This month, Aaron is talking to Dr. Rafat Abonour about multiple myeloma. Multiple myeloma is a cancer that forms in white blood cells, and Dr. Abonour tells Aaron about how the disease affects patients, and the cutting edge of research into treatments. And we get a nice story about biking.
The 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.
Dr. Aaron Carroll: Welcome back to the Healthcare Triage Podcast. 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 II diabetes and Alzheimer's disease.
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. Welcome.
Dr. Rafat Abonour: Thank you.
Dr. Aaron Carroll: Thank you for joining us.
Dr. Rafat Abonour: Thank you for having me.
Dr. Aaron Carroll: Can we start a little bit? We're always interested in hearing about the backgrounds of our guests. How did you get to this position? How did you get interested in your research? How did you get here?
Dr. Rafat Abonour: I started wanting to become a transplant surgeon, but then I ended up doing just a hematology fellowship and bone marrow transplant. I did my research on plasma cells. These are the cells that cause multiple myeloma. Then I started doing gene therapy and gene therapy wasn't exciting and dangerous, so I needed to focus on something. I knew plasma cells and I loved myeloma patients, so I decided to focus on that.
Dr. Aaron Carroll: Let's see, what are plasma cells?
Dr. Rafat Abonour: Plasma cells are the cells that make antibodies to help us fight infection. We need them. That's how we survive a hundred years, 70 years, whatever. What happen is that one of these plasma cells become malignant and start reproducing itself and causing harm to the patient.
Dr. Aaron Carroll: They are a type of white blood cell?
Dr. Rafat Abonour: Yes, sir.
Dr. Aaron Carroll: Okay. Where are they made?
Dr. Rafat Abonour: Well, they actually start in the lymph nodes and then they migrate to the bone marrow where they reside. Your first encounter was, for example, let's say tetanus or pneumonia bacteria in the blood. Then these cells mature, become plasma cells, produce memory antibodies to help us fight infections when we get exposed again to the pneumonia. They reside in the bone marrow. When we need them, they get out, they make more new antibodies to help us fight infection.
Dr. Aaron Carroll: Can you talk a little bit more about how they work when they're working right? How exactly do they help us fight infection?
Dr. Rafat Abonour: Well, they produce a specific antibody. We have a repertoire of plasma cells that are capable of recognizing different pathogens, from the mumps, to the measle, to the influenza, to the pneumonia. Every time we get exposed to one of these pathogens, these plasma cells proliferate and produce more antibodies to fight the infection.
Dr. Aaron Carroll: What happens when they produce the antibodies? What happens next?
Dr. Rafat Abonour: Well, the antibodies bind to the pathogens and you just neutralize it or help other cells gobble it up.
Dr. Aaron Carroll: Okay. What happens when things go wrong?
Dr. Rafat Abonour: Well, when things goes wrong is that one of these plasma cells start accumulating in the bone marrow. 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. You just have a monoclonal protein, doesn't cause harm to the patient. What happen next is that tons of these cells start accumulating in the bone marrow, so you have like 10/20%, but it's still not causing harm.
We call that condition smoldering myeloma. 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. About 70% of patient with myeloma will have either osteoporosis, holes in the bones or they start breaking bones. They just try to lift a bag and then they break a bone in their back or something like that. Myeloma can affect the bones, can cause anemia, can cause very high calcium level because you're leaching calcium out of the bone.
So the patient become unable to think and may go into a coma, or they can actually get kidney damage. We call these the CRAB criteria for diagnosing myeloma. The C is for high calcium, the R, renal or kidney failure, A, anemia or bone disease. You have a lot of these abnormal cells in the bone marrow and you have one of these criteria, then that patient has multiple myeloma.
Dr. Aaron Carroll: What makes the plasma cells go bad? What goes wrong?
