Dr. Michael Shapira, MD shares an early vaccine for myeloma and his work to raise the age ceiling for allo and auto transplants


Originally posted on mPatient Myeloma Radio

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Dr. Michael Shapira, MD
Haddassah Medical Center
Interview date: April 18, 2014


Dr. Shapira shares work done to test a myeloma vaccine from Vaxil called ImMucin that targets the MUC1 oncoprotein, found in about 70% of myeloma patients. This vaccine was used in an early clinical trial to test safety, but the study results look promising, even when used without other therapies. He also describes his work to increase the upper age limit effectively for transplantation including autologous and allogenic and how he has been able to reduce graft vs. host side effects of allogeneic transplant with multiple strategies.

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Full Transcript
Jenny: Welcome to today’s episode of mPatient Myeloma Radio, a show that connects patients with myeloma researchers. Learning from these wonderful men and women is a very important part of receiving outstanding care. It’s important to support their efforts and by participating in their clinical trials, we can help them come to more discoveries at a quicker pace.

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We have a new site called myelomacrowd.org. That’s the first all-inclusive site for myeloma. We invite you to take a look at that site and also to think about becoming a contributor where you can see many options to share what you know to help other myeloma patients.

Today, we are very fortunate to have with us Dr. Michael Shapira. Dr. Shapira is a senior physician in the Bone Marrow Transplant Department at the Hadassah Medical Center in Jerusalem, Israel. Dr. Shapira also performs work as a researcher and professor in the Bone Marrow Transplant Department in Hematology. He specializes in transplantation and treatment for elderly myeloma patients and has helped move forward improvements in transplant, including reduction of symptoms in graft-versus-host.

Prof. Shapira is serving as a principal investigator on several clinical studies, some of which we’ll cover today. Now, I have several people in the myeloma Facebook groups request this interview and as part of this, I’ve included their questions. Dr. Shapira, there’s great popular demand to hear from you.

Dr. Shapira: Thank you very much. It’s a pleasure to be on your show.

Jenny: Thank you so much for all you’re doing for myeloma patients. I guess my first question — this is how this interview began — there’s a Vaxil drug called ImMucin to treat — and I’m not sure how you say it — MUC1 expressing myelomas both with active and smoldering myeloma. I guess this is an immunotherapy. So first, maybe you can describe what is MUC1.

Dr. Shapira: MUC1 is an oncoprotein. That means that this is a protein that should not be on a regular cell, but is exists on several types of cancer cells, among which is myeloma, but not only. Some several solid tumors also express MUC1. Not all tumors in the specific type express MUC1. For example, in myeloma, which is the issue of our talk today, not all myelomas express MUC1, but we developed an interest in this oncoprotein and we’re not the only one. We wanted to make a vaccination against that hoping that the immune system will help us fight against myeloma.

Jenny: How did you discover MUC1?

Dr. Shapira: MUC1 was described years ago. It’s not our discovery. Vaxil Bio, founded by Dr. Lior Carmon from the Weizmann Institute, developed a way to make a very small peptide-like vaccine that hopefully — and we think it is — will be able to induce immunity against MUC1 regardless of the HLA, which means regardless of the immune systems, specific immune system ID of the patient.

Just to make it clear that in the past, it was very difficult to induce immunity against tumor cells with a very specific protein. We had to make specific protein type of HLA, specific type of MHC, which is the biological ID of our cells. That made it very difficult to make immunotherapy as a wide and acceptable treatment because you had to have a specific drug per patient. Our vaccine makes it easier to make vaccination for all patients regardless of their HLA.

Jenny: How does a patient know that they have MUC1? What test is identifying that?

Dr. Shapira: We perform bone marrow biopsies of patient with active myeloma and we stain the cells, the myeloma cells, against MUC1. It’s a very easy test. It takes a few hours and then you know whether the myeloma cells are MUC1 positive or negative.

Jenny: Is this a FISH test or a GEP test or is it a separate test?

Dr. Shapira: It’s a FACS cell sorting test.

Jenny: And do most myeloma researchers use this test or is this something special.

Dr. Shapira: You need to have the specific antibodies with the fluorescent color on them in order to make this test.

