What is Leukemia? with Dr. Aaron Gerds

Podcast Transcript

Nada Youssef:      Hi, thank you for joining us. I'm your host Nada Youssef and you're listening to Health Essentials podcast by Cleveland Clinic today. We're broadcasting from Cleveland Clinic main campus here in Cleveland, Ohio. And we're here with Dr. Aaron Gerds. Thank you so much for being here today.

Aaron Gerds:     Thanks for having me. I'm thrilled to be here.

Nada Youssef:   And Dr. Gerds is currently a hematologist at Cleveland Clinic Cancer Center and assistant professor in hematology and medical oncology at the Cleveland Clinic Taussig Cancer Institute. And today we're talking about leukemia and please remember this is for informational purposes only and it's not intended to replace your own physician's advice. All right, so let's just start with very basics. What is leukemia?

Aaron Gerds:     Leukemia can be a very fearful word, I know, but there are, I think it's important to remember there are so many different types of leukemia. When someone comes to me as a leukemia doctor and says, "Well, what is leukemia?" It's almost like I walk into Sherwin Williams and say, "I want some blue paint." You look at the wall, there's all these paint chips of hundreds of different kinds of blue, so really, I think the key there is that there's so many different types of leukemia. But we can break this down to a couple of different simple groups. There's acute and there's chronic. Acute means something that comes on very quickly. It's generally pretty aggressive, if we don't treat it, people can pass away from it within days to weeks. There's also chronic leukemia, which means it usually comes on much slower and even without treatment, patients can live years.

These terms are very old. They date way back before we had any formal classification systems, 50 plus years ago. More recently we started to divide them as well into myeloid and lymphoid groups, meaning that's the cell of origin. Are they from a certain group of blood forming cells in the bone marrow or another certain group of blood forming cells? Really we can think about any leukemia with this kind of two by two table, acute versus chronic, myeloid versus lymphoid. Of course with each of these groups, there's many other subsets of leukemias based on what types of immature cells we're seeing, what type of mature cells we're seeing in all the other different features within the disease. But the basic breakdown is acute versus chronic, myeloid versus lymphoid.

Nada Youssef:   Okay. When I start with the questions, just feel free to explain both categories because I know the questions might be different for each one, but I want to know how it affects the body. What actually happens to your body when you have leukemia?

Aaron Gerds:     Leukemia starts when some of your blood forming cells acquire a mutation. A mutation in a gene generally either that is important for the development of these cells, the growth of these cells or the maturation of these cells. These mutations will happen. And then the blood, the ability for the bone marrow to form blood will become altered in some way. Either you make too many of a certain subset of blood cells or their maturation is interrupted, their ability to mature is interrupted and you stopped making enough of these blood cells. And so usually the first signs and symptoms of this disease are akin to having too much or too little of these blood cells in your bloodstream and things kind of stem from that.

Your blood is so important. We often joke in hematology that hematology or cardiology, being here at the Cleveland Clinic, we always like to poke, have a little fun with our colleagues over in the cardiology department, but we're like, well the cardiology is, they're just dealing with the organ that gets to pump the blood around. Blood's the most important thing, but it's within leukemia you kind of think about it, all the symptoms and things that can happen from leukemia stem from having too much or too little blood. If your blood levels become low, you often feel anemic. Anemic is another term for having too few red blood cells that can lead to shortness of breath. It can lead to issues with heart failure even or kidney failure. And people often report feeling very tired, fatigued or rundown. And that's often a early sign or symptom of the disease as well.

If you have too many white blood cells and those white blood cells are very, very sticky. Say they're very immature cells for instance, or this happens in acute myeloid leukemia, they can kind of clog up the blood vessels of the brain or the lungs and cause confusion or shortness of breath that way too.

Nada Youssef:   There are many, many types as you mentioned, that exist. Can you talk a little bit about the different types?