Dr. Rafat Abonour: Actually, a lot of research going on in term of environmental exposures, and just this week got a big settlement against Roundup because when patients develop multiple myeloma from using that. We think there is toxic exposures, farming communities, there's increased risk of multiple myeloma near factories and near mining communities. For example, I have patients near a mine in Southwest Indiana where multiple people who worked in that mines develop multiple myeloma. The questions is, what did they dump into the water?
I mean, these people are drinking well water. We think chemical exposure plays a role in making these plasma cells become malignant and multiply and cause harm and cause disease.
Dr. Aaron Carroll: Okay. Once we have a concern, they've met the CRAB criteria, what happens next to help make the diagnosis?
Dr. Rafat Abonour: We do several things. Number one, obviously we need to do blood tests to see if they're anemic, they have high calcium, or they have kidney failure. The second thing is that we look for this abnormal protein, because myeloma start from one plasma cells. The protein they produce is unique. We call it monoclonal protein. 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 the free light chain. We check that.
The second thing we have to look and see what they have in the bone marrow. 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 okay and some of them do poorly. The genetic makeup of the myeloma can help you distinguish these three groups.
Dr. Aaron Carroll: That was actually going to be my next question, is, are all cases of multiple myeloma the same, or are they all very different or they fall into a bunch of categories?
Dr. Rafat Abonour: Yeah. I mean, I think the term multiple may not be really because of multiple lesions within the patients. I think it's multiple presentation of the disease. I have patients who do very well. They get one kind of treatment and they go on and stay in remission forever. Then we have patients who within a year or two, they relapse and they actually don't do well. That's about 20% for each group. Then the rest, the 60%, those patients have multiple relapses, but you can control the disease and they can live long life.
Dr. Aaron Carroll: What is the treatment for the most part?
Dr. Rafat Abonour: Yeah. The treatment has evolved. It used to be more chemotherapy or traditional drugs that cause hair loss or blood count abnormalities. Now we have these ... We call them novel drugs. They work on things that influence the proliferation of the cells or their interaction with the neighborhood where they live. These cells cannot really find hospitable environment within the bone marrow to grow. 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. Some patient may need maintenance therapy after you do the stem cell transplant.
Dr. Aaron Carroll: For the most part though, it's drugs?
Dr. Rafat Abonour: Yes, it is drugs.
Dr. Aaron Carroll: What's the typical course of treatment?
Dr. Rafat Abonour: Most patients will require what we call induction treatment, which is trying to control the disease, trying to improve the symptoms. That will take three to four cycles. The cycle is about four weeks. After that you do the cell transplant, which is a two components. One's collecting the stem cells that support the use of high-dose chemotherapy. Then you give this big-dose chemotherapy which kills everything in the bone marrow, but you have the patient's stem cells that make blood cells stored.
The next day you give it to the patients and these cells will grow and make healthy blood cells.
Dr. Aaron Carroll: This is when you're doing a stem cell transplant.
Dr. Rafat Abonour: Yes.
Dr. Aaron Carroll: You're actually transplanting the patient's cells back into their own body?
Dr. Rafat Abonour: Yes.
Dr. Aaron Carroll: How does that work?
Dr. Rafat Abonour: What you do, is you collect the patient's own stem cells first, and these cells live in the bone marrow. What you do is you give a specific hormone that stimulate these cells to grow every day for four days. On 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. You collect only the stem cells and you store them, you give the blood back to the patient.
You do this in the outpatient in the blood bank, 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.
Dr. Aaron Carroll: How do you be sure that you're not collecting bad cells or that those won't turn into bad cells?
Dr. Rafat Abonour: Yeah. We have looked. Actually, we did research on that. What we're looking for is specific marker on the surface of these cells makes them stem cells, called CD34. We look to see if we collect any myeloma cells. We did very sensitive assay. Two things. One is that the myeloma cells don't mobilize that effectively. The second thing is that they don't freeze well. Basically, the products we give back to the patients, very unlikely to contain any myeloma cell.
