in line with the clinical experience that we have with CAR-T cell therapy.
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LC: I agree, and I think it was very interesting that at this same meeting, we saw the patient-reported outcomes from KarMMa-3, which was a study that you led [2]. This very much matched those observations, and that agrees with what I see in clinic as well. Although, I think as long as treatment is successful, I think with the bispecifics, we tend to see some of the same improvement that we see sometimes with CAR-T [3‐5]. The challenges with the old therapies when it doesn’t really help [or] work well, patients, of course, don’t feel better. Paula, I think with the patient-reported outcomes, there is this definition of minimally important difference, which is the minimal numerical change on the particular domain that is considered to be clinically significant and that allows [us] to have those percentage comparisons. Do you think that matches the perception that we clinicians have when we see the patients?
PR-O: I think that there is still probably room for improvement regarding patient-reported outcomes—how we measure it, what do we ask, and how patients are answering to those questions. But I think that the more and more that we use these scales and these measures, the more that we are able to interpret this data, because that is one important aspect. And probably, although nothing is perfect, I think that it has a correlation with what we see clinically regarding the improvement in the health status, the improvement in the physical functioning, and all the different domains that are classically evaluated. For sure, there are other toxicities that are not being evaluated in these questionnaires, somehow. And this, for example, now that we have these novel therapies, for example targeting [G protein-coupled receptor, class C group 5 member D] GPRC5D, now with all these oral complications, and so on. Some of these adverse events or these symptoms that patients may have are not always captured with all these questionnaires. So, I mean, we can improve—but definitely, I think that we can get good information that can be really close to the clinic and the improvement in the patient condition.
Real-World Evaluation of Outcomes in Relapsed/Refractory Multiple Myeloma Patients that are Triple-Class Exposed After Receiving 2 or More Prior Lines of Therapy—Radwanski et al. Abstract 3358 [6]
PR-O: Okay, so maybe now, Luciano, we agree, we can move to another very interesting abstract that was presented by Dr Radwanski regarding real-world evaluation of outcomes in relapsed/refractory multiple myeloma patients. [Patients were] triple-class exposed, but earlier in their treatment course, so only after receiving two or more prior lines of therapy. This is the population that was indeed enrolled in the KarMMa-3 [study]. Patients that were considered triple-class exposed earlier, not waiting for having three or more prior lines of therapy, that this is also our reality in the clinical scenario today. This is a retrospective analysis that included 557 patients that was performed in different databases from 2017 to 2023. The 83% of the patients reached triple-class exposure status within three lines of therapy. And there was, as we also know with other studies, an inferior real-world [progression-free survival] PFS, and also real-world overall survival for patients that were triple-class exposed as compared to patients that weren’t triple-class exposed. So also, they found that patients that had already received the three main classes of the agents were frequently retreated with those agents, sometimes in different combination, even after being already refractory to that particular drug. So, the question for you is, how you think that we can optimize the outcomes or reduce the burden in this population of triple-class exposed patients?
