MPE webinar | EHA 2026 highlights

[music] >> Right. Um, good afternoon everyone. I'm Charlotte Haynes from Myeloma Patients Europe and I would like to welcome you all to this webinar that's been organized by MP on the highlights from the 2026 European Hematology Association Congress. >> [music] >> I'm the scientific and patient information manager in the medical education and scientific engagement department at MP. >> [music] >> And I'll be the moderator of this webinar. Can we have the next slide, please? Okay. Um, so we'll just start the webinar with a short introduction [music] and housekeeping rules. And then our speaker, Dr. Johan Lund, will give a presentation on his highlights from the EHA 2026 Congress. After the presentation, we'll have a question and answer session before we close the webinar at 6:00 p.m. Central European Time. Um, next slide, please. So I just like to, um, give some housekeeping rule rules and a quick reminder on how to use Zoom. [music] So, um, there'll be a question and answer session with the presenter after the end of the presentation. Please use the Q&A function, which is found on the toolbar at the bottom of the window, to ask questions to our presenter. You can also click on the like button to upvote a question, which will let us know, uh, which questions you're most interested in. Please don't wait until the end to ask your questions as we'll try to group them by topic while the presentation is ongoing. Uh, you can also use the chat window to chat with other participants, share [music] your experiences or comments on the current discussion. But, um, please do not use the chat function to ask presenter any questions. [music] Use the Q&A feature for that purpose. If you're facing any technical difficulties, please do let us know in the chat as someone from the MP team [music] will reach out to you. So, I'll just let you know that your videos are disabled and you're on mute and but this webinar is being recorded and it will be available on our website [music] www.mp-europe.org and on our social media channels. Thank you. [music] So just a brief overview of the EHA annual conference. This is a global gathering of hematologists, researchers, clinicians, >> [music] >> patient advocates and industry partners. It serves a key platform for presenting cutting edge research and clinical findings, sharing [music] best practice in medicine and clinical practice, advancing hematological education through sessions, workshops and poster presentations. This year was the 31st edition of the congress. It [music] took place in Stockholm, Sweden. There were an estimated 14,000 people attending in person and around 4,000 attendees online. So this is by far the largest number of people that have attended the EHA congress [music] so far. So next slide, thank you. And just to let you know that we also undertook some filming of the EHA with the authors of some of the key clinical trials in the fields of myeloma, high-risk smoldering multiple myeloma and AL amyloidosis. And you can find [music] and watch these on our YouTube channel. And the next slide. So I would like to now welcome our speaker Dr. Johan Lund who will be describing his highlights from EHA 2026. [music] Dr. Lund is a senior consultant and affiliated researcher, Department of Hematology, Karolinska University Hospital and the Department of Medicine, Karolinska [music] Institute of Stockholm, Sweden. So really I'm delighted to have you here Dr. Lund and we shall hand over to you [music] now. Thank you. >> Thank you very much. The there's all over that this is any opinions where my personal ones. Uh but yeah. So we start with talk about treatment of newly diagnosed myeloma. [music] You know, 90% there was not so very much new uh >> [music] >> topics, you know, last year. We saw also that, okay, the DVRD or the quadruplet in first-line treatment was set [music] up a standard in all of Europe. And yeah, that is still You so You remember 17 years of PFS in first-line of treatment that was extremely good and that is what we see. That is how we will treat the patients the last couple of the last [music] coming in years. But there were some actually new data on those patients [music] also, but you know that we try to the over always have the discussion, can we give those quadruplets all patients? [music] And both both the Imroz and the CeFiC studies have done those sub-analysis on frame patients see that, okay, they have about the same PFS and overall survival. But then it comes question, okay, but how did how did the patients [music] change? And now we got the results actually from the quality of life and see that, yes, patients [music] with four drugs have a better quality of life than the patients with three drugs. That tells me when as a myeloma doctor that, yeah, we should [music] treat any patient every patient with those four drugs, not try to be kind in some way. Patients and then get away with their treatment if the patient [music] can't persist on it. Uh the myeloma is always worse than the side effects. But yes, and then the question is whether, okay, new immunotherapies, such things, when [music] can we see them in first-line of treatment? And we've been waiting for years to see the studies and we still have no results. But for example, CAR T cell 6 with the CAR T cell in first-line of treatment. We We're waiting for the this data. So, what can we do [music] something more about, for example, maintenance? The automatic for trial [music] shows that, okay, we take this up as maintenance therapy after autologous stem cell transplant. Maybe maybe not. The four into the sea. You can have the check with every fourth week, every fourth week then, and every fourth week. And we don't see that. Yeah, the problem is the side effects. The cumulative incidence of [music] grade three and four infections. Uh so, we still not know, and we will wait for the overall survival and progression-free survival data. We can see [music] that, yes, the