Aaron: Welcome back to the Healthcare Triage Podcast. This Healthcare Triage Podcast is sponsored by Indiana University School of Medicine, whose mission it is to advance health in the state of Indiana and beyond by promoting innovation and excellence in education, research, and patient care. IU School of Medicine is leading Indiana University's first grand challenge: the precision health initiative with bold goals to cure multiple myeloma, triple negative breast cancer, and childhood sarcoma, and prevent type-2 diabetes, and alzheimer's disease.

And, that's perfect, because today we're going to be talking about multiple myeloma. Our guest this week is Rafat Abonour, who's the director of the myeloma program at Indiana University School of Medicine. We're going to be talking today about multiple myeloma and where the cutting edge research is. What people are doing, what people are thinking, where we might be going.

So, welcome. Thank you for joining us.

Rafat: Thank you for having me.

A: Could we start a little bit, we're always interested in hearing about the backgrounds of our guests. How did you get to this position, and how did you get interested in your research? How did you get here?

R: So I started wanting to become a transplant surgeon, but then I ended up doing just a hematology fellowship and bone marrow transplant. And, I did my research on plasma cells; these are the cells that cause multiple myeloma. And then, I started doing gene therapy, and gene therapy was an exciting and dangerous. I needed to focus on something. So, I knew plasma cells and I loved myeloma patients, so I decided to focus on that.

A: So, let's say, what are plasma cells?

R: So, plasma cells are the cells that make antibodies to help us fight infection. We need them; that's how we survive, you know, 100 years, 70 years, whatever. So, what happened is that one of these plasma cells become malignant and start reproducing itself and causing harm to the patient. 

A: So, so they're a type of white blood cell?

R: Yes, sir.

A: Ok. Where are they made?

R: Well, they actually start in the lymph nodes and then they migrate to the bone marrow where they reside. You know, so you get your first sort of encounter was, for example, let's say tetanus or, you know, pneumonia bacteria in the blood, and these cells, you know, mature, become plasma cells, produce memory antibodies to help us fight infections as, you know, when we get exposed again to the pneumonia.

And they reside in the bone marrow. When we need them, you know, they get out, they make more new antibodies to help us fight infection.

A: So, can you talk a little bit more about how they work when they're working right? How exactly do they help us fight infection?

R: Well, they produce a specific antibody. So, we have a repertoire of plasma cells that are capable of recognizing different pathogens, you know, from the mumps to the measles to the influenza to the pneumonia. And, so, every time we get exposed to one of these pathogens, these plasma cells proliferate and produce more antibodies to fight the infection.

A: And, so what happens when they produce the antibodies? What happens next?

R: Well, the antibodies bind to the pathogens, and you just neutralize it or, you know, help other cells gobble it up.

A: Ok. So, what happens when things go wrong?

R: Well, when things goes wrong, is that one of these plasma cells start accumulating in the bone marrow. So, you initially have, for example, maybe 5% of abnormal plasma cells in the bone marrow. They don't cause any harm. We call that condition MGUS (monoclonal gammopathy) of undetermined significance. Just having a monoclonal protein doesn't cause harm to the patient. But, what happens next is that tons of these cells start, you know, accumulating in the bone marrow. So, you have like 10/20%, but it's still not causing harm. So, we call that condition smoldering myeloma. And then, eventually what will happen is that these plasma cells can affect the patients in different ways. One is that it can weaken the bone. So, about 70% of patients with myeloma will have either osteoporosis, holes in the bones, or they start breaking bones..

So, they have, you know, they just try to lift a bag, you know, and then they break a bone in their back or something like that. So, myeloma can affect the bones, can cause anemia, can cause very high calcium level, because you're leeching calcium out of the bone. So, the patient become, yeah, uh, unable to think and may go into a coma, or they can actually get kidney damage. So, we call these sort of the CRAB criteria for diagnosing myeloma. The "C" is for high calcium, the "R" renal or kidney failure, "A" anemia, or bone disease. So, you have a lot of these abnormal cells in the bone marrow and you have one of these criteria, then we, you know, that patient has multiple myeloma. 