Jenny: And is this test available in the US? Do you know?

Dr. Shapira: The staining, yes. It’s a commercially available test.

Jenny: We’ve started doing a lot of discussion on this show about specific genetic mutations and specific translocations deletions and things like that. And so, I’ve been very proactive in talking to people that they need to understand their disease biology. And so, I just never heard of MUC1 before.

Dr. Shapira: We’re not aware that MUC1 changes the biology of the disease; rather, it’s a target for the immunotherapy, so we cannot say that the MUC1 patient is with high risk of progression or lower risk of progression as compared to other patients.

Jenny: Okay. When you say that not all patients have MUC1, what percentage of patients have MUC1? Do you see it also on smoldering and MGUS?

Dr. Shapira: Our patients, we tested them in a small study that we’ve done, and we’ll be talking about it in the coming minutes. We found MUC1 positivity in about 70% of the patients.

Jenny: Seventy percent, but not everyone. And does it go across different high risk features or no? You didn’t see any kind of pattern?

Dr. Shapira: It’s not related at all.

Jenny: Well, can you explain first what MUC1 does?

Dr. Shapira: The biology of MUC1 is not the issue here. I think that the issue is our ability to use that as a target for the immune system against myeloma. We were not using the specific features of MUC1; rather, we’re using the fact that this is something to discriminate between the normal cells and the abnormal cells.

Jenny: Do you want to describe your study? Because you have a phase two study that is now closed, is that correct?

Dr. Shapira: Exactly.

Jenny: Okay. Do you want to explain what that study was and then what you found?

Dr. Shapira: Yes. As I said a few minutes ago, Dr. Carmon the founder of the firm Vaxil Bio, developed a way to produce a small protein, a peptide, which will be immunogenic against MUC1. In this case, we were able to make vaccines against other things, but in the context of this study, it was against MUC1.

What we aimed to do in this study is to first of all assess the feasibility of finding patients which are suitable for this vaccination, meaning to see whether we can find patients that are MUC1 positive, and this was successful. We found 15 patients out of the 19 patients that we sampled.

We wanted to see the safety of this drug because it was never tried in humans. We found that the drug was very safe. The side effects were very limited in a very short while. It was very easy to use this vaccination and we really didn’t see any outstanding or longstanding side effects. We wanted to see whether we’ll be able to get immunity against MUC1, specific immunity against MUC1.

We found that all patients responded to the vaccine. This was actually truly amazing for me because peptides are known to be very low inductors of immunity, so I was really astonished by the fact that all patients developed specific immunity against the imMucin. We had the control to show that this is specific and not just generally increased immunity. And so, these were the main aims of the study.

We had a secondary aim, to see what these vaccinations will do clinically, meaning to the myeloma. This was not the aim of the study because if you want to assess that, you’ll need truly a large number of patients, which is the next study we’re planning, but this study was aimed against safety and immunogenicity, and this was the number of certain patients we needed. But this very limited and small group of patients, we saw that 11 out of the 15 patients with myeloma responded clinically to the vaccination.

We had eight patients with a stable disease for several months and three patients that achieved CR (complete remission). I think two achieved stringent CR (complete remission). Up to date, we’re just finalizing the paper to be submitted for a journal. Currently, which is I think  approximately two years after we started the study, we still have four patients out of these 11 patients that responded that are still with an ongoing response.

Jenny: And this is all single-agent response, right?

Dr. Shapira: It’s not only single-agent response. They received no standard therapy against myeloma, no proteasome inhibitors or IMiDs or chemotherapy, and most of them are a long while after the last vaccination. They are on practically no maintenance. They had maintenance of the vaccination. It has taken place — I think the last patient was like a year ago, but we have other patients that are close to three years. And since the end of the vaccination that was for the first patient, which was like two and a half years ago, they get no treatment and are still with ongoing response.

So I think if we’re looking at the myeloma field, it looks like a very promising maintenance because it’s very easy to get, the side effects are very limited and don’t necessitate  admissions in an outpatient clinic or any injection and doesn’t suppress the marrow. There’s no side effect to our knowledge of a secondary cancer like you see with Revlimid, so it’s very interesting.