Dr. Aaron Carroll: 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 ... Or is that just, you just have to take the risk?
Dr. Rafat Abonour: The stem cells are the cells that make white cells, red blood cells and platelet, and the process of developing multiple myeloma doesn't really start at the stem cell level. Stems start probably around when they mature to white cells and before they divide into lymphocytes or neutrophils, different part of the white cells. It's at the lymphocytes level when they become B-cells, the B-cells become plasma cells. Maybe it's between the B-cells and the plasma cells.
Dr. Aaron Carroll: This question may be totally naïve. 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 since those cells are less likely, or is that just too hard to do?
Dr. Rafat Abonour: Well, it's very hard to do. We have done what we call allogeneic transplant, donor stem cell transplant. The problem is that most patients with multiple myeloma are in their late 60s, so allogeneic transplant is very risky. We actually lose a large number of these patients and despite doing an allogeneic transplant, some patients have relapsed, so it's not really a routinely used approach. Maybe in the young patients you may consider an allogeneic transplant.
The issue with allogeneic transplant is the risk of a graft-versus-host disease. The immune cells from a donor do not like where they're living in the patients, so you get damage to the skin, liver and the intestine. The other thing is that the advantage of allogeneic transplant used to be the graft-versus-disease. Unfortunately, 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 allogeneic transplant.
Dr. Aaron Carroll: Interesting. Okay. Patients get a round of drugs and then stem cell therapy?
Dr. Rafat Abonour: Mm-hmm (affirmative).
Dr. Aaron Carroll: What's the usual course after that?
Dr. Rafat Abonour: Three months later, they recover from the stem cell transplant. Then some patients are considered for maintenance therapy. Two things. One, we give them medicine to keep their bone from breaking down. We do that as an infusion or injection once a month. Then sometimes we give 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? Is it the chemo pill or is it some other strategies that we are trying actually to explore here?
Dr. Aaron Carroll: How many different types of drugs are available? I mean, is it that everybody gets the same cocktail of drugs or is it individualized?
Dr. Rafat Abonour: When I started working on multiple myeloma, we had only this traditional chemotherapy. In 2003, the first-in-class drug was approved, which is a proteasome inhibitor. Proteasome inhibitor, just think about it like you have a garbage disposal and you just clog it. Just the accumulation of toxic stuff and the cells start dying. That's how proteasome inhibitor works. These are amazing. I mean, these drugs have changed the course of the disease. Now there are three drugs in that class available.
In 2006, we got a class of drugs approved called the immunomodulatory drugs. 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. 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. The company that makes that drug started developing next generation of that drugs that cause less neuropathy.
We actually have two drugs in that class now. We have three immunomodulatory drugs, three proteasome inhibitor. Then more recently, the FDA approved drugs we call a monoclonal antibodies. These are drugs that recognize the surface of myeloma cells and help eradicate these myeloma cells. Protein that bind to the myeloma and bring the immune cells to try to eradicate them.
Dr. Aaron Carroll: How do you decide which of those to use?
Dr. Rafat Abonour: Well, that's a great thing. That's why we do clinical trial. In the clinical trials, we find the best combination. First of all, now we know that one drug is not enough. You have to use a cocktail of drugs. The good things for a patient today is that you have different cocktails. Based on their medical condition, you can find the right combination therapy.
Dr. Aaron Carroll: When you say their condition, what do you specifically [crosstalk 00:15:33]?
Dr. Rafat Abonour: 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. That's good news for the patient is that we can tailor the therapy toward their conditions and their actually desire. I mean, some people would like only oral regimen. They don't want to go to infusion. They can't really go twice a week to the clinic to get chemotherapy. We have oral regiments for them.
Dr. Aaron Carroll: When you say there are cocktails, is it multiple drugs in a class, or you're picking drugs from each different class?
Dr. Rafat Abonour: Exactly. We pick the drugs from different class. Basically, what we do is synergy without overlapping toxicity.