overall response rate is extremely good if you combine if you give give those drugs after the stem cells transplant. >> [music] >> But still, we have to see side effects and progression-free survival. And we >> [music] >> already have so very good progression-free survival. So, this will be hard to put in this drugs. [music] Uh yeah. They also showed the new we have waited and waited waited for a long long time with those new with those cell mods. New iberdomide, mistic domide. The old ones lenalidomide and pomalidomide. Uh >> [music] >> and they have a much better affinity to the cereblon com- complex and probably much better drugs. Uh much more potent. And now we can see that this when when we changed lenalidomide to iberdomide in this [music] quadruplets. And you know, CFE is and the trial, we can see that they had an overall response rate about 92%. And here we actually have a better one. So, if you change lenalidomide to iberdomide, you get a better overall response rate and probably much better results in the future. Uh But then then the question is whether okay, the side effects. Yes, but the same neutropenia and maybe actually those new two new drugs I'm demide, elotuzumab have better side effects than lenalidomide when it comes to [music] GI and other things. So, that could be something in the future, but no no data that show that we should change today. >> [music] >> And you can also this is a very extreme extremely expensive combination if you would you know, the belantamab mafodotin. They are trying to get [music] into second line of treatment. And here's the study in first line of treatment in combination with daratumumab, but far too expensive to use in most countries. >> [music] >> And actually the results are not much better. The overall response rates are 92%. So, [music] this maybe this will be something, but I think the belantamab will that will be something in second or later lines. Yeah, but more interesting when it comes to relapse truly other relapse patients second, you know, the tech majestic three study. That was extremely good data when it comes to ASH this year. >> [music] >> And now I have done it on cytogenetic and functional high-risk patients. You know, the overall survival and PFS data are on all those patients are astonishing, really good to use the combination of teclistamab and daratumumab in second [music] or later lines of treatment. Uh we have not seen those kind of data anytime. [music] Uh but then they change they have also fi- looked at subgroups in the cytogenetic set high-risk group. And also what we say as clinician the functional high-risk, that means that the patient who have have very short type on progression They know that those patients are in a cell transplant, but you know that those patients are in a very bad setting. And you know and this when you look at the cytogenetic high risk Uh sorry. [music] Uh you can see that yeah. The patient in the tech Dara group they have very good data even if I have a cytogenetic high risk profile. And you see [music] if you got a standard therapy they have a very worst prognosis. But when you come to the uh Franklin high risk status even worse. Really bad results in standard risk really in the in high risk patient with standard therapy. But if you gave them those this kind of combination with a bi-specific antibody and see the CD 38 CD 38 antibody they got close to the same results as the standard risk patient. This is very good. And maybe we we should could use those drugs in second line of treatment for those [music] high risk patients. I think that we will not be able to use it for every patient not not in many years. And then all also waited for the majestic nine study. Second line of treatment with single doses single doses teclistamab. Very good PFS data. Yes, so that's something we can use. We know that we all all new drugs will be used in the latest line of treatment and then they will be successfully moved to first line of treatment. We saw that in daratumumab we used the fifth line of treatment and now we use the first first line and it will probably be the same. Teclistamab bi-specific used in fourth or fifth line treatment today. Tomorrow it will be the second line and maybe in first line in some years. This was also interesting and in monumental at what quit the mob in common the combination with daratumumab plus minus or with pomalidomide. Uh this one the interesting data is near not here but it's better to have talquetamab daratumumab versus daratumumab pomalidomide. We know that that would be much better. [music] But what's interesting about the those graphs does not differ. They they don't show that but you see that adding daratumumab to talquetamab that is very good but adding pomalidomide to that combination does not do anything. So we thought before but okay pomalidomide and immunomodulatory drugs would >> [music] >> in some way do something synergistic with the bispecifics but here they can show that it's probably not the bispecific probably not the immunomodulatory drugs it's more the CD38 antibodies but are synergistic. [music] We'll see that in the future. And here also is a study that you can show that okay carfilzomib in combination with immunomodulatory drugs are quite good in the second line of treatment. They can show that lenalidomide is >> [music] >> as good but there are maybe better options in second line of treatment. Yeah, some new data on uh CAR T cells. This is a very interesting one. You know the [music] in vivo CAR T cell showed on ASH late-breaking ASH and abstract ASH three patients. Now we have 18 patients in this study. >> [music] >> You know that in normal ex vivo CAR T you produce the CAR T cells outside the patient and it takes four, five, or six weeks. Here you just inject a retrovirus into the patient and then it produces its own in the CAR T cell in the patient. And the results are so don't need a lymphodepletion. They have the off-the-shelf. It's just a virus. And everything is in the patient. >> [music] >> And now we can say that 100% of patients are MRD negative 6 months after. >> [music] >> So, very, very good results as well. Uh 18 treated patients, that's it today. And all are in complete remission. One patient had [music] a a plasmacytoma that they rate I radiated and is now also in >> [music] >> complete remission. So, this is maybe the future and it's much, much, much cheaper than the CAR-T cells that are provided today. Uh Also, a new dual CAR-T cell, BCMA and CD19. Uh CD They say that it's multiple myeloma progenitor that also is killed. I don't believe that, but that's that's my belief. But, interesting is that manufacturing 3 days, it's expands. You you you produce it ex vivo, but it expands in the patient. That means that it takes less, much less time to produce it and give it to the patient. Uh and uh Yeah. Very good [music] results. 