Jenny: Well, I see why people are really excited for me to talk to you. I understand it. I have a few questions about this and I want to work into — usually, I’ll leave it for the end for questions, but I have several patients email me questions about the study, so I think I’ll ask them now. Dana asked, “Do you have plans for US trials for this and will they be for smoldering patients?”

Dr. Shapira: The current plan — I mean, as you know, we live in a very business-pointed and focused to medicine unfortunately, so the company is trying to raise money in order to have the study that will finalize the clinical data of imMucin, enabling them to have it accepted by the EMEA and the FDA, which will be for patients after autologous transplantation as a maintenance treatment, a planned study for groups. I hope that later on when the company would be larger, we could use that in smoldering myeloma and as a post-allogeneic transplant therapy. They’re focused — and I do understand them — at the best possible indication for the vaccine to enable them to survive financially.

Jenny: Well, she has also asked if it was used as a single agent, but you already covered that. So your next study is planned for when? The last study was a phase two, so this one would be a phase three?

Dr. Shapira: Hopefully, yes. Well, it depends on money. We have to raise the funds in order to initiate the study to finalize the protocol. It will take a while. I guess if somebody is interested in investing in the company, this will — I’m not a part of the company, so I’m free to suggest that, but if they have funds, they’ll do it faster.

Jenny: I understand. How would somebody qualify when they were able to open the study? What would they need to look like in order to qualify for that study?

Dr. Shapira: As it looks now while we’re building the next protocol, it looks like we are looking for patients that have achieved at least partial remission with the induction therapy of myeloma and the ongoing autologous transplant that we vaccinated before and after the transplant.

So in order to be qualified for the study, you’ll have to have a good performance status to be a responder, at least to be a partial responder for the induction therapy, and several other qualifications like liver function, like all studies, but these are the two main points which would be determining whether the patient can be qualifying for the study.

Jenny: Can you explain the difference? Because in our last show, we talked a little bit about vaccines and we talked mostly about T-cell research. And then someone else had mentioned peptide vaccines. So what’s the difference between a peptide vaccine or a different kind of vaccine for myeloma therapy?

Dr. Shapira: Most vaccines we had until now are mainly used for prevention of infectious diseases like vaccination against hepatitis or diphtheria or other types of infections. We’re using proteins, which are very large molecules. And in order to make them, you make — it’s very easy to make, but they cause a lot of side effects. You need several vaccinations in order to use them.

Here, what we are using is a very small protein. Peptide is like a shred of protein. We’re using only the part, the epitope, which is important in our eyes in the whole protein. It’s a very small part of the protein. Usually, the side effects of this vaccination will be low, but the vaccine efficacy will be also very low. This is something new that we were able to show with our vaccine, that we were able to get low side effects and very good immunogenicity.

We found specific T-cells against the MUC1 developing in the patients. We saw that the soluble MUC1, you can see — in some patients, you can see that they have MUC1 positivity also in the serum as a protein, floating protein, and you’ll see that these proteins are going away and the patient is becoming negative with this test, so we show that despite the fact that we are using a peptide, we’re able to get very good immunogenicity.

Jenny: Well, it’s very exciting for myeloma patients to think about this. I know that you said it had been used in solid tumors or a target had been used, a MUC1 target. I know several researchers have said, “We need to stop looking at myeloma maybe as a biological disease or cancer as a biological disease and look across cancers that we might share some different features.” So is there anything happening in the solid tumor or all those with MUC1 that’s either added to your study or that you found from that study?

Dr. Shapira: What we are initiating now at Hadassah is also a study in breast cancer, MUC1-positive breast cancer. I have no current details about that. Those are different researches.

I have a patient, a US patient, who came to Hadassah with metastatic breast cancer. She came with no evidence of disease, the reason she was not qualified to any study. She’s been vaccinated with the MUC1 as an off-study patient. At the time, we had enough vaccines to do that. She’s currently gained two years after the vaccination and is free of treatment in the disease.

Jenny: Wonderful!