A: What makes the plasma cells go bad? What goes wrong?

R: So we actually, a lot of research going on in terms of environmental exposures, and just this week got, uh, big settlement against Roundup, because they, when, patients develop multiple myeloma from using that. So, we think there's toxic exposures; farming communities, there's increased risk of multiple myeloma, near factories and near mining communities. For example, I have patients in, near a mine in southwest Indiana where multiple people who work in that mine's developed multiple myeloma, you know, and the question is what did they dump into the water, I mean, these people are drinking well water. And so, I think, we think chemical exposure plays a role in making these plasma cells sort of, um, become malignant and multiply and, you know, cause harm and cause disease.

A: Ok, so once somebody is-- Once, we have a concern, they've met the CRAB criteria, what happens next to help make the diagnosis?

R: So, we do several things, and number one, obviously we need to do a blood test to see if they are anemic, they have high calcium, or they have kidney failure. The second thing is that we look for this abnormal protein, because myeloma starts from one plasma cell. The protein they produce is unique, we call it monoclonal protein. So, we do a specific blood test to check for that monoclonal protein, and find it. We have to find a monoclonal protein or we find an abnormal part of that protein race, we call it a free light chain. So, we check that.

The second thing, we have to look and see what they have in the bone marrow. So, we do a bone marrow biopsy to see the number of these abnormal cells and what type of cells. We do genetic analysis on those cells to see what they do, because myeloma patients, some of them do very well, some of them do ok, and some of them do poorly. And, the genetic makeup of the myeloma can help you distinguish these three groups.

A: So, that was actually going to be my next question. Are, is sort of all or all cases of multiple myeloma the same? Or, are they all very different? Or, do they fall into a bunch of categories?

R: Yeah, I mean, I think the term multiple may not be really because of multiple lesions was in the patients. I think it's multiple presentation of the disease.

A: Ok. 

R: So, I have patients who do very well. They get one kind of treatment, and they go on and stay in remission forever. And then, we have patients who within a year or two, they relapse and they actually don't do well. And then, so that's about 20% for each group. And then the rest, the 60%, those patients, you know, have multiple relapses but you can control the disease and they can live a long life.

A: So, what is the treatment for the most part?

R: So, the treatment has evolved. It use to be more chemotherapy or traditional drugs that cause hair loss or blood counts abnormalities, but now we have these, we call them sort of novel drugs. They work on things that influence the proliferation of the cells, or their interaction with the neighborhood where they live.

So, these cells can, you know, not really find hospitable environment within the bone marrow to grow. So, these are new drugs that, in combination, have produced amazing results. We still consider high-dose chemotherapy and stem cell transplant as part of the treatment to improve the outcome, and some patients may need maintenance therapy after you do the stem cell transplant.

A: So, for the most part, though, it's drugs?

R: Yes, it is drugs.

A: And so, what's the typical course of treatment?

R: So, most patients will require what we call "induction treatment," which is trying to control the disease, trying to improve the symptoms, and that will take three to four cycles, the cycle is about four weeks. After that, you do the stem cell transplant which is two components: One is collecting the stem cells that support the use of high-dose chemotherapy; then you give this big dose chemotherapy which cause everything in the bone marrow, but you have the patient's stem cells that make blood cells stored. So, the next day, you give it to the patients, and these cells will grow and make healthy stem cells.

A: So, this is when you're doing a stem cell transplant, you're actually transplanting the patient's cells back into their own body.

R: Yes.

A: How does that work?

R: So, what you do is you collect the patient's own stem cells first, and these cells live in the bone marrow. So, what you do is you give a specific hormone that stimulate these cells to grow every day for four days, and the fifth day, their blood is full of these stem cells. What you do is you take the blood out, and you do a process like dialysis - a process called "apheresis." So, you collect only the stem cells and you store them, you give the blood back to the patients, and you do this in the outpatient in the blood back for four hours, five hours a day. Sometimes in one day, you get all the stem cells you need, sometimes you need up to three days.