Aaron Gerds:     Yeah, sure. The main categories, again, acute and chronic. And then within acute leukemia we often think of acute lymphoblastic leukemia and acute myeloid leukemia. Those are going to be the kind of two most common categories people talk about. Acute lymphoblastic leukemia are from the lymphoid cells. Again, the other kind of way we divide up the leukemia. Acute lymphoblastic leukemia is the one we often think about in pediatrics, so there's really, if we look at the incidence across ages and when the disease happens, there's a big hump in children and then in middle life it kind of goes away and then there's a second hump in adult life. There it's a disease of both children and older adults. The lymphoid cells often contain certain mutations that we can actually target with new therapies, which is really exciting, targeted therapy. And the set of chemotherapies we use for that disease are different than the acute myeloid leukemia.

If we look at acute myeloid leukemia. Again, these are acute leukemias that come from the myeloid lineage in the bone marrow. That tends to happen in older folks, not really so much in the young. Instead of two humps when we're looking at age, it just tends to happen as we age. And really the average age of the onset of diagnosis is around 70 or so. Definitely a disease that's more common in older folks. Again driven by mutations and often a patient will present with too many white blood cells and too little red blood cells and platelets cells. And that kind of tips us off to what's going on and sets us down the path. Again, the reason we make these distinctions is because the treatment for these diseases is so different. The types of chemotherapies or targeted therapies we may use are very, very different.

Nada Youssef:   Which types of those with the leukemia, which one is the worst?

Aaron Gerds:     I get this question a lot. What kind is the worst? Is this if I'm going to get one, is this the one I want to have? Or is this the one that really, really bad one? I get that question a lot and it almost goes back to there's so many types of leukemia, even within very precise groups of leukemia. Say if you take acute myeloid leukemia, there's a whole bunch of types of leukemia subsets of that acute myeloid leukemia and it really depends on within that group. If we take, again just acute myeloid leukemia, acute myeloid leukemias with a certain chromosome called inversion 16 we feel like that's a pretty good one. We can cure a lot of those patients with just chemotherapy alone.

But if we take that same acute myeloid leukemia, if we look at the chromosomes of that acute, those cells, and if they have like a lot of chromosomal errors or errors in genes or in chromosome seven or 17P in certain abnormalities, those are really aggressive and chemotherapy will not cure those patients. And we want to think about different treatment. Even within a category of leukemias, there's a range. There are good ones and quote unquote bad ones within that, within those groups.

Nada Youssef:   I know you mentioned how they develop and you mentioned it can develop from bone marrow. Can you explain again how it develops some of the leukemia, the two different ones?

Aaron Gerds:     Yeah, yeah. Leukemia all starts with a mutation. Leukemia is actually a form of cancer. I think a lot of people may not realize that. And all cancers start with acquiring a mutation in a cell. We have a genome, there are 70,000 genes in every one of our cells and every one of our cells has the same genome and what makes your skin cells skin cell and your let's say kidney cell a kidney cell is what genes are turned on and off. And there's a whole system that regulates a lot of that. And if we look in leukemia cells specifically, what has happened is there are particular mutations that happen in a or a small set of genes that not only change how the cell behaves, but also what other genes in within the cell are turned on and off. And that one mutation or set of mutations leads to abnormal growth of those cells.

Again, same for leukemias, all cancers. And that starts in your bone marrow. Your blood comes from your bone marrow. And so when a bone marrow cell, a particular cell, what we call a bone marrow stem cell gets this, gets a mutation of this nature in it, that ultimately will grow up to be a leukemia.

Nada Youssef:   You can, you'll be able to detect it early.

Aaron Gerds:     That's a really interesting question. There's been a lot of focus now on this thing called CHIP, clonal hematopoiesis of indeterminate prognosis. Clonal means that all the cells are the same. I don't know if you remember Star Wars at all, and they had the Clone Wars where all, they're all off of Boba Fett. They're all kind of, or his father, Jango Fett, and they're all identical genetically. And so if we look at these cells, they're all genetically identical or relatively genetically identical so they're clones. Hematopoietic means blood forming, so bone marrow cells. Indeterminate means we don't know. And prognosis means prognosis.