Dr. Shapira: I have to point again that this was a study with very low number of patients. It was not aimed at a clinical response, so the fact that we found something is very stimulating for us, but this was not the aim of the study. That’s the reason we have to have the next study determining whether this clinical activity that we saw is really something.

Jenny: That was one of the other questions by someone named Suzie. She said, “Were there results of a vaccine response with or without chemo and pre- and post-dosing?” Your answer is “yes”.

Dr. Shapira: Yes, absolutely, no chemo, IMiDs, no proteasome inhibitors, nothing.

Jenny: So if you added those — and you’re a transplantation expert, so in your practice and your research, would you imagine that you would use — you will be using those in combination, it sounds like, for phase three because you’ll be incorporating transplant.

Dr. Shapira: Absolutely, yes. I think that the main point with any immunotherapy is to get to the point of a minimal residual disease in order to achieve the best results. The lower amount of tumor that you have, the easier it will be for the immunotherapy to work.

If you look at myeloma, the best timing tumor-wise of this deduction or chemotherapy will be post-autologous transplant. When you have a good induction — we have very good inductions that are enabling us to get a partial response, a very good partial response in most of the patients, followed by stem cell transplant and autotransplant, and then to use immunotherapy.

Another benefit of the usage of autotransplant is because the suppression of the immune system, which is a side effect of the chemotherapy that we are introducing in the autologous transplant, makes kind of an immune hole for the new of the immune system that will arise after the immunization. So if you will do the vaccination in a non-immunosuppressed patient, a non-transplanted patient, maybe the response will be lower. This was shown in other types of immunotherapies in other types of cancers, so I guess it will be the same here.

So there are two good reasons to do that after autologous transplant, the achievement of minimal residual disease and also the reduction or the suppression of the immune system at the point of the induction of the immunotherapy, and then we’ll have a better response, clinical response later.

Jenny: And so, the goal is to knock down the tumor burden and then have an impact. I have a question and this is also a question by one of the other patients. “How frequently do you think that vaccine needs to be given?” I know you probably haven’t gotten to that stage yet because you’re just testing the safety of that.

Dr. Shapira: Yes, but what we used also — we wanted to see the immune response, so what we did is vaccination every other week, every two weeks, a vaccine that was given for six cycles, and then there was a possibility to continue for another six cycles. So patients came to our outpatient clinic, received the vaccination, stayed for about half an hour just for our records and then went home.

That’s the schedule we’ve used. We are not aware of other schedule because we’ve never tested that, but in the future eventually when we’ll be able to start testing again, then maybe we’ll increase or decrease the frequency of the vaccinations, but this is the frequency we’re using now.

Jenny: It’s just beginning. So if someone wanted to join this study, let’s say they did start a phase three study and they were from United States, would they be able to do that?

Dr. Shapira: It’s an open question. We planned the study to be in the Israeli centers naturally and possibly in the world. The question of the US is still open. It depends on whether they’ll be interested on applying this therapy for the US patients. It’s an open question.

When you have competing studies and you’re not able to record enough patients, it’s not wise to open a new center, so we’ll see that. We’ll get in contact with our colleagues we work with in the States. If we see that there is an interest in joining the study, then naturally we’ll be calling these researchers and it would be easier for US patients to join.

Jenny: Yeah. Would there be anything to prevent a US citizen from coming to your facility if you had it there?

Dr. Shapira: Nothing.

Jenny: That would be great. That was all the questions. Another question was how does imMucin differ from Stimuvax, if you are aware of this drug? I guess they’re both signal peptide domain drugs.

Dr. Shapira: This is actually a question for Dr. Carmon. He’s so knowledgeable about this. I can’t specifically say what are the specific differences between those two, but I think what I heard from him is that we got better immune responses than Stimuvax, but this is actually not my expertise.

Jenny: I saw that you also did work with transplant with NK cells and this is may have been past work, but would you like to describe how you’re using NK cells? Because I know that’s some other form of immunotherapy.