A: How do you be sure that you're not collecting bad cells or that those won't turn into bad cells?

A: - won't turn into bad cells.

R: Yeah, so we have looked, actually, we did research on that. So, what we're looking for is a specific marker on the surface of these cells make some stem cells called "CD34," and we look to see if we collect any myeloma cells, and we did very sensitive assay, and two things: Myeloma cells don't mobilize that effectively, and the second thing is that they don't freeze well. So basically, the product that we give back to the patient is very unlikely to contain any myeloma cells.

A: Knowing that the stem cells could then-, are you assured that the stem cells won't then develop into cells which will turn back into myeloma, or is that, you just have to -

R: So, the stem cells are the cells that make white cells red blood cells and platelets -

A: Right.

R: And the process of developing multiple myeloma doesn't really start at the stem cell level.

A: Okay.

R: Stems start probably around when they sort of mature to white cells and before they divide into lymphocytes or neutrophils - different part of the white cells - it's at the lymphocytes level: you know, when they become B cells, the B cells become plasma cells - so maybe it's between the B cells and the plasma cells.

A: So, I guess-, I'm not - and this question may be totally naive - given that we know that whatever was in this person that such that their cells could develop into myeloma cells, would they be better off with someone else's stem cells in the sense that those cells are less likely? Or is that just too hard to do?

R: Well, it's very hard to do. So, we have done what we called "allergenic transplant" - donor stem cell transplant. The problem is that most patients and with multiple myeloma are in their late 60s. So, allergenic transplant is very risky; we actually lose a large number of these patients, and despite doing the allergenic transplant, some patients have relapsed. So, it's not really a routinely used approach. Maybe in the young patients and you may consider an allergenic transplant. The issue with allergenic transplant is the risk of a graft-versus-host disease that -

R: - that immune cells from the donor do not like where they're living, and the new-, in the patients. So, you get damage to the skin, liver, and the intestine. But the other thing is that the advantage of the allergenic transplant used to be that the graft-versus-disease. And fortunately, the myeloma cells tend to hide from the immune system, and we don't get a very good graft-versus myeloma effect when we do allergenic transplant.

A: Okay. So patients get a round of drugs, and then stem cell therapy - what's the usual course after that?

R: So after three months later, they recover from the stem cell transplant, then some patients are considered for maintenance therapy. So, two things: One, we give them medicine to keep their bone from breaking down, we do that as a infusion or injection once a month, and then sometimes pills of these novel chemotherapy drugs that will help maintain the response.

I think the research should be focusing on what to do after transplant when the patient have minimal residual disease. How can we improve the patient IMMUNE response to eradicate the residual disease?

A: Right.

R: Is it the chemo pill or is it some other strategies that we are trying actually to explore here.

A: How many different types of drugs are available? I mean, does everybody get sort of the same cocktail of drugs or is it individualized?

R: So, when I started working on multiple myeloma, we had only this traditional chemotherapy. In 2003, the first in-class drug was approved, which was proteasome inhibitor. And proteasome inhibitor is, just think about it like you have a garbage disposal and you just clog it, and just the accumulation of toxic stuff, and the cells start dying. So that's how proteasome inhibitor works. And these are amazing, I mean, these drugs have changed the course of the disease.

Now, there are three drugs in that class available, and in 2006 -

R: -2006, we got a class of drugs approved called the "immunomodulatory drugs." And the first in class was the drug thalidomide; that drug that caused a birth defect when it was used in the 50s for motion sickness and nausea associated with pregnancy. And this drug, we didn't understand how it works for a long time, but it worked. But the problem was using thalidomide for a long time, it can cause nerve damage.

A: Okay.