100% of the patients response. And there we go. Maybe a quite good median follow-up. >> [music] >> We'll see, but this will probably Uh but the best thing with this is that no maybe no icons and no delayed neurotox- neurotoxicity. That is the problem with the CAR-T with the Carvikti cell. You have the all the icons and the Parkinsonism, the Guillain-Barré syndrome and the cranial nerve palsies. And if you can get rid of that, we have a much better option. And there also been some study. I just saw this picture. And an allogeneic anti-BCMA CAR-T cell as you produce [music] an allergenic cell. That means that you can have it on the shelf and provide any patient [music] or with a with a cell and it's not the patient's own cells. Good response rate, but no no more results than this. Yeah, then there's the question about the treat the high-risk smoldering myeloma patients. [music] Uh personally, I'm not very convinced on this. Uh we have the Quila study, you know, where you have daratumumab and maybe they showed overall survival benefit and they are that got the daratumumab. The problem is that in the control arm in that study, all [music] patients indeed not get the daratumumab when they started treatment. Uh Oh, wait. I'm not not convinced yet. But there >> [music] >> are lots of some studies. This is elotuzumab high-risk smoldering myeloma and they should have a smoldering myeloma with high-risk risk criteria. Then give all the patient this and yes, this >> [music] >> they respond. Have a median follow-up of 40 months. All patients are alive. Yes, they should be. They are not actually treatment demanding from beginning. The progression-free survival is 96%. Yes, but you have no control group. [music] So, actually, we are not sure that this is good. And you know, all know that if you provide those patients with the bispecific antibodies, they got side effects. Uh infection rates, they got this and the CRS, of course, is such things, but the infection are the big problems. Maybe if you provide a patient in early alliance, the side effects are not that worse, but Well, we'll see. I will I I want to see the control with the status with control arm and overall survival benefit, then I will be convinced. >> [music] >> And this is even more interesting. The Saji Kumar that's a great researcher. He has to ask this question when is he giving a when is presenting why this trial smoldering trial a smoldering myeloma trial. Uh and he can he can show that okay, we have a reduced risk of progression with lenalidomide. And that daratumumab is approved due to the Aquila study. Uh but it's still remain unknown. >> [music] >> So we set up this study on and you combine four drugs carfilzomib [music] virus smoldering myeloma patient. Actually >> [music] >> due to our guidelines today not treatment one, but they got the combination of carfilzomib lenalidomide daratumumab and dexamethasone for induction and for consolidation and then maintenance lenalidomide and daratumumab. But ended up in overall survival, yes, quite good, but five out of those patients 87 patients actually died during the study. In five years and two had a cardiac arrest. And I don't I'm not sure, but but you got cardiac problems with carfilzomib. When the COVID, yes, of course you got you got a problem with infections. Possible leukemia, yeah, we probably got in anyway. [music] Unknown. But this yes, it's a good study. You can show some kind of results, but you have no control arm, so >> [music] >> we don't know if the patient actually has benefits from this. And this is also another one teclistamab proves the depth of response and >> [music] >> pretty fast versus lenalidomide in high-risk myeloma. The same setting, [music] but here you have an actually a randomized trial between lenalidomide and teclistamab. This is something I believe in more. >> [music] >> We know that patient probably probably will benefit from lenalidomide. They they have a better definitely the not worse [music] survival rate if they if they get lenalidomide than if they didn't get it. And here we can see that, okay, progressive free survival is much better with you give them teclistamab. But still you don't have any overall survival data. So, you give a very potent drug with >> [music] >> potent side effects for 3 years and then see what happens [music] later on. Yes, we will see what happened later on, but uh the overall survival I will data we will get in many years. Hopefully. What I think is actually maybe one of the most interesting things is the treatment of AL amyloidosis. You know, AL amyloidosis is has been a huge problem. It was a huge problem 10 or 15 years ago with we had very bad treatment options for those patients. They died from the organ failures. Uh nephrotic syndromes or the especially the cardiac symptoms symptoms. And here they presented some studies on bispecific antibodies. With the linker study with linvoseltamab with the BCMA CD3 a bispecific antibody, and this is good. If you provided them the with a sufficient dose of lenvosep, I would see a rate of 100% >> [music] >> and this is not