Dr. Aaron Carroll: Okay. What is the usual course? You have your treatment. You're in maintenance. How do most patients do?
Dr. Rafat Abonour: 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 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.
Dr. Aaron Carroll: Do you treat them again?
Dr. Rafat Abonour: 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 of the newer strategy. For example, one of the newer strategy will be what we call CAR T-cells, which is basically taking the patient own immune cells, expand them, genetically modify them to make sure that they can recognize myeloma and kill it. We put two genes. One to recognize myeloma and one killer genes. That's why we call it chimeric receptor antigen T-cells, CAR T-cells.
I mean, these kind of therapy is now used in clinical trial in relapsed patients. We may be able now to use it in clinical trials for the high-risk patient upfront, before they get to relapse and have a horrible disease that's hard to control.
Dr. Aaron Carroll: How hard is it to do that?
Dr. Rafat Abonour: First of all, you have to collect the patient T-cells with the lymphocytes that become the killer cells. Basically, it's like we collect the stem cells. We do apheresis. We take the blood out, separate the white cells from the rest of the blood. 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. Then you incubate them with a virus that get the two genes inside the cells, after you expand these cells.
Then you bring them back and take in back to the patient. It's a very expensive process. 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.
Our goal is to try 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 if they start relapsing in a year and you give them a very expensive therapy. Our goal is to try to make CAR T-cells more specific, safe, and maybe less expensive.
Dr. Aaron Carroll: How expensive is it?
Dr. Rafat Abonour: Well, I mean, for the commercial products this 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 CAR T-cells.
Dr. Aaron Carroll: What's the usual prognosis for a patient who develops multiple myeloma?
Dr. Rafat Abonour: Really has improved significantly. If you look at patients when they were diagnosed 15 years ago, 20 years ago, we're saying you can live on average two or three years. Now, I think if you look at patients, depends on their stage. If you have stage one disease, you would think these patients should live at least 15/20 years.
Dr. Aaron Carroll: Can you tell us what stage one is?
Dr. Rafat Abonour: Stage one is we look at certain things. We look at the chromosomes and inside the bone marrow. Are the good chromosome, bad chromosome? We look at something called LDH, is enzymes in the blood. We look at albumin. If these are normal...And there's another protein, we look at the blood called beta-2 microglobulin. If these are normal and the cytogenetics are good one, that's stage one. These patients, if you look at their five-year survival, more than 93% are alive at five years.
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.
Dr. Aaron Carroll: What are the other stages?
Dr. Rafat Abonour: Stage two and three. Three is the high risk where you have high beta-2 microglobulin, high LDH, low albumin and bad cytogenetics in the bone marrow.
Dr. Aaron Carroll: Okay. It's more about the actual chromosomes and what the cells look like, than how quickly you caught it, or how much ... Obviously metastasize is a totally different meaning.
Dr. Rafat Abonour: Sure. Well, yeah. I mean, myeloma is always sort of detected at advance or all over the body. It's unlike other tumors. It's just always systemic disease, but if you detect it at early stage before you have a lot of myeloma, you have a lot of bone destruction, I think you're going to 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.
Why don't we treat all smoldering myeloma? Because the 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. Only specific group of smoldering myeloma, which we call them high risk for progressing. Half of them will progress to myeloma within two years. We're doing clinical trials on them. There are two kinds of clinical trials.
One use these 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 within 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 this myeloma cells visible to the immune system? Can we make the immune system recognize myeloma?
What we're trying to do is actually generate a vaccine from these myeloma cells and then inoculate the patients with this vaccine with the hope that they develop immunity that will eradicate the myeloma.
Dr. Aaron Carroll: Would the vaccine be tailored individually to patient, or is this the kind of vaccine for everybody?
Dr. Rafat Abonour: Yeah. We take the myeloma cells and generate a vaccine from their myeloma cells.