LC: Thanks, Paula. I think this is, of course, a very revealing abstract. I think of course we tend to learn most of the information that informs our practice from clinical trials. But sometimes, there are some new answers that can only be clear when you look at those large datasets and see how really things perform in the real world. Sometimes [it is] going [to] be quite different. And I think when you and I think about triple-class exposed patients or the triple-class exposed patients who are reflected in many clinical trials, those are patients from maybe 5 years ago, where it would take patients four or five lines of therapy to really be triple-class exposed. Patients who were exposed, for example, to a monoclonal antibody as part of a relapsed/refractory treatment in third or fourth line. But with those therapies advanced to early lines of therapy, [it] is not uncommon that patients achieve triple-class exposure status already on the second line, sometimes you know, third-line therapies. There’s some other abstracts we will discuss today that go well into this topic. And that’s a challenge, right? Because now we have, you know, at least in the US—I think it’s very similar in Europe—approvals that follow lines of therapy. So, you have drugs or CAR-T cell therapy that has been approved for patients with four lines of therapy [Food and Drug Administration; three prior therapies for the European Medicines Agency] [7‐10] who are triple-class exposed, and then you have those patients who are triple-class exposed in second or third line and cannot access those therapies. And data like [these] really reveal that it is not the number of lines of therapy, it’s really the exposure that seems to matter most. I think it is a challenge for us to be able to use therapies or not in a sequence that makes sense. We have this lack of evidence from clinical trials on how to treat patients who are triple-class exposed but have one or two prior lines of therapy. And I think that’s where there’s the need and an opportunity to develop new evidence for drugs with new mechanisms of action. I’d love to hear your thoughts, Paula, but I think in this day and age, given the plethora of options that we have, it’s almost unjustifiable to repeat a drug for which the disease is already shown to be refractory. Many times, you upgrade [i.e., switch] within a certain class, you know, patients who receive bortezomib in prior lines and might be refractory, then it’s meaningful and makes sense to use carfilzomib [3]. Same thing with lenalidomide or pomalidomide. But we really need to think hard and try everything possible to introduce a drug with a new mechanism of action and, I think, to help generate data for the really innovative and transformational agents, such as CAR-T and bispecifics, in those early lines of therapy.
PR-O: Yeah, I 100% agree. I think that we, as you mentioned, we do what we can with the tools that we have in our hands. Unfortunately, the indications for the novel therapies are beyond this. So, you need to somehow find a way to get the patients [treated] until they can be able to receive CAR-Ts or bispecifics. And I think this kind of data really highlights that need, and helps also [with] informing, and eventually helping also in the new phase 3 randomized studies that are already moving these therapies earlier, to be able to show that indeed this is an unmet medical need—that patients with early-line relapse, but that they are already triple-class exposed, are doing very poorly with the standard regimens.
Real-World Safety and Efficacy of Teclistamab for Patients with Heavily Pretreated Relapsed-Refractory Multiple Myeloma—Dima et al. Abstract 91 [11]
LC: I totally agree. And I think, a good segue to that, Paula is the next abstract that we have. It’s from Dr Dima, who reported on results of five US academic centers. There [were] quite a few abstracts with a similar design at this meeting. They collected 102 patients to describe the real-world efficacy of teclistamab, a [B cell maturation antigen] BCMA–CD3 T cell engager. And what they report is the patients of the real-world had—of course, they were sicker than patients who were on the MajesTEC-1 trial, which is the pivotal trial that led to the teclistamab approval—they had worse performance status, more cytopenias, more high-risk features. But despite those substantial patient–population differences, the early response rate was pretty similar to what we see on MajesTEC-1. But of course, we don’t have long-term data. We don’t have duration of response because, you know, this drug has only been approved in the US for a little bit over a year now. So, Paula, are you surprised to see those? At least in the short term, are real-world outcomes comparable to clinical trials? And what do you think that message is we can get from this, in terms of inclusion of sicker patients into clinical trials?
PR-O: So, I am not surprised. I think that this is also something that we have seen as well for the CAR-T real-world data, no? So that despite enrolling patients... that... will not meet the eligibility criteria for the particular study, patients are still able to receive the drug to get good efficacy and, more importantly, I will say similar safety, which I think is very relevant. So that reflects that physicians are well trained, well educated, that they are able to deliver these drugs safely, and that the efficacy is comparable. And I think that this is critical, you know, for us to see that the data that we see in the trials are then similar to what we see in the real-world setting, because we cannot forget that some of these drugs are only approved based on single-arm, phase 2 studies. So, it is very relevant for us to see that the outcomes are maintained in the real-world setting. Regarding having this for being more open to enroll patients or sicker patients in clinical trials, I think that will be great from our perspective and from the patient perspective. But I think that we also need to be cautious because these drugs need to be approved, and so we need to somehow create the scenario in which safety can be really evaluated properly. And this is, I mean, a simple example. If your patient enters the trial with a severe thrombocytopenia that is not related to disease burden, how can you then say whether that drug that you are giving to that patient, that is phase 1, phase 2 data, is not causing, I don’t know, more cytopenias to that particular patient? So, I think that it is a balance to be inclusive and allowing patients that may have problems related to myeloma vs allowing sick patients that make [it] difficult [for] the interpretation of the safety data of that particular drug, particularly if we are speaking about single-arm studies.