first-line, it's second or third or fourth-line of treatment, but it's good. And but most interesting is that you got, you know, the involved free light chain that it's a light chain that deposits into the organs, and you [music] want to get rid of that as fast as possible from the blood thing. And that you reduced it to less than 20 mg per liter by day 15 on treatment. That is really fast, and that's much better than other options you have with those patients. And that also meant that >> [music] >> you got a renal response in 73% of the patients in 9.5 months. And the cardiac response in 50% of patients in 9.5 [music] months. And that is much better than as a clinician as but okay, if I have a cardiac problem with my patients, it will be better in 1 or maybe 2 years with standard therapy. So, this is good. And this is another attempt to make [music] but this is another bispecific antibody. It has lower affinity to the CD3. [music] That means that they have a the T cells are not that very much activated, so you get probably less CRS. And those patients uh also had 100% overall response rate. And even faster removal of the involved free light chain, less than 1 week. And so, actually in my clinic today, we we we you know, we used to draw VCD in first-line treatment and then we have lots of other combinations. We use venetoclax for example in second-line of treatment. Most of the patient have the trust ligation 11:14. But I think that I would change to this in many ways my patients >> [music] >> because I want the I want the results early. I can't wait for it. If I have [music] frequent most if I have the chronic problems, I can't definitely not wait for one or two or three months. I will know that the patient will get worse for every day. [music] So, this is worth it. And also, we've seen for 10 or 15 years all those trials that try to find an antibody against towards that actually goes [music] into the organ and they remove the light chain from the involved organs. And this is an antibody. Yes, against lambda or kappa chain. And uh when they used this, we can see no results at all. Because when when when when when they looked into the database, they saw that okay, most of the patient are actually lambda. 80% of the patient are lambda isotype. But the patient with kappa isotype, they could actually say "Hey, but okay, it's P value is good. So, kappa." And they can also show in the lab that okay, it's definitely for kappa is much better. So, this could actually work in the rows and fits for the patient with AL amyloidosis and the with the kappa isotype. Yeah. So, what's happened? Yeah. What I would say is my take-home message from EHA this year is that okay, you should use the quadruplets in first line for all patients. We have the data on my specifics. We have data on [music] CAR-T maybe, but the solid data are on [music] the quadruplets with the CD38 antibody, bortezomib, lenalidomide, and dexamethasone. We can maybe change We can definitely change the We can maybe the lenalidomide to some other immunomodulatory drugs. We can change bortezomib for maybe for something else, but you should use the four drugs or drugs. And not only for the young and fit, you should use it also for the older, the frail patients. They still have the benefit. You have overall survival, you have PFS, but you also have benefit in quality of life. So, remember that the multiple myeloma, you get symptoms of that. That's nothing you want [music] to have. Expect to get the side effects because you can always remove the drug, the side effects, and you can't remove the myeloma myeloma or the or the or the organ damage from myeloma. And in second or later lines of treatment, yes, we have the good chances to get the good results with with CAR-T cells approved. [music] We get better and better CAR-T cells. The one we we have today, the Carvykti, it's good, but we're always concerned about the later side effects, the neuropathy. That's something we dislike. [music] And so, we're looking for something better or something better with less or less side effects, but there are options coming. But you also see extremely good results with the bispecifics in second or later lines of treatment and [music] especially in combinations with CD38 antibodies. So, we will see in some years, but that's So, we we have to discuss see more of the studies and discuss with the authorities see if we can get it approved. And in AL amyloidosis that have been a very very bad >> [music] >> prognosis, we can see better better. We can see VCD, that's a very good option. But now when we [music] see the results with the bispecifics, we can see that okay, the the the the plasma cell clone is not so malignant in most of those patients. [music] It's the problem is the organ damage. So, they seem to be quite easily treated with bispecifics with very very good overall response [music] rates. And this is my personal opinion, but it's still not clear on when to and how to treat smoldering myeloma. Daratumumab is approved and uh we'll see if we are going to use it. Lenalidomide shows yeah, some kind of results, but [music] there you have the side effects and I know one can stand it. And [clears throat] combinations, yes, you really really have to show [music] overall survival but it's if you go to give treatment to a patient with smoldering myeloma, no symptoms at all, the combination of three or four drugs that give them side effects and maybe there was a side effects for rest of their lives with peripheral neuropathy [music] peripheral neuropathy or maybe also some of those drugs actually give secondary cancers. So, [music] I'm not convinced yet, but the the day I see the overall survival data, I would also say, yes. Yeah, I think again, definitely in time. But, it's open for questions. >> That's great. Thank you very much, Dr. Lund. Yes, definitely we've got a good amount of time for some questions. Um I know you just um >> [music] >> you ended your presentation questioning