What we're detecting in people who do not have blood cancers, do not have any diseases at all, we test their blood, we can find mutations in their bloodstream that can ultimately lead to leukemia. Not very common in younger folks, like say you check the blood of someone who is 30, you're pretty unlikely to find that. But if you check the blood of someone who say is 80 and has no normal blood counts, no evidence of leukemia at all, in roughly 10 to 15% of those people, we'll detect mutations that are common in leukemia and there is a risk of developing a hematologic cancer over time with those folks when they have those mutations. Roughly a percent or so per year, and we think that these CHIP states where we acquire a mutation in our bone marrow that's hiding in there, there's these clones that could over time lead to this disease. And we think that's how a lot of these leukemias happen, particularly leukemias like acute myeloid leukemia or a related disease called myelodysplastic syndrome.

We think when it happens in younger folks, say children or people in their say 20s or 30s even, they probably had some sort of predisposition for it. Maybe one gene wasn't mutated but was very susceptible to mutations. There was a preexisting first hit and then once a second hit or a true mutation was acquired, then the leukemia happened. But for most people who get leukemia, it's actually because they've acquired a mutation in some of their, one of their bone marrow cells, the blood making cells over the span of their lifetime and that eventually, this CHIP thing, which eventually turned into a leukemia.

Nada Youssef:   What organs aren't affected by it and can it spread?

Aaron Gerds:     Yeah, so mainly the bone marrow, which is actually a tissue, not an organ, but it's a very important system. And so that's the first thing we think about. Again, when you get a leukemia, often the bone marrow is not able to make enough blood or at least effective blood. And a lot of patients we'll see that have maybe a normal white blood cell count, but those white blood cells aren't acting properly and they can't fight off infection like they should be doing. That's usually one of the main things we see. Other organs and tissues certainly can be involved as a result of that. If the blood cells are low or too high, other organs can kind of get in trouble with this. But mainly it has to do with the bone marrow's inability to produce blood and hand in hand goes the immune system too. And that's the other key feature there. The immune system often becomes weakened in these states and people could become susceptible to infections, which is a real serious complication of having a leukemia.

Nada Youssef:   Now, when I was searching this, I saw a lot of this lymphoma. People are wondering if leukemia and lymphoma are related at all?

Aaron Gerds:     Yes, they are.

Nada Youssef:   They are.

Aaron Gerds:     They're cousins.

Nada Youssef:   Oh, they're cousins.

Aaron Gerds:     I would say they're kind of cousins. Lymphoma is specifically a cancer of the lymph tissue. You have lymph nodes say like in your armpits, your neck, your groin. The spleen is part of the lymphatic system, if you will. And so it's a cancer of the lymph system. Your lymph cells originate in your bone marrow. For example, a T-cell or a thymus educated cell, they'll be born in your bone marrow. It'll circulate around in your blood, it will go to your thymus gland, which is usually more present in kids than adults. It'll get educated and then becomes a T-cell part of the lymphatic system or part of the, part of the immune system, the greater immune system.

If a cancer happens as part of where the T-cell is the predecessor, it often becomes a lymphoma, but you can also get leukemias of T-cells too. It's somewhat of an antiquated term to separating out lymphomas and leukemias. I think the simplest way to think about it, lymphomas are solid, so they usually cause enlarged lymph nodes, solid masses. Where leukemia is more in the bloodstream, it's liquid, it kind of flows around and pumps around with the blood. I think that's the simplest way to separate them out. There are some that you can't tell the difference.

There's this thing called small cell lymphocytic lymphoma or SLL and then there's CLL or chronic lymphocytic leukemia. They're actually the same disease, but it has two different names, whether it's mostly in the lymph nodes or mostly circulating around in the bloodstream. Same disease, two different names. Makes it completely confusing.

Nada Youssef:   A lot of investigation to find out what your patients have. Let's talk about the early signs of leukemia. Are there any?