LC: I totally agree. I think those points are very well taken and you know, really reassuring that when you go to the real world and we can use things more at the physician discretion, the safety has remained very similar, and so has the efficacy, so that’s very reassuring.
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Teclistamab in Relapsed Refractory Multiple Myeloma: Multi-institutional Real-World Study—Mohan et al. Abstract 545 [12]
PR-O: Now we move forward to our next abstract that was presented by Dr Mohan. This is again a real-world, multi-institutional study focusing on teclistamab therapy in relapsed/refractory multiple myeloma, including five US academic centers with 89 patients treated. Importantly, and I think that this was a common factor in several of the real-world studies of teclistamab in relapsed/refractory multiple myeloma, there was 37% of the patients who did receive prior BCMA therapy. This is different for the MajesTEC-1 trial, the pivotal phase 2 study, and definitely this prior exposure trends towards a worse overall response rate. The overall response rate for the real-world cohort was 55%. Just to remind that the overall response rate for MajesTEC-1, so for teclistamab in the pivotal trial was approximately 60% [13], but in this study the real-world patients had more penta-drug refractory disease, much more BCMA exposure, a higher proportion of high-risk cytogenetics, and also a much larger proportion of extramedullary disease compared to the patients that were enrolled in the trial. So, what do you think is the applicability of this real-world experience to clinical trial outcomes?
LC: So, I think that’s great, Paula. I think we see here a population that, as expected, does not match perfectly the population of MajesTEC-1. So, more patients with prior BCMA-directed therapy, patients who are sicker, more heavily pretreated myeloma. And it’s true you see some encouraging activity, you know, the response rate being very close to what we saw on MajesTEC-1 and without any new kind of safety finding. And I think studies like these are very important, and then I’m glad to see that the [American Society for Hematology] ASH abstract committee start to recognize that and give more airtime, so to speak, for those studies, because that’s the only way we have to learn about populations that are not represented in the clinical trials. I think in our practice it gives a lot more freedom, so to speak. It gives some more endorsements, so to speak, to treat patients that perhaps will not have been eligible for MajesTEC-1. We had a publication earlier this year, with a small series of patients with poor renal function, with creatinine clearance less than 30 [mg/dL] [14]. We have the patients on dialysis and that’s up, you know. Teclistamab, as I’m sure any other bispecific, is perfectly fine to be used on those patients [15‐17]. There’s no renal clearance of the antibodies. An antibody like any other gets cleared. And there’s just some logistics challenge that can easily be overcome. So, they really can extend that transformational therapy for patients who otherwise don’t have other options. So, I think that I find that quite reassuring.
PR-O: Yeah, and indeed there was a similar poster presented at ASH from the French group with similar experience in patients with dialysis [18]. So, definitely that real-world study helps us [treat] these more difficult-to-treat patients that are not enrolled in the trials. Also help us, you know, informing on the patients to those outcomes. Definitely, this is very relevant.
Real-World Treatment Patterns and Clinical Outcomes Among Triple-Class Exposed and B-Cell Maturation Antigen (BCMA) Exposed Multiple Myeloma Patients—Mian et al. Abstract 542 [19]
PR-O: Moving forward now to our next abstract that was presented by Dr Hira Mian. I think that this is also something that is very relevant. So, we are now moving into the post-BCMA [settings], and we really need to understand what are the real-world treatment patterns and outcomes of patients that have already received the three main classes of drugs plus a BCMA-directed therapy. So, in this study they enrolled 344 patients who were all of them triple-class exposed and had received a BCMA agent. They found out that patients that were triple-class exposed and BCMA exposed had rapid treatment discontinuation, reflecting a short duration of response of the next treatment and a short progression-free survival. I think that this is one of the most relevant topics that are coming back and forth regarding optimized sequencing. How can we salvage patients after [they are] BCMA exposed? And what is your opinion about this, Luciano?