um the efficacy of treatment [music] the high-risk smoldering multiple myeloma. We do have a couple of questions around um smoldering multiple myeloma. Um >> [music] >> so, there's a question about what is the most convincing argument that waiting is safer than using modern immunotherapy right now to sort of stop the disease at [music] its right before it progresses. >> It's all about the side effects. If you have a smoldering myeloma, you know that a rate [music] of patient always some patient will get myeloma, but low lots of patient will not get a symptomatic [music] myeloma at all. So, you know that you have to treat if you have to treat 50 patient, 25 of them that maybe benefit from it, but the rest of them will never ever have benefit from this. And you don't know don't know which patient that have benefit. That means that you have to have a drug that is very very safe. >> [music] >> And I can actually I can accept that a tumor map for example, that's that that's that's a good drug and then not not much side effects. Uh and but when it comes to that you have the progression, then you don't have that option left. Uh so, today we have lots of other options. So, maybe we can use this drug or tumor map. But, to use lenalidomide for example, you have secondary cancers, you have infections, you have the gastrointestinal problems. Um we get dizzy. You have You're [music] not made when you have that for 1 or 2 years, you have not a normal life. And the bi-specifics, they You have the problem with the infections. >> [music] >> Uh my patient with uh I give the bi-specifics, they can't meet their grandchildren because they got so infected. Great. >> Yeah. Yeah, so there's a potentially quite [music] a big uh cost to the treatment. Um would you mind just um stopping sharing your slides? And then [music] uh >> Yeah, I click >> See you all later. >> [laughter] >> Great. Thank you. Okay, so we've now got quite a few um questions that have come in through the chat. So um there are some questions around um I [music] think there was uh around predicting um are you able to predict when inactive multiple myeloma um could become active and how can you um make [music] that prediction? >> Well, that is a great question. And that is uh the There's no We can't do that today. Uh if we could do that, then it would be no problem at all to treat multiple myeloma. Right. Well, that is the big question. We don't We don't know. That means that if we are going to treat multiple myeloma, we treat too many [music] patients. Some will benefit and some will not. And we don't know But if we got that blood sample or that blood test, that would be marvelous. Yeah. Yeah. Right. Thank you. I think [music] that covers the question around was there or maybe uh are there any new markers or blood tests that can tell us exactly when the disease is starting to get activated, say before any actual damage happens to the bones or the kidneys? >> No, just the ones we use the crit and then there we we can measure it >> [music] >> in the function we can maybe measure it. There were some bone markers maybe we could use but we don't use them in the clinic but yeah, we've seen that in some clinical studies that can show the bone marker but we have not used them to [music] show progress or we've used them just to show that okay, we have a bone disease. Maybe that could be used but I've seen no studies on that. Uh so just before the M protein and see what happens with it and then see the creatinine levels, calcium levels and then of course the >> [music] >> hemoglobin and such things. That's what you can do today. >> Right, thank you. And um are there any specific protocols for some gear protection, antioxidant strategies or metabolic support to protect >> [music] >> bodies before active treatment actually becomes needed? >> No, there are no protocols on that things. But we we think that we could have them but no, we don't [music] have anything. I I just tell my patient to live a healthy life. Don't smoke, [music] don't eat too much and out out go out have a walk and but to do some exercise. That's that's the most important things. >> Okay, >> [music] >> thank you. And so we also still questions around CAR T. Um could you tell me how does Teclistamab compare with CAR T in terms of progressive free survival but also in terms of the cost benefits [music] of the two different treatment options? >> Well, that's a question that we also ask ourselves. Yeah, Teclistamab you know the Teclistamab uh but it's three and then you have the CAR T to four. But you can you can you [music] can actually see that okay, they're quite similar population both both those trials. [music] And the PFS in the normal patient setting is slightly better in the Kymriah. Slightly better. If you look at the high-risk patients as we did now in the in the EHR and in the Medicare 3 data, you can see that it's better. It's better to do with the the combination Kymriah than the Kymriah than the car victi in second line of treatment. So, maybe it's better. But then you have the side effects. Now, we have the Kymriah, you get side effects from the beginning, but >> [music] >> in 6 months, everything is normal. Patients they have a normal life for some years until they progress again. And if you are on Kymriah in combination with Kymriah, you have not slight not the normal life. You get infected all the time in that. So, yeah. That is the problem. If the cost-benefit Yeah, you can calculate [music] a cell but I think it's the same. It will cost 1 million a year. Yeah, it's the I think it's about the same cost. If you look [music] if you are on combination of Kymriah and Kymriah for 3 or 4 years, it will be at the same cost as car victi. Okay. Okay. Thank you. >> Um and then there's a question about car T and how it's used across the world. It's someone's noted that it seems to be used more in America >> [music] >> and if you've got any views as to to why that is the case. >> Yeah, it's only about