R: So, the company that makes that drug start developing next generation of that drugs that caused less neuropathy. We actually have two drugs in that class now. We have three immunomodulator drugs, three proteasome inhibitor. And then more recently, the FDA approved drugs we call a "monoclonal antibodies." So, these are drugs that recognize the surface of myeloma cells and help eradicate these myeloma cells - so protein that bind to the myeloma and bring the immune cells to try to eradicate them.

A: So, how do you decide which of those to use?

R: So, that's a great things, that's why we do clinical trial, and in the clinical trials, we find the best combination. So, first of all, we now know that one drug is not enough; you have to use a cocktail of drugs. So, the good things for patient today is you have different cocktails, so based on their medical condition, you can find the right combination therapy.

A: So when you say "their condition," what do you mean, for example?

R: So, for example, if somebody has significant nerve damage, you want to avoid drugs that cause further nerve damage. If somebody have advanced kidney failure, you want to avoid the drugs that can be too toxic if you have kidney failure. So, that's a good news for the patient is that we can tailor the therapy toward their conditions and their actually desire. I mean, some people like only oral regimen; they don't want to go to infusion, they can't really go twice a week to the clinic -

R: - a week to the clinic to get chemotherapy. We have overall regimens for them.

A: So, when you say their "cocktails," is it multiple drugs in a class or you're picking drugs from each different class?

R: Exactly, we pick drugs from a different class. So, basically what we do is synergy without overlapping toxicity.

A: Okay. So, what is the usual course? You have your treatment, your maintenance, how do most patients do?

R: So, most people, as I told you, they really do well, they stay in remission for a long time. Now, the average time in remission may be five to seven years. But unfortunately, we have these about 20% of patients who relapse within the first two years - we call these our "high risk." Risk of what? Risk of shorter remission, shorter survival. That's where really a lot of research going on to try to improve the outcome of these patients.

A: So, do you treat them again?

R: Yes, we treat them again. We try to find novel combinations, we try to find clinical trials for these patients, we're trying to employ some newer strategy. For example, one of the newer strategy will be what we call "CAR T cells," which is basically taking the patient's own immune cells, expand them, genetically modify them to make sure that they can recognize myeloma and kill it. So, we put two genes: one to recognize myeloma and one killer genes. So, that's why we call it "chimeric receptor antigen T cells - CAR T cells."

So, these cells, I mean these kind of therapy is now used in clinical trial and relapse patients, but we may be able now to use it in a clinical trials for the high-risk patient upfront before they get to relapse and have a horrible disease that's hard to control.

A: How hard is it to do that?

R: So, first of all, you have to collect the patient T cells with the lymphocytes that become the killer cells. So, basically, it's like we collect the stem cells: We do apheresis - we take the blood out, separate the white cells from the -

R: - white cells from the rest of the blood. And then when you take these to the lab - I mean to the processing/manufacturing facility - you separate the specific cells, we call them "T cells," and then you incubate them with a virus that get the two genes inside the cells after you expand these cells. And then you bring them back and take them back to the patient.

So, it's very expensive process, and the FDA, as you know, approved two CAR T cells - one for lymphoma and one for leukemia - that are very expensive. But there's a lot of different companies are working on it. We at Indiana University School of Medicine put together grants and we have a center - the Brown Center for Immunotherapy - we're almost ready to recruit the director of that, and our goal is to improve on the safety of these products, the specificity of these products, and improve the sustainability. 

I mean, unfortunately, if you look at some of the clinical trials, these cells lasted about a year; that's not good enough because if they start relapsing in a year and you give them very expensive therapy. So, our goal is to make CAR T cells more specific, safe, and maybe less expensive.

A: How expensive is it?

R: Well, for the commercial products is almost $400,000 they charge for that. If we produce it locally, it may cost us probably $40,000. But that's why our goal is to see if we can start making our own cartridges.

A: So, what's the usual prognosis for a patient who develops multiple myeloma?