Aaron Gerds:     Certainly there are. There was some recent press around a patient that we had who thought they had a bug bite and eventually went and sought out treatment. And it turned out, well, it wasn't so much a bug bite, but a manifestation of their acute leukemia. Now I'm not saying that everybody who has a bug bite has leukemia or vice versa, but sometimes what happens is we are looking at a symptom of a patient for a completely different reason or something that's almost unrelated and we notice that their blood counts are abnormal. That often could be a first tip off. Most patients who have leukemia, feel tired. They may have fevers, they often feel like I said, anemic because their red blood cells are low and they're not getting enough oxygen pumping around to their tissues and they feel just anemic. Some patients will be thrombocytopenic, meaning their platelets are very low and they get a lot of bruising and bleeding.

Those are probably the most common symptoms that happen in patients who have leukemia. But there's also a fair chunk of patients who we just happen to find it on routine screening or just by happenstance by checking their blood for a completely different reason. Particularly those patients with chronic leukemias. They can often be asymptomatic or not have any symptoms at all.

Nada Youssef:   Now you talk quite a bit about genomics and well, is this a hereditary link? Leukemia then.

Aaron Gerds:     That's always a question and we actually here at the Cleveland Clinic have a molecular hematologic pathology board where we get together a pathologist, molecular biologist and hematologist and we talk about different cases where we've had a patient with a disease and we look at the mutations that are inside this using our in house panel where we look at 62 different genes that are commonly mutated in these diseases. And we spend part of the time discussing, well do we think there's a hereditary link in this particular individual?

We'll go through and see the mutations and other variants that may not be fully mutations but might be a little off. And we'll kind of look at the genomics that we have in front of us and say, "Well, should we refer this patient to genetic counseling?" It's we don't really know how much is inherited and how much isn't. Certainly these things can run in families. Older reports would say maybe 5% of leukemias were inherited and run in families where 95 were sporadic or just popped up in individuals. But there are emerging reports that say maybe that number is higher, that there are maybe even upwards of a quarter of cases might be more hereditary than we think. One in four even. A lot of this work is being done by collaborators of ours. One of our collaborators, her name is Lucy Godly over in Chicago and we've been working a lot with her to try to unravel some of the questions around around this. Is it more hereditary or not hereditary? But so it's really unclear because these studies are really hard to do.

Nada Youssef:   Based on the pathology lab, that's when you would find out if that patient should be seeing a genetic counselor or not.

Aaron Gerds:     Yeah, certainly we do two things. We take a very detailed history, we ask questions. Does anyone else in your family have a leukemia or a lymphoma or a cancer? And we start taking, well what, is there any medical problems with your grandmother, your grandfather, your aunts, uncles, cousins. And we kind of try to do a really accurate family history. And that couples with what we see genomically inside of these leukemia cells and we take that information together and say, "Boy, there's some family members here with some kind of questionable things going on and there's these kind of mutations, or at least variants of concern, differences in the genome that we might want to investigate further," and then refer the patient to genomic counseling.

Nada Youssef:   Makes sense. Are there risk factors that increase your chance of developing leukemia? If so, what are they?

Aaron Gerds:     Yeah, so for most patients, leukemia can almost be seen as a process of aging. Again, as we all age, we acquire these mutations in our bone marrow. That whole CHIP thing we were talking about earlier. But for some patients there are exposures that can increase the risk of developing leukemia over time. Probably the most well known one is a chemical substance called benzene. It's an industrial paint thinner kind of compound, but also happens to be the most common carcinogen in cigarette smoke. And there is a clear link between benzenes and the development of leukemia. Ionizing radiation is another risk. Patients or people who are exposed to high doses of ionizing radiation can develop leukemia. I'm not talking about an ankle x-ray when you twisted your ankle when you were 12. I'm talking about people who have either worked in the field of radiation or were involved with radiation disasters before there were a lot of kind of regulatory oversight with these things.