Dr. Shapira: Yes. NK cells are nonspecific killer cells that are floating in our blood, and also, we are able to increase their number in the lab. What we are doing is for several types of cancers, not only for myeloma. We’re inducing immunosuppression by chemos, and then infusion of killer cells that are being introduced, non-specific donors, non-match donors, and infused into the bloodstream of the patient, followed by a stimulants that are given subcutaneously in order to increase the longevity of these killer cells, and we can do that in a few cycles. …with the protocol, but we saw very interesting responses both in solid tumors and also myeloma.

Jenny: And this is a whole separate class of drug, right?

Dr. Shapira: Yes. It’s not a drug. It’s a therapy. Absolutely. Exactly. It’s not related to the vaccination. It’s the development related to the standard care of myeloma.

Jenny: So when it comes to immunotherapies in these different approaches, do you see the future of being able to use them together? For example, maybe this signal, this peptide vaccine and then a different therapy with NK cells, or it’s just too early to think about that?

Dr. Shapira: I don’t think that there is any contradiction of the usage of both. The vaccination is an induction of the specific response while the NK is a non-specific response. This is exactly what we have in our body. We have the specific immune system like T-cells and we have the non-specific, which is like NK or neutrophils or the complement system, so there’s no reason not to use both of them together.

Jenny: Well, I think patients are excited about moving towards that. I also saw that you have a lot of expertise in transplant both allogeneic and autologous, especially in the elderly. So would you like to share what you’re working on for that?

Dr. Shapira: What I’m truly proud of is the change that we did in the medical field. It wasn’t just me, it was the whole group. We changed the upper limit age of allogeneic transplantation. In the past, it was widely accepted that there is no possibility to transplant patients above the age of 40 in the beginning, and then 50, which was kind of frustrating because most of the hematological diseases that are being triggered by transplant appear in patients older than 40 or 50. Myeloma is, AML is, MDS, Non-Hodgkin’s Lymphoma, CML, so it was an added treatment and you have no ability to use that.

We showed it in our work and definitely this has changed the attitude of many hematologists. We showed that if you assess the biological age of the patient rather than the chronological age of the patient, then you can transplant safely patients above the age of 60. We also did a couple with the age of 70. It’s not published yet.

So if you carefully look at them, we know that 60 is — people at the age of 60 are young, not like the 60 of years ago. I think it’s the same with patients above the age of 70. Particularly for me, it’s age discrimination, not sending a patient to transplant just because of his or her chronological age is high. We have to truly assess the biological age and we need to see the patient is in good clinical shape with no serious medical history.

Then this patient can undergo transplant safely and enjoy the effect of allogeneic transplantation. This is what we showed and it definitely has affected the insurance companies and the hematologists.

Jenny: You are saying this is for allogeneic, right? Because that’s really remarkable.

Dr. Shapira: Allogeneic, Definitely. Autologous is more though. An autologous transplant for patient at the age of 70 plus sounds easier, much easier if you compare it to allogeneic transplantation, but we did also allogeneic transplantation for patients above the age of 70. It’s really age discrimination and we don’t like that.

Jenny: So how do you determine biological age? You’re looking at what factors of fitness or health? You’re saying not a lot of comorbidity type of things, so how do you define that?

Dr. Shapira: Medical history, seeing whether the patient had any heart condition, longstanding untreated hypertension or diabetes, renal problems, et cetera, just standard comorbidities, but also their physical capabilities. How physically shaped is the patient? We have many — I’m sure in the States also — many, many patients around the age of 60 which are totally physically active. They work. They’re able to do their jobs. They’re able to enjoy gymnasiums and they’re physically in very good shape. These patients are good candidates for transplants.

Jenny: So is it more of a mindset change or has something changed in the therapy to make it safer and more effective?

Dr. Shapira: Definitely both. Therapy has changed because we showed in the beginning of the ’90s that we’re able to use a much lower dose of chemotherapy for  the induction of allogeneic transplantation. This is what is news nowadays throughout the world, which is called RIC, which are the initials of Reduced Intensity Conditioning. We showed that you don’t have to kill the patient in order to kill the marrow and have the engraftment of the new marrow. You can use easier drugs. You can use lower doses of these drugs and still have engraftment of the cells without the major side effects of the transplant.