R: It really has improved significantly. If you look at patients when they were diagnosed 15 years ago, 20 years ago, we were saying you can live on-average two to three years. Now, I think, if you look at patients, depends on their stage: If you have stage-one [stage I of stage I, II, III] disease, you would think these patients should live at least 15, 20 years.

A: Could you tell us what "stage I" is?

R: So, stage I is we look at certain things: We look at the chromosomes and inside the bone marrow - are they good chromosome/bad chromosome; we look at something called "LDH" - enzymes in the blood; we look at albumin. So, if these are normal,  there's another protein we look at in the blood called "beta-2 microglobulin." So, if these are normal, and the cytogenetics are good one, that's a stage I.

And these patients, if you look at their five-year survival, more than 93% are alive at five years. So, the stage may influence how long they live, but we are seeing more patients living with myeloma and starting to die from something else compared to what we did 10, 15 years ago.

A: What are the other stages?

R: So, stage II and III?

A: Mm-hmm.

R: So, III is the high-risk, where you have high beta-2 microglobulin, high LDH, high or low albumin, and bad cytogenetics in the bone marrow.

A: Okay. So, it's more about the sta-, like the actual chromosomes and what the cells look like than how quickly you caught it or how much-, obviously, metastasized is a totally different meaning.

R: Well, yeah. I mean, myeloma is always sort of detected at advanced or all over the body; unlike other tumors, it's always systemic disease. But if you detected at early stage before you have a lot of myeloma, you have a lot of bone destruction, I think you're gonna do well.

Now, the trick is what we're doing is a lot of research going on is,  first of all, as I told you, myeloma is preceded by two conditions: MGUS and smoldering myeloma. So, why don't we treat all smoldering myeloma? Because that treatment can have side effect, and we don't know if it really can cure patients. If we have a curative regimen, then we can use it early on and take some risk.

So, only specific group of -

R: - group of smoldering myeloma - which we call "high risk for progressing," you know, half of them will progress to myeloma within two years - we're doing clinical trials on them. And there are two kinds of clinical trials: One used is combination chemotherapy that we have the novel agents - the monoclonal antibodies, the proteasome inhibitor - we put them together, and what we're trying to do was in two years to see how many patients are we putting in really solid remission, with the hope to cure these patients.

The other approach to the high-risk multiple myeloma is that can we actually make these myeloma cells visible to the immune system? Can we make the immune system recognize myeloma? So what we're trying to do is actually generate a vaccine from these myeloma cells, and then inoculate these patients with this vaccine with the hope that they developed immunity that will eradicate the myeloma.

A: So, would the vaccine be tailored individually to each patient?

R: Yes. So, we take the myeloma cells and generate a vaccine from THEIR myeloma cells.

A: So, is that the kind of thing that's just gonna have to - do you think will be commercially, like, there'll be a company that does that? Or is that where just you need to go somewhere that's doing it in a lab?

R: I think we should be commercially available, but that's the hope - that you can generate a vaccine for each patient: you just send the cells, and they process it, and they send you a vaccine.

A: What do you think the most exciting work's being done right now? Or what is the most exc-, what area? I'm not saying where in the country; I mean what area is the most exciting work?

R: For me, for example, I am actually looking and trying to figure out, "Can we prevent the development of multiple myeloma?" So, I'm doing a clinical trial in patient with monoclonal gammopathy of undetermined significance [MGUS], and I'm trying to see if we can actually prevent him from developing multiple myeloma. So, let me tell you the background of that.

A: Sure.

R: So, in my practice, I see a lot of monoclonal gammopathy of undetermined significance, and I have seen patients who lost the monoclonal gammopathy.

R: - So, how did it disappear? So, in the 6-8 patients I have seen they lost weight, and by weight loss, they lost the monoclonal gammopathy.

A: Really?