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LC: Yeah. So very, very intriguing data. I think there were a series of retrospective and prospective studies that set the benchmark for triple-class refractory disease. But of course, now, with the anti-BCMA-based therapies—CAR-T and bispecifics being the obvious go-to therapy for those patients—we just moved the goalpost further, right? Now, we have this challenge of patients who have received not only the three main classes of agents but also a BCMA-directed therapy. And [it’s] not surprising that treating those patients is very hard and there’s really a near complete lack of data. In a way, it does not surprise me. There is a lot of discontinuations. I think at this point, patients oftentimes have low physiological reserve, but also very often the treatments don’t work. I think that’s really the biggest problem. When we already, you know, exhausted some of your better options.
There is always this observation about African Americans vs White patients. It’s a little bit difficult to make a conclusion. I think in the US, African American could be a surrogate for lower income, lower healthcare literacy, harder access to treatment centers. So that certainly might be a factor.
We saw in this study that also there’s the healthcare providers choosing CAR-T before bispecific antibodies. And it kind of makes us wonder why that is. I think that perhaps the most obvious explanation is that CAR-Ts have become available earlier. [They] have become available first before bispecific antibodies were available, particularly during the period of this study, 2019 to 2022. I think also, we now are learning. I know we have seen data from elranatamab, we have seen data for teclistamab, and we’ve seen data for talquetamab being used post-BCMA-directed CAR-T, giving pretty good efficacy, very close to what you get from patients. At least in terms of the response rate for patients who never receive the BCMA-directed therapy. This gives us a clue that, you know, that is one of many ways to sequence those therapies. But I really think if this study were to be repeated in the last 12 months, we would probably see a very different scenario. I think the uptake of the bispecific antibodies has been really fast for reasons that are pretty obvious for us that are in the field, that you know you essentially bypass a lot of the challenges for CAR-T cell therapy, including apheresis slots, manufacturing slots, the availability. [Also], this perception that the patients have to be fitter to endure the period between collecting the cells and being able to treat the patients. I think it’s just [a] matter of time before bispecifics move up to be more frequently used than the CAR-T cell therapy. And then we’re going to have a challenge, Paula, to learn how different bispecifics can be sequenced, or how CAR-T might perform after bispecific antibody.
PR-O: No, I think that you raise the points, you know, that probably the time frame where the study was performed, given their [CAR-T cell therapy] approvals, definitely is a very important point.
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The Additional Disease Burden Accompanying a Delayed Diagnosis of Multiple Myeloma: Utilising a Large Real-World Evidence Base—Quinn et al. Abstract 3771 [20]
LC: So, going back now, we’re talking about patients with myeloma refractory to four classes of therapy, and I’m going back to the very beginning. Going back to initial diagnosis. We have this study presented by Dr Quinn with myeloma patients from the UK, two national surveys, trying to draw a picture of the circumstances how patients were diagnosed and one of the surveys had near 600 patients, the other had a little bit over 600 patients. And what was described by Dr Quinn that the pain was the most frequently reported symptom at time of the presentations and patients with a delayed diagnosis have of course, more symptoms and were more likely to experience mobility issues. I don’t think that surprises us, Paula—we deal with myeloma patients every day. What do you think in your circumstances, which I think are probably quite different from the one we have in the US, what do you feel are the reasons more frequently patients have a delay in diagnosis? And any recommendation that you can give to the general public or to the primary care provider about being more aware in allowing early diagnosis?