the different health care systems. They have uh Yes. The insurance companies that think that it's very good to use very many expensive uh treatment option because they got benefit from that. They pay for it. And in Europe, we [music] think one for another time before we actually accept everything. But we have different systems in Europe as well. As you can see that in Germany, they use lots of car with T. And then now we do that in Sweden as well. Uh but not in Norway, they're not in Denmark. I [music] say that the difference between the countries. And that is that is the authorities who who to pay for this. >> Okay. Right. I'm just looking at the other questions that we received. We received quite a good amount of questions, so thank you everyone for that. They were quite varied. Um were there any discussions on minimal residual disease? Um specifically in relation to stopping treatment [music] if sustained negative MRD. Um and do you use MRD to stop What are the main restraints? Like cost of NGS machine, training lab technicians. >> Yeah, it's not the cost problem the MRD. If you do the flow cytometry in 10 to the minus five, it costs about what it would be about $2,000. >> Sure. >> Uh that's 20 2,000 euro we can say that's in different European setting. Uh so that's not so costly, but we don't know how to use it. And I I use it Um um when when my [music] patient then I I but I really not know how to use it because I know that okay, if it business MRD negative, he or she will benefit from maintenance therapy. If it's MRD positive, she and he will definitely benefit from maintenance therapy. So Yeah. But we think that we in future can use this for stopping therapy. Yes, we think they try to have, for example, the CD38 antibodies for 2 years MRD negative when they say get rid of the treatment, but we are not convinced that that's correct way. The way we use the MRD today is in clinical studies as a surrogate net market for overall survival. That's okay to use it. But to use it [music] to choose treatment, I'm not sure today if we have the improves. But there are definitely studies ongoing that that will [music] show us. But the problem is that all patients, even the MRD negative ones, will benefit as a group from getting more therapy. That is because we don't think that we cure any [music] patients today. We probably do, but we don't think so. But we yep. And since we think that we not know if we treat cure any patients, we can't use it because in any time the patient will relapse. And then we know that when the patient relapse, we know that it this patient would have [music] great benefited from a prolonged treatment. The whether or whether not he or she was [music] MRD negative. Thanks. >> Thanks. So, do you feel like that it's >> [music] >> uh question of actually just having to wait for more uh research to be published about this and longer follow-ups of patients before being able to to think about whether it can be used in actually stopping treatment? >> Yes, we have to do the more more more studies. We have to say talk about functional functional cure. That says that, okay, 5 years of MRD negativity when we say the patient [music] is cured. That is we say. And that could mean that okay, 5 years of MRD negativity, then we should definitely stop treatment. Yeah, but that's how we could use it today. Maybe. >> Right. Thank [music] you. Um and then sort of changing to looking at newly diagnosed or very early diagnosed, are there any signs in research or practice that very early diagnosis should be treated or should patients still [music] be left untreated? >> That's the same question as we talked about the smoldering myeloma. >> [music] >> If you have early detection and to treat the patient to see what this patient treatment wanted, yes, of course, it's much better to see the patient when we see small bone lesions before the patient gets break all the bones in the body. Yes, of [music] course. Uh but if it's we find a treat the disease that early, yes, we already do that. We found all the MGUS patients, [music] not all patients, but but we found lots of patients with MGUS. They are early on the journey to becoming a multiple myeloma patient, but we don't know will die from something else. So, [music] should we get the right one? >> Thank you. And um related to that, there is a >> [music] >> um sort of question around if someone's unsure whether they have MGUS or smoldering myeloma, and they don't know anything about their risk status because they've actually not been allowed to talk to a hematologist at this stage. So, I guess they've been told that they either have MGUS or smoldering myeloma. Um what would be the recommendation there where they feel they're not able to access [music] um services of of a hematologist? >> If you're an MGUS, no, the treating doctor that the doctor that actually documents it and then diagnoses you [music] as an MGUS or smoldering should be able to say if this is MGUS or a smoldering myeloma. Yes. And no one else than an hematologist that can actually say that this is smoldering [music] myeloma. You can find the M protein in the as a GP, of course, but and you have to refer the patient to the hematology department to get the diagnosis of multiple myeloma. And of course, as a patient, you should know if you have MGUS or smoldering myeloma. That's uh something that won't ever occur. [music] >> Right. So, it's not necessary to to necessarily go to a hematologist. It's more that you need to talk to your primary [music] care provider to understand that. >> Your primary care provider can definitely diagnose you with the MGUS. And if you have a low M protein and every other blood levels are okay, you [music] you are an MGUS patient. But if you see that M protein is rising, of course, you should get a a referral to the hematologist, definitely. Yeah. >> Okay. Thank [music] you. Um we Okay, so [music] we have um a question here about um recommended maintenance therapy after [music] autologous stem cell transplant for multiple myeloma. Um would the recommended maintenance therapy be lenalidomide, and what are the side effects of that [music] treatment? >> The recommendation today from the from the EHA and EMN is maybe that you should have a combination. But yes, lenalidomide is sufficient as a some treatment that is as maintenance treatment. Uh you should have a low dose and and so beginning. Um uh yes, >> [music] >> you can get the side effects. All patients can and then the close to all patients get the side effects. The problem with side effects is that you [music] have some kind of fatigue, you can get a gastrointestinal problems, can be anyhow, and they come very very very very It takes a long time for them to appear, and you don't often notice [music] that this is side effects. Many of my patients think that, "Okay, the life is not better with this. I have a problem with stomach, fatigue, you know, I have a cancer." And when I ask them about this, and then, "Okay, we have to stop [music] treatment." We start to stop lenalidomide one or two or three weeks with him, okay. This is how life should be. So, that is the problem with lenalidomide maintenance. [music] It's And if you have a maintenance with daratumumab, for example, you don't get those side effects. >> Right. So, we do have a couple of questions specifically around [music] lenalidomide. So, someone said if a high-risk myeloma patient with a VGPR is stable after 6 years on maintenance with lenalidomide and Velcade and still tolerate treatment, would you stay with that rather than move to one of the more recent drugs [music] therapies to maintain the remission? >> I always say that you know what you have, but you would don't know what you get. If you have a good risk once and has been on the same level in 6 [music] years, I should go on. If you get side effects, get rid of it and see what happens. To don't I would not change it [music] that that that that No. >> I see. And actually, this goes back to what we're talking about about what is Oh, no, sorry, we've answered that. Um and then on So, it's quite um an interesting question here about um is it possible to create an artificial system in a patient's body? So, uh artificial immune system in a patient's body. So, it must be about the in vivo CAR T work. >> Okay, as I did I'm not sure I get the question correctly. >> So, the question is is it possible to create an artificial immune system in a patient's body? So, I I I think maybe that's related to the in vivo CAR T and you were talking about perhaps. >> You can't you can't create an artificial immune system because an immune system is about extremely complex. Of course, you can have an allogeneic stem cell problem to get the immune system from some [music] some some other from a donor, but that immune system will directly attack yourself. That is the problem. Uh and create an artificial immune system that means that you should have all the white blood cells to protect any virus and tumor and a bacteria and a fungal agents. I think that's that we are not there. Maybe in the future, [music] yes. But as you say with the CAR T uh that is actually you create with a lentivirus, a virus that infects infects T cells and redirect those T cells and uh and so they attack the myeloma cells. That is possible today. But that is one antigen and one [music] and and not for any >> Yeah, I can I realize it's um early days for the in vivo CAR T cell [music] therapy work, but do you have any ideas of when you think that you know might be an actual possibility and in real practice or what the steps are that would need to be taken before that could even [music] be considered? >> Um, you've had them already in the clinical trial and they seem to be efficient. They seem to work. They seem to be safe. Maybe safer than the CAR T cells we have actually on the market today. Uh, so they have to do the phase two and phase three studies. Maybe not the phase even the phase three studies. They can be in the market >> [music] >> in a couple of years. Yeah. And uh and what's very interesting about those I I I I don't know this is stuff that I can tell you but I saw a possible price for those >> [music] >> in vivo CAR T cells. They were cheap, much cheaper than the CAR T cells we have on the market today. So that could actually be a big big issue for the market. >> Right. Okay, that's really interesting. Thank you. >> [music] >> Um, and so sticking with yeah, sort of comparing different types of CAR T cell therapies, um, someone has asked why is um, ciltacel um, [music] in their opinion better than ide-cel? So I guess question is is it? And if it is >> Right. Here's what I think about the ciltacel is much better than ide-cel. [music] Yes, that is we we we see the PFS data. I I think I thought that I saw the first data on CAR T cells. I saw the lymphoma yeah you cured lymphoma with CAR T cells. That's very good. Then I saw the first data on ide-cel. We have a PFS progression free survival rate of 18 months. 50% of patients relapse. I saw this can't be anything [music] actually in myeloma. They're too costly for this this little benefit. Uh, and then we can see that okay the PFS data for >> [music] >> ciltacel is more than three years. That is exciting. Uh I know that the authorities always count on I you know, the quality, how many years of a good life and quality, and how much that could cost. And I just said it's too costly actually, [music] and you don't get that anything from it. Uh probably it's the way I have different epitopes on the anti- uh on the antigen on the BCMA. [music] And they call Carvykti is more efficient, it's works better there. That that's could be the only difference, [music] but no one knows actually. Yeah. >> And thank you. Right, I think we've uh nearly come to the end of this Oh, I think uh >> [music] >> there's a new question. Right. [music] Um okay, so in patients with multiple myeloma who are MRD negative after autologous stem