R: So, we think obesity is an inflammatory state can stimulate plasma cells. So, what we're doing actually, we're putting a trial together in which we start accruing here; we're going to look at patients who are undergoing weight-reduction surgery, and what we're going to do is screen them for MGUS. And then those who are positive for monoclonal gammopathy, we're going to follow them after the surgery and look at the group that lose weight versus the group that doesn't lose weight.

A: Sure.

R: Are they going to lose the MGUS or not? So, if we can prove that they lost this abnormal protein, that's a good thing, and we're going to explore and see why. Is it because they lost certain inflammatory proteins when they lost the weight, or not? And so, that would be a great advances, you know.

A: Is obesity a known risk factor for myeloma?

R: Yes, if patient who are (?~25:07)OP-, let me tell you: If somebody has monoclonal gammopathy and they are obese, they have four and a half a chance of developing multiple myeloma compared to non-obese patients.

A: Interesting.

R: Yeah. So, this is a big study that was done at St. Louis VA hospital, because they have records on patients who develop myeloma, and they know their weight, and they know if they MGUS or not. So, the obese - four and a half time chance.

A: Is type 2 diabetes tied up in that, too, or is it just the obesity?

R: I think it's just the obesity. I haven't looked at it, I'm not familiar with any data on diabetes.

A: So, besides the prevention, what else is...?

R: So, prevention - I think the other thing is that we really need to screen, we need to see in this area that we talked about - in the high-risk area: near farming community, near mining community, near factories that was -

R: - factories that was dumping a lot of these chemicals - can we understand how many people *do* have these pre-myeloma conditions. It will be interesting to understand that, because then we will study the impact of this environment on these preconditions. And then what we would like to see is predisposing factor in addition to the chemicals; if you have certain gene, will you get myeloma when you're exposed to a certain pathogens. So, I think that's exciting to us.

And then finally, can we find a way to deal with high-risk myeloma? I think that's really the most frustrating condition we deal with. And my goal is to really understand the immune makeup of these patients, and try to understand how we can enhance it to help us eradicate the disease.

A: How are - I mean, just because clearly we live locally - how are patients doing here locally, and what kind of studies are we doing locally to try to help?

R: So, that's a great question. As you know, Indiana University issued this great grant challenge grant trying to really cure three diseases and cancers in Indiana, and multiple myeloma was selected as one of these diseases. And so, one of the proposals that we have is that we want to understand how myeloma patients do in Indiana. We want to understand their diagnosis, their treatment, their outcome, their side effect. 

In addition, we want to understand their genetic makeup and also understand the myeloma genetic makeup and the environment. So, we're putting together what we call a "cohort of patients," we want to analyze 1,000 patients with myeloma and pre-myeloma conditions in Indiana. We started actually accruing patients in November and we have more 170 patients thus far enrolled. 

So, what we're doing is we're looking at their baseline genetic information: we take saliva, we take blood - and when we do a bone marrow biopsy, we take the myeloma cells -

R: - we take the myeloma cells and the neighborhood where they live inside the bone marrow cells, and we try to analyze them. And the goal is to try to understand do they have a predisposition to certain things, what is their immune profile, what's their ability to metabolize certain drugs or not - and then sort of correlate the natural history of the disease: what's their genetic makeups, the myeloma genetic makeups, and the micro-environment within the bone marrow makeups.

A: Are you looking at their broader environment as well: where they live, where there they might be exposed to...?

R: Exactly. So, we are doing that in collaboration with a group down in Bloomington, because by zip code, you can figure out where they live, what their exposed to, and things like that. And we have survey that we ask the patients to help us understand their occupations and where they grew up - things like that.

A: So, how long do you think that'll have to take to get all the patients you want?

R: Since November - that's about four or five months - we have 170 patients, so hopefully we can accrue all these patients within two, two and a half years.

A: Are those all new diagnoses, or -

R: No.

A: - are those all patients you're picking up?

R: Our patients from newly diagnosed relapsed patients.

A: How common is myeloma to begin with?