Dr. Aaron Carroll: Is that the kind of thing that 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 in a [crosstalk 00:23:11]?
Dr. Rafat Abonour: I think this should be commercially available. That's the hope, is that you can generate a vaccine for each patient. You just send the cells and they process it and they send you a vaccine.
Dr. Aaron Carroll: What do you think the most exciting work's being done right now? Or what area? I'm not saying where in the country. I mean, what area do you think is the most exciting work?
Dr. Rafat Abonour: For me, for example, I am actually looking at trying to figure out, can we prevent the development of multiple myeloma? I'm doing a clinical trial in patient with monoclonal gammopathy of undetermined significance. I'm trying to see if we can actually prevent them from developing multiple myeloma. Let me tell you the background of that.
Dr. Aaron Carroll: Sure.
Dr. Rafat Abonour: In my practice, I see a lot of monoclonal gammopathy of undetermined significance. I have seen patients who lost the monoclonal gammopathy. How did it disappear? In the six to eight patients I have seen, they lost weight and by weight loss, they lost the monoclonal gammopathy.
Dr. Aaron Carroll: Really?
Dr. Rafat Abonour: We think obesity is an inflammatory state, can stimulate plasma cells. What we're doing actually, we're putting a trial together and we start accruing here. We look at patients who're undergoing weight reduction surgery. What we're going to do is screen them for MGUS and then those are positive for the monoclonal gammopathy, we're going to follow them after the surgery and look at the group that lose weight versus the group doesn't lose weight. Are they going to lose the MGUS or not?
If we can prove that they lost this abnormal protein, that's a good thing. We're going to try to explore and see why. Is it because they lost certain inflammatory proteins when they lost the weight or not? That will be great advances. You know?
Dr. Aaron Carroll: Is obesity a known risk factor for myeloma?
Dr. Rafat Abonour: Yes. If patient who are ... Let me tell you if somebody has monoclonal gammopathy and they are obese, they have four and a half chance of developing multiple myeloma compared to non-obese patients.
Dr. Aaron Carroll: Interesting.
Dr. Rafat Abonour: Yeah. This is a big study that was done at St. Louis VA hospital, because they have records on patients who develop myeloma. They know their weight and they know if they had MGUS or not. The obese, four and a half time chance.
Dr. Aaron Carroll: Is type II diabetes tied up in that too, or is it just the obesity?
Dr. Rafat Abonour: I think it's just the obesity. I'm not familiar with any data on diabetes, but-
Dr. Aaron Carroll: Besides the prevention, what else is-
Dr. Rafat Abonour: Prevention. I think the other thing is that we really need to screen. I mean, we need to see in these area that we talk about, in the high-risk area, near farming community, near a mining community, near 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. I mean, because then we will study the impact of this environment on these preconditions. Then what we would like to see is a predisposing factor in addition to the chemicals.
If you have a certain gene, will you get myeloma when you're exposed to certain pathogens? I think that's exciting to us. 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. 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.
Dr. Aaron Carroll: I mean, just because clearly we live locally, how are patients doing here locally? What are we doing? What kind of studies are we doing locally to try to help?
Dr. Rafat Abonour: That's a great question. As you know, Indiana University issued this Grand Challenge grant, trying to really cure three diseases and cancers in Indiana. Multiple myeloma was selected as one of these diseases. One of the proposal 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.
We're putting together what we call a cohort of patients. We want to analyze 1000 patients with myeloma and pre-myeloma condition in Indiana. We started actually accruing patients in November, and we have more than 170 patients thus far enrolled. What we do is we're looking at their baseline genetic informations. We take saliva, we take a blood, and when we do a bone marrow biopsy, we take the myeloma cells and the neighborhood where they live inside the bone marrow cells, and we try to analyze them.
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. Then correlate the natural history of the disease with their genetic makeups, the myeloma genetic makeups and the microenvironment within the bone marrow makeup.