cell transplantation and are receiving daratumumab plus lenalidomide maintenance, how do you [music] manage persistent grade 1 2 neutropenia? Do you prefer maintaining lenalidomide at the >> [music] >> um versus is it lenalidomide 10 mg with GCSF support or reducing the dose to 5 mg? Is there evidence that maintaining the higher dose improves long-term outcomes enough to justify GCSF [music] support? >> There's no evidence at all. You know, so I would definitely go down to 5 mg. You have a maintenance therapy and you should be on that therapy for years. You can't have GCSF every week. But yes. I I would definitely go down 10 mg every other day or 5 5 mg every day. That's the first thing I do. Uh in the maintenance therapy setting >> [music] >> to use the GCSF you can't do that, but then I will have to have a discussion with the patient. Do you want to [music] take this medicine every week or two times a week for the rest of the treatment period? Maybe maybe not. That is >> Thank [music] you. Um we have some reassuring information around that they were the first patient on the ISA RBD phase two study. Um [music] they were about 4 years 3 months on remission in remission for just under 4 years, but they have high risk uh multiple myeloma and have been taken off lenalidomide for the last month. Um >> [music] >> and they just wonder what kind of risks there might be for not continuing the lenalidomide treatment. >> I think there's not not much risk at all. If you go on with this isatuximab, that is sufficient, I think. Uh you will get side effects on lenalidomide. You will get carcinoma uh in the skin cancers, those things, if you continue [music] any longer with lenalidomide. So, and today we know that we have really treatment [music] options in second, fourth, and the third and fourth lines as well. So, I think definitely if it's if the doctor >> [music] >> her her or his doctor recommended to get off lenalidomide, I would. And I also have done that with my own patient in this study. >> I see. [music] Um and so, we have a question around sort of kidney function. Um [music] so, the example here is around after eight cycles of chemotherapy when creatine level remains at 300 in a patient who's not yet [music] started dialysis, if kappa and lambda levels return to normal after these eight cycles, [music] is it already too late for the affected kidney, or is there a chance that kidney function will recover by the end of the myeloma treatment? >> I don't know, actually. Eight months is quite a long time. Um there there still is [music] a chance, yes, but it will get less and less the longer the time. Yep. >> Okay. >> Yep. >> Okay, so I think this is the last question now. So, we have Oh, no, I see they sent it another one popped up. So, we've got 5 minutes left, but so this is the last question so we'll just go through them. Um with 10% [music] plasma cells we are told the disease is asymptomatic. However, could severe social around the symptoms could severe fatigue and tingling be caused by low-grade toxicity from the M protein damaging nerves and tissues even before traditional criteria [music] met. DDE heart 2026 discuss recognizing these symptoms not as just make coincidences, but as a a direct biological effect of [music] early clonal activity. >> I don't think that you get a clue if it's an early clonal activity or something, but we know that yes, the products the M protein can definitely do damage [music] at those levels. You can have a You can definitely have that for example AL amyloidosis or >> [music] >> we talk about not the MGUS with like MGUS or MGNS [music] with like with a renal problem, you can definitely get before that and you can get And also you can get a new [music] neuropathy from the M protein at low levels. So, yes, if you have some symptoms and you have some kind of smoldering myeloma or MGUS uh that actually could be the problem. So, yeah, we see some patients I get a referral from the from the neurological department and definitely from the nephrologist. >> Okay. Okay, so I I this last [music] question is uh uh So, there is just So, there are just a couple of minutes left. Um >> [music] >> and this may be more of a an individual question. Um so, this is around being on lenalidomide for 3 years post [music] stem cell transplant and just had a BCC removed. Um is this likely to be an ongoing issue from here? Sure exactly what's there meant there. >> Well, I don't know BCC. What is that? >> A basal cell >> Okay, basal cell carcinoma. Okay, basal cell carcinoma. It could be due to the development by we don't But we know that the risk of getting skin carcinomas, especially basal cell carcinomas, uh squamous cell carcinomas, and so forth, are raised if you have the lenalidomide treatment ongoing. Yes. So, maybe there is something that's around that you can get a basal cell carcinoma unless you have lenalidomide or not, of course. [music] >> Okay, thank you for answering that. And then this is will be the final question. Um [music] in a Thank you so much. In an MRD negative patient after autologous stem cell transplantation [music] receiving daratumumab lenalidomide maintenance, is persistent neutropenia >> [music] >> ANC around 1.5 * 9 per liter commonly due to lenalidomide even if the patient tolerated the same dose well before transplantation? >> Yeah, but 1.5, [music] that's okay to have. That's not a problem. So, just go on. >> Right. okay. That's [music] great. Thank you so much. I know there's a very varied questions and I didn't quite manage to group everything together. So, I apologize for that. They all came in, but they were so helpful and a really useful presentation overview of EHA 2026. [music] I think also just to say I know we haven't had any questions about AL amyloidosis, but it was really interesting to see that promising data that you that you highlighted around treatment for that. So, it's great and thank [music] you. Thank you so much. >> Thank you for listening. >> [music]