R: Myeloma is about one and a half percent of all cancers, and we're trying to figure out the exact incidents in Indiana is probably 1,200 new patients diagnosed a year.

A: Clearly the NIH has to give money to this, but how else do you put money together? Are there foundations? How else does myeloma research get done?

R: As an avid runner, about 15 years ago we were sitting with patients trying to figure out how we could support myeloma research at Indiana University, one of my patients said, "Why don't we do a 5K for myeloma?" And I said, "Well, everybody has a 5K for myeloma; how about we do something different? You guys come to me -

R: - you guys come to me from all over Indiana for a second opinion - why don't you go to your community and spread the word about the disease?" And they said, "Wow, that's exciting." But I'm not going to be riding a car to go there; I'm just gonna run. 

In the first year, I wanted to go run to Fort Wayne. 

A: Okay.

R: But that was a huge distance - 

A: That's for people who don't live in Indiana.

R: - that's 120 miles; I said, "I'm not ready." [A chuckles] So, what we did is the first four years, we split it - one day of running, one day of cycling.

A: Okay.

R: So, we did about 50 miles of running and the rest is cycling -

A: [undertone] That's still a lot of running.

R: So, that's how "Miles for Myeloma" started. And then, because the distance is getting like 200, 250 miles, it's just two days or three days of cycling.

A: Okay.

R: So we come from St. Louis to Indianapolis, from Columbus, Ohio to Indianapolis, "Miles for Myeloma," we have raised almost 5 million dollars. But the most exciting thing about the whole thing is that we have patients who ride with us, -

A: Right.

R: - it's organized by family of patients that do that. And so the thing about it is that makes me really excited is to see my myeloma patients riding.

A: Yeah.

R: And I still remember one day - because you know you get these guys who want to ride with you and they're very really amazing cyclists, and this is not a race - this a group of people trying to ride together to support each other and spread the word about myeloma. So, if you have somebody already in Indianapolis and the other person still in Terre Haute, it's not fun -

A: No.

R: - it's hard. So, I remember one time I want to tame the group a little bit, so I stopped everybody, and I said, "Do you know why we're doing this?" Because of myeloma. What we're going to do about it: we're going to spread the word, we're going to try to raise awareness, we want to make sure that everybody understands this disease needs to be cured. So, I said, "How many of you are riding with myeloma today?" And there were two people. And I said, "How many of you riding -

R: - riding with myeloma and still on treatment for myeloma?" One guy.

[positive music underscore]

I said, "Okay, so this guy is gonna lead us, and everybody has to follow him."

A: Right.

R: "Do not pass this guy." [A laughs] So, I was kinda probably doing it because I was tired.

A: Right!

R: I want to slow the pace down a little bit. So, this guy grabbed a bottle of water, poured it over his head, and we actually stopped at the bottom of a hill, and this guy was climbing so fast [A laughing] I was working hard to stay with him, and I said, "Oh my gosh, why did I say that!?" 

But it was amazing to see how excited he was, how aggressive he was climbing that hill, and it just makes me know that today myeloma patients can live a normal life; it's not a disease that stops you from living your life, and that's why we need to tailor the therapy so they can live a healthy quality life, and hopefully we can find a combination [music ends] that cure them so that they don't stay on treatment forever. 

A: This Healthcare Triage podcast is sponsored by Indiana University School of Medicine whose mission is to advance health in the state of Indiana and beyond by promoting innovation and excellence in education, research, and patient care. IU School of Medicine is leading Indiana University's first grand challenge - the Precision Health Initiative - with bold goals to cure multiple myeloma, triple negative breast cancer, and childhood sarcoma, and prevent type 2 diabetes and Alzheimer's disease.

Thanks again to our guest, Rafat Abonour, for our discussion of multiple myeloma, what causes it, what we're doing about it, and where things might be going in the future.

Listen to the Healthcare Triage podcast each and every month for information about health, health policy, health research - we'll see you next month.

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