Dr. Aaron Carroll: Are you looking at their broader environment as well, where they live, where they might be exposed to?
Dr. Rafat Abonour: Exactly. We are doing that in a collaboration with a group down in Bloomington, because by zip code, you can figure out where they lived, what they're exposed to and things like that. We have survey that we ask the patients to help us understand their occupations and where they grew up, things like that.
Dr. Aaron Carroll: How long do you think that'll have to take to get all the patients you want?
Dr. Rafat Abonour: As you see, I mean, since November that's about four months, five months, we have 170 patients. Hopefully we can accrue all these patients within two, two and a half years.
Dr. Aaron Carroll: Are those all new diagnoses or are those-
Dr. Rafat Abonour: No.
Dr. Aaron Carroll: ... just patients you're picking up?
Dr. Rafat Abonour: Our patients for newly diagnosed, relapse patients.
Dr. Aaron Carroll: How common is myeloma to begin with?
Dr. Rafat Abonour: Myeloma is about one and a half percent of all cancers. We're trying to figure out the exact incidents in Indiana. It's probably about 1200 new patients diagnosed a year.
Dr. Aaron Carroll: 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?
Dr. Rafat Abonour: As an avid runner as you know, about 15 years ago we were sitting with patients and trying to figure out how we can support myeloma research at Indiana University. One of my patients said, "Why don't we just do 5K for myeloma?" I said, "Well, everybody has a 5K for myeloma. How about we do something different? You guys come to me from all over Indiana for a second opinion, why don't you go to your community and spread word about the disease?"
They said, "Wow, that's exciting, but I'm not going to be riding a car to go there. I'm just going to run." In the first year I wanted to run to Fort Wayne, but that was a huge ... You know? 120 miles.
Dr. Aaron Carroll: That's far away for people to go live in Indiana. Yeah.
Dr. Rafat Abonour: I said, "I'm not ready." What we did is in the first four years, we split it one day of running and one day of cycling. We did about 50 miles of running and the rest is cycling.
Dr. Aaron Carroll: Still, a lot of running.
Dr. Rafat Abonour: That's how Miles for Myeloma started. Then because the distance started getting like 200/250 miles, it's just two days or three days of cycling. We have come from St. Louis to Indianapolis, from Columbus, Ohio to Indianapolis, Miles for Myeloma. We've raised almost $5 million. The most exciting thing about the whole thing is that we have patients who ride with us. It's organized by family of patients that do that.
The thing about it is that makes me really excited is to see myeloma patients riding. I still remember one day, because you get these guys who wants to ride with you and they are very, really amazing cyclists. This is not a race. This is a group of people trying to ride together to support each other and spread the word about myeloma. If you have somebody already in Indianapolis and the other person's still in Terre Haute, it's not fun.
Dr. Aaron Carroll: No.
Dr. Rafat Abonour: It's hard. I remember one time it was like, I want to tame the group down a little bit. I stopped everybody and I said, "Do you know why we're doing this?" Because of myeloma. What are we 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 understand this disease need to be cured. I said, "How many of you riding with myeloma today?" There were two people. I said, "How many of you riding with myeloma and still on treatment for myeloma?"
One guy. I said, "Okay. This guy is going to lead us and everybody has to follow him. Do not pass this guy." I was kind of probably doing it because I was tired. I want to slow the pace down a little bit. This guy grabbed a bottle of water, pour it over his head and we actually stopped at the bottom of a hill. This guy was climbing so fast. I was working hard to stay with him. I said, "Oh my gosh, why did I say that?" It was amazing to see how excited he was, how aggressive he was climbing that hill.
It just makes me know that today myeloma patient can live a normal life. It's not a disease that stop you from living your life. That's why we need to tailor the therapy so they can live a healthy quality life. Hopefully we can find a combination that cure them so they don't stay on treatment forever.
Dr. Aaron Carroll: 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 II diabetes and Alzheimer's disease.
Thanks again to our guests, 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.