PR-O: Yeah. So, I think that one of the reasons for delayed diagnosis is that symptoms of myeloma are not unique—some are quite common. So, myeloma typically arises in the elderly or patients in their sixties, seventies where, for example, bone pain is quite common. So, there [are] symptoms that are not specific for the disease that can be presented in the general population quite frequently: asthenia, bone pain, fatigue, and so on. And sometimes, [a] patient [goes] to the primary care physicians, receives painkillers, pain doesn’t improve, keeps on going (I mean, moves to another place). So, I think that there is the need for this continuous medical education for primary care physicians to really, if you have a patient with bone pain, particularly spinal pain that does not improve, go and check the labs, go and perform a protein electrophoresis. If you have a patient with a known deterioration of the kidney function, [a] patient that is not hypertensive, no diabetes, check the urine, check the proteins in the urine. So, there are a lot of things that we can keep on teaching, you know, our primary care physicians, because the good news for myeloma is that you can detect it in the blood. It’s as simple as that. You have a biomarker that is easy to detect. So, if you perform a protein electrophoresis in those patients with anemia, bone pain, kidney insufficiency, and you detect the monoclonal protein, those patients will be sent for a full workup much more earlier, and it is as simple as that. I think it’s a matter of training, education, and raising this awareness. And this needs to be done repetitively because you do it once, you see the improvement in the diagnosis, but then, 6 months later, then again, you know, you need to repeat, so that would be my recommendations.
LC: I agree, and I know, for us and some specialists it’s in a way easier, because the patients come to us because already somebody already suspected.
PR-O: Exactly.
LC: But when you are out there, in the real world, being a primary physician, you’re going to see a thousand back pains that are degenerative disease until you see one myeloma.
PR-O: Exactly.
LC: So, recognizing the red flags is important, but is also very, very challenging. And I think for us, Paula, sometimes I tried to convey this, once the treatment, the diagnosis is suspected, I think there’s a sense of urgence in myeloma that people do not always get. Sometimes we see patients present with renal dysfunction, somebody suspected myeloma of finding a paraprotein and is still going around and taking weeks to do referral. You know, and to me, somebody with a light chain of 4000, and loss of renal function, is urgent. That patient needs treatment this week.
PR-O: Definitely.
LC: Yeah. So, I think there’s a little bit of kind of an old mentality that myeloma is a disease of the elderly, without much room for improvement, we don’t need to rush. And given the therapeutics that we have now, and a potential to prevent morbidity and mortality, early institutional therapy is crucial.
PR-O: Definitely. Yeah, couldn’t agree more.
Outcomes of Patients with Newly Diagnosed Multiple Myeloma Experiencing Treatment Failure After Upfront Quadruplet Therapy and Autologous Stem Cell Transplantation—Ravi et al. Abstract 1989 [21]
LC: I’ll do our last abstract, and I’d love to get your take on something that we actually put together from our group. My colleague, Dr Ravi, presented this poster. So, we all know, and I think, one of the main themes of this meeting was the success of quadruple therapy, right? We saw that with the ISKIA trial and with the PERSEUS trial, with wonderful, wonderful depth and duration of responses [22, 23]. However, as we know painfully too well, there’s no such thing as a perfect therapy that works for everybody. And unfortunately, as we gain follow-up on prior experience with quadruple therapy, we start seeing patients who have a progression. And then you have this situation that is not well reflected on existing clinical trials of patients who have one prior line of therapy, but they have been quad-exposed. And I think we have made some assumptions over the years that well, if you’re exposed but not refractory, you’re still going to do very well. And we use that a lot, for example, for treatment with CD38 monoclonal antibodies. So, what we did here, we took patients from... we got 248 consecutive patients from our institution who received quadruple therapy. That was either [daratumumab plus bortezomib/lenalidomide/dexamethasone] dara-VRd or [daratumumab plus carfilzomib/lenalidomide/dexamethasone] dara-KRd, both in clinical trial and patients treat[ed] as standard of care, and the good news is [only] 41 patients had progression. So, with the medium follow-up that exceeds 2 years. So that’s the good news. Well, when you look at the patients who have progression after quadruple therapy, most of those patients got [a] transplant, they all had the intent to transplant. We really see three patterns: (1) the patients who progress while [receiving] quadruple therapy, (2) patients who progress on the first year, and (3) those patients who progress beyond the first year. And what we see is, for the patients who progress early on, of course there’s less use of monoclonal antibody, more use of chemotherapy. For patients who progress later, beyond 1 year, we have more use of monoclonal antibody. But nevertheless, the responses are not so great. For the patients who progress early, the response is in the 20% to 30% range. Even the patients will progress after 1 year, the response rate is a bit over 60%. [In] the early progressors, the survival is less than a year, and for those who progress beyond 1 year, the progression-free survival of the next therapy is just about 8 to 9 months. So, it looks like even if you reuse a CD38 monoclonal antibody more than a year after, the responses are not that great, and the duration [of] their response is not long. And for our patients who have an early progression, they are in really big trouble. So, Paula, I want to hear from you, have you had this experience? Does that surprise you? And how do you think that can inform us on the management of those fortunately uncommon but yet very challenging patients?
PR-O: Yeah. So no, the data does not surprise me. Unfortunately, you know, because we all hope that we will be able to rescue these patients, but the reality is that those patients that fail rapidly to this quadruple therapy are having a very poor outcome. So yeah, this is what we see in the real setting. And this is very important, because maybe these patients will be future candidates for these novel therapies.
LC: I agree. And I think this speaks to the importance again to account for exposure when we make clinical trial eligibility and when we make regulatory approval. Because you [have] those patients progressing 6 months after dara-VRd and they have one line of therapy. But we know nothing that you use is going to work, but yet they cannot access drugs that have been approved for triple-class refractory patients because they haven’t had enough lines of therapy.
PR-O: Exactly. So, probably what we are going to have is more patients that are eventually cured or never relapsing or not relapsing early, and the proportion of those that will have suboptimal outcomes with these very intensive therapies at the beginning are the ones that are going to be very, very difficult to treat and will deserve to be treated with the novel therapies early on.
LC: I totally agree.
Closing
LC: Well, this has been a very informative and pleasant discussion that we had for the last several minutes. And I would like to acknowledge this support from Pfizer for this podcast and turn the stage to my co-host today, Dr Rodriguez-Ortero, so she can say some final words.
PR-O: Yeah, so just thank you, Luciano. It has been a pleasure for me to be here with you discussing these abstracts and—until the next time.
Medical Writing.
Medical writing support was provided by William Clafshenkel, PharmD, PhD, of Nucleus Global and was funded by Pfizer.
Authorship
The authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship of this article, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.
Declarations
Conflict of Interest
Luciano J. Costa has received honoraria from Amgen, Bristol Myers Squibb, Celgene, Janssen, Karyopharm Therapeutics, and Sanofi; has acted as consultant for AbbVie, Adaptive Biotechnologies, Amgen, Bristol Myers Squibb, Celgene, Janssen, and Karyopharm Therapeutics; has received research funding from Amgen, Bristol Myers Squibb, Celgene, Janssen, and Juno; and has participated in Speakers’ Bureaus for Amgen and Sanofi. Paula Rodriguez-Otero has received honoraria from AbbVie, Celgene, GSK, H3 Biomedicine, Janssen, Pfizer, and Sanofi; has acted as a consultant for AbbVie, Bristol Myers Squibb, GSK, Janssen, Pfizer, and Sanofi; has participated in Speaker’s Bureaus for Bristol Myers Squibb, GSK, Janssen, and Sanofi; and has received funds for travel expenses from Pfizer.
Ethical Approval
This article does not contain any studies with human participants or animals performed by any of the authors.
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