And then lastly, chemotherapy. Our colleagues who take care of patients who have solid tumors have done such a phenomenal job treating these patients and that they're living much longer and they've been exposed to more chemotherapies, cytotoxic chemotherapies, genotoxic chemotherapies that can lead to mutations and ultimately cause leukemias. Say a patient has breast cancer and gets, taxane or some other chemotherapy to treat their breast cancer, that ultimately could lead to the development of a leukemia because the chemotherapy that they got to kill the breast cancer also caused a mutation or damaged the DNA and some of the blood forming cells that lead to a cancer. That's another risk factor for developing leukemia.

Nada Youssef:   Do we understand yet the cause of leukemia besides aging?

Aaron Gerds:     Yeah, so I definitely think the acquiring mutations as we age or just acquiring mutations by random chance alone and then some of these exposures, increasing that risk, but it all comes back down to acquiring a mutation that leads to abnormal growth of blood making cells. That's where it's coming from. I think the real key we need to figure out going forward, is determining earlier who's at greatest risk for developing these and perhaps increasing surveillance or maybe even intervening in the future. I think that's going to be the real key to lowering the incidence and improving the longterm outcomes with leukemia.

Nada Youssef:   Now, I know you mentioned this a little bit earlier, but I want to ask you this question. It's often considered a childhood illness as you mentioned, and the most common cancer in children under 15 but can we talk a little bit about why that is? Talk about adult versus kids?

Aaron Gerds:     Yeah, so I think that one of the key factors here too, it's almost a bit of perception. Cancer in children is very uncommon. Cancer in adults is common because again, no matter what tissue we're talking about, we acquire mutations in those tissues as we age. You think about skin cancer. Probably not going to get a lot of sun exposure if you're a one year old, but if you're say 70 and you lived by the beach your whole life, you've probably got a lot of sun exposure so your risk for melanoma or other skin cancers are going to be much higher. It's the same with blood cancers too. We all age, we're more likely to acquire these mutations in our blood system, in our blood making cells that can lead to leukemia.

Cancers in general are uncommon in kids, less common than certainly compared to adults. There's a bit of a proportion thing. Why ALL? I don't know if anyone really knows the answer, but if you look, the peaks in the number of people overall getting ALL in kids versus adults, they're pretty close. And in fact actually there are probably more people with ALL that are adults, especially older adults than there are actually kids. It's just the fact that kids don't get too many other cancers. And that it rises to the top of the list. Where in adults, you think about it, you hear these statistics, like one in 13 women will develop breast cancer over the course of their life. On autopsy series, one in six or one in eight men have prostate cancer. That's usually not happening in children. I think it's more of a, just a relative increase in leukemias in children as opposed to an absolute increased risk of leukemias in children.

Nada Youssef:   The reason it's so increased in children, it's a gene mutation as you mentioned, they could be even born with it versus risk factors that they didn't go through yet.

Aaron Gerds:     Yeah, there's probably some factor that's inherited that increases their risk. They've inherited something we call a polymorphism often, which is not a mutation necessarily, but a different code of the gene that makes it more susceptible to becoming mutated. Probably that's the case. That and then they go on with that polymorphism and then something happens where the mutation actually happens and then causes leukemia. But I think it's just, it looks like leukemia is a childhood disease because kids don't get too many other cancers period. And it's just the most common of a kind of an uncommon situation. But then in adults, cancer's really common, particularly other cancers of solid organs like again, breast cancer, lung cancer, prostate cancer where leukemia kind of slides down the list because compared to those it's much less common.

Nada Youssef:   That's great information. Okay so jumping into treatments, how do we diagnose leukemia? How do you detect it?

Aaron Gerds:     There's a lot of things. The big thing is really taking a look at the blood. That is our first and most important clue. Whether we actually do something called a blood smear, where a drop of blood is placed on a slide, a glass slide, and we smear the blood across that, not with our fingers but with another slide. And then it's preserved and we look under a microscope. And that way we can look at the individual cells in the bloodstream and that is our best clues to get started on a diagnosis. We can use other techniques like flow cytometry where individual cells are put through a machine and we can look at the proteins on the surface of the cells to kind of tell us are they normal or abnormal.