Also, I’m seeing that there’s been a remarkable change in the health of patients above the age of 60 and 70. I can’t really call them elderly. Sixty is young nowadays, but they were thought to be elderlies at the time and I think the age burden has changed because of nutrition, because of anti-chemical disease therapies, because of better control of hypertension and diabetes, because of changes in attitude for smoking.

I think there’s been a remarkable difference in the health of people above the age of 60. I think the combination of both changed the reality, and this enabled the change in attitudes for many patients and their physicians.

Jenny: Now, there was a lot of work also that you were doing to reduce host-versus-graft, which is part of at least the allogeneic transplant. Would you like to share what you have done there?

Dr. Shapira: What I did is try to use less immunosuppressant agents systemic-wise and try to use them locally or try to immunomodulate the immune system rather than having a very severe systemic immunosuppression.

Just a short introduction, when we’re using allogeneic transplantation, we have to use prophylactic doses of immunosuppression agents, but when GVHD appears, what is the standard care nowadays is high-dose steroids, which is a very nonspecific immunosuppression. When this fails — everybody uses a different type of immunosuppression, but in general, it’s very systemic, which is if it works, it still leaves the patient as a target for very severe infections and morbidity or mortality.

What we did is the usage of a specific drug which is not an immunosuppressant, but rather immunomodulating, or the use of standard drugs only locally. For example, we developed a way to infuse steroids directly to the organ which is affected, for example, the liver or the gut. That’s a very, very strong immunosuppression in the affected organ, but not having a very severe immunosuppression systemically.

By that, we managed to double the survival of the patients having refractory graft-versus-host disease in our institution, a real life result, not study results, which are initially higher than the real life, but this real life result is doubling of the survival, which is great. It’s still not perfect, but they’re really great.

The other thing that I’m doing, this is something that’s still very early for the animal work. We discovered that if you transplant two donors at the same time in a mouse, you get increased anti-tumor effect while you get decreased GVHD. We are working on that to understand exactly what’s happening, but this is a very interesting pathway that hopefully we’d be walking through in the future in the pre-clinical and hopefully later on in the clinical field.

Jenny: That’s unique. I’ve never heard of that before, so that will be exciting to see what you find.

Dr. Shapira: Yes. I have a lab worker — I don’t do the work, but she’s a believer. She saw enough animal studies. She knows that this method works. We still don’t understand how, but she definitely — we have dozens and dozens of mice. We have more than a few experiments that we did and in all of them, we had the same response. It increased the anti-tumor effect and decreased GVHD. It’s very interesting.

Jenny: Wow!

Dr. Shapira: Usually, what we see is when we are able to increase the anti-tumor, you’ll get more GVHD and vice versa. When you decrease the GVHD, you’ll get less anti-tumor, so this is really exciting for us.

Jenny: When you find something like that in the lab, how long does it take to get to the clinic with that kind of hypothesis or discovery?

Dr. Shapira: It depends really on the methods or the specific acts that are doing that. For example, we see that the reason is because of change at the molecular level, then we’ll have to introduce some drugs, new drugs, and this will take a very long while. If we’ll see it’s on the level of cellular components that are changed, maybe this will be easier to bring to the clinical test.

Jenny: Just an overall question, when do you look at using the allogeneic transplant versus the autologous transplant?

Dr. Shapira: In myeloma or in general?

Jenny: In myeloma.

Dr. Shapira: It’s very accepted to use autologous transplant as an upfront treatment for patients that have responded to the induction therapy and are felt to be eligible for auto transplant physically. Allogeneic transplant is a complicated issue. Patients with myeloma — at least in the past, we’re very sensitive to the allogeneic effect, and the morbidity or mortality was tremendous. So I think that most patients that are transplanted now, these are patients that are highly refractory, but they’re young and strong and you’d think that they have a chance to withhold the allogeneic effect while being out of any other therapies which are standard therapies.

In our institution, we don’t get patients for an upfront tandem transplant or a very early allogeneic transplant after failures. The issue is open, but all previous studies show that the sensitivity of myeloma patients for allogeneic effect is high, the morbidity is high and the mortality is high, so many people are reluctant to send or to accept patients for allogeneic transplantation.

Jenny: And we have interviewed another doctor who specializes in allogeneic transplant, just remarks that if you have graft-versus-host for the first hundred days, that’s not a good thing, but if you have it kind of as a chronic long-term, it could actually be good for an anti-myeloma effect. Have you found that to be true as well?

Dr. Shapira: Yes, definitely. What we hope in the future is to combine the imMucin, the anti-MUC1 vaccination as a post-transplant care because you change the immune system. You change that and we hope to direct the new allogeneic immune system against the myeloma easily while using the imMucin.

Jenny: And if the objective is to knock down the tumor burden and then give the vaccine, could you see it being a preventative course for either an MGUS or smoldering patient in the future?

Dr. Shapira: I hope yes.

Jenny: Well, everybody would be excited about that.

Dr. Shapira: I suggested to a few colleagues of mine that are myeloma physicians, I suggested that with the new drugs that we have nowadays, we are able to achieve a second MGUS state in patients. Patients as we know that MGUS progresses into myeloma, and I think that there are patients that we are able to get them back with the induction and with transplant.

Definitely we have a few patients like that with very prolonged response without any therapy, but also with the good maintenance that we have nowadays, I think that there’s an increase in the number of patients that achieved this so-called second MGUS state, which is very interesting. Again, these patients will hopefully be candidates for the imMucin.

Everybody knows these patients that have remarkable response to the treatment and a very, very prolonged progression-free survival, which is resembling the MGUS, although they still have protein in the blood in a very low dose, in a very stable dose. So I think if you disregard the old effects on the skeleton and the old effects on the kidneys, then if you look at them carefully, you may see these patients with second MGUS states.

This is the definition that has to be worked on, but I’m sure that we can define these patients, find them, and then isolate them for further therapy, further studies. They are different types of diseases and a different type of disease response as compared to others.

Jenny: Let me ask you for a minute about recruitment for clinical trials. I know European networks — I don’t know the way it works in Israel – is different from how they recruit in the United States, but — I guess two questions.

What’s the impact of patients being willing to participate in clinical trials? Is that a challenge for you in Israel or do you have a network that has a better approach than how the US does it? Because I know some of your approaches better than how US does it.

Dr. Shapira: Actually, I think myeloma is an excellent example for that because in Israel, there’s a very strong patient union, which is highly interested in the development of new therapies for myeloma, and also for the introduction of proven therapies into the Israeli basket. We have a different insurance program here. It’s different from the States. It’s a national insurance, health insurance, but they are very strong in their contact with the physicians. They are very strong in their contacts with patients. They are strong in the introduction of patients into studies and also to the whole introduction of novel therapies into the Israeli basket.

So definitely, the recruitment of patients is important for the development of new drugs and definitely the cooperation between physicians and the patients is important for future therapies.

Jenny: That’s one of the goals of this series, is to help give exposure to the amazing work like you are doing.

Dr. Shapira: If you’re interested, the name of the group in Israel is called AMEN, which is a very nice name. It’s the initials also of the Israeli myeloma group. You can contact them and learn from their experience because they’re very, very strong here in Israel. I think it’s the strongest patient group in general in Israel; very well-organized.

Jenny: I will contact them. That’s fantastic. Well, Dr. Shapira, thank you so much for joining us today. You’re doing really remarkable work. I know I’ve used that word several times, but what you’re doing is changing the field of myeloma, so thank you so much for being willing to participate on the show and share what you’re doing.

Dr. Shapira: Thank you very much for the invitation. We truly hope that we’re changing the field of myeloma. We don’t know that yet, but we hope that this is the beginning of a new era in myeloma.

Jenny: Well, we love to see it when researchers are pushing forward into new areas and trying new things. So if there’s anything that we can do to support your work, we’d love to do it.

Thank you for listening to another episode of Innovation in Myeloma. Join us next week for our next mPatient Radio interview as we learn more about how we as patients can help support a drive for cure for myeloma by joining clinical trials.



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  1. Pingback: Vaxil Drug Shows Significant Promise In Myeloma: Vaccine Trains Immune System To Destroy Cancer Cells - The Myeloma Crowd

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