The lastly, one of the things that we use is a bone marrow biopsy. Bone marrow biopsy is a way of going to the source. Your blood doesn't come from the sky, it comes from your bone marrow, so it makes sense to go and look there. I often use the analogy of if you're driving down the expressway and you saw all the Fords didn't have doors on their trucks, you'd probably go to the Ford factory and say, "Why aren't you putting doors on your trucks?" And so when we see abnormal blood counts, we often go to the bone marrow to say, "Well what's going on here? Why aren't you making blood?" And that's how we often find these leukemias.

And then in addition to that, we augment our diagnosis by looking at the chromosomes inside the leukemia cells. Through testing called cytogenetics. And then we also look in, look at the mutations inside these cells using more molecular type techniques to make the diagnosis.

Nada Youssef:   You mentioned earlier chemotherapy can cause leukemia so how do you treat cancer?

Aaron Gerds:     It seems kind of silly to use chemotherapy to see to treat something that was caused by chemotherapy, but in fact we use chemotherapy. But I think one of the more other important points is that for some patients with chronic leukemia, we simply watch them closely because they can live many years with this leukemia. If you look at a patient with essential thrombocythemia, which is a fancy way of saying the patient has too many platelets due to a mutation in a gene, usually one of those genes that include JAK stat, JAK, NPL or calreticulin. Those patients can have lifespans that approach the normal population even without chemotherapy.

I think it's really important to know what kind of leukemia before we apply the treatment. And for many patients we do observation. We just keep an eye on things to make sure it doesn't change or get out of control. But for some patients we definitely have to intervene. I think there's been some really interesting examples of how medicine has been pushed forward through the treatment of leukemia. One example is a medication called imatinib. There's this type of leukemia called chronic myeloid leukemia or chronic myelogenous leukemia. It is caused by a specific mutation called the Philadelphia chromosome or BCR-ABL.

Once this gene was identified, this abnormal chromosome, this mutation was identified, they did crystal instructors of it and they saw that it made this protein, this tyrosine signaling kinase thing. If you kind of imagine it like a Pac-Man, we then designed a wedge to stick in Pac-Man's mouth so it wouldn't work anymore. That drug was imatinib. It took a disease that without a bone marrow transplant people universally died within three years of diagnosis and it cured people with a pill. Unreal. Every targeted therapy developed in cancer medicine has been trying to live up to imatinib since. It really lurched the whole field forward in a very dramatic way.

I could talk for hours on it because it's such an interesting story about how treatments are developed, how the FDA thinks about things, how advocacy groups got involved. It's really an interesting story but I think it's a clear example of how leukemia was able to push the entire cancer field forward.

Another thing is CAR T-cell therapy, which is very exciting. CAR T-cell therapy is an immunotherapy. We know immunotherapies work in leukemia. Don Thomas who was awarded the Nobel prize for developing bone marrow transplant realized very early on that it wasn't the chemotherapy that we were giving with bone marrow transplant but it was the new immune system from somebody else that was going and killing the leukemia cells. We knew from a very early time, many, many years ago that immune cells can be used to kill leukemia cells and other cancer cells too.

But obviously bone marrow transplant comes with a lot of side effects. One way of trying to get around that is we actually take the patient's own T-cells, which is a type of lymphocyte, type of white blood cell. We take it out of them, we engineer and reprogram it, kind of lift open the hood, fiddle with the inner bits, put it back together, grow a whole bunch of them in a Petri dish. We basically primed them to kill, look for a certain protein on the surface of the cancer cell, grow the whole bunch of them in the Petri dish, and then give them back to the patient. We're taking the immune cells, reprogramming them, growing a whole bunch of them, putting them back in the patient to kill the cancer cells.

And this technology has been absolutely amazing in treating acute lymphoblastic leukemia, particularly patients who have gone through several lines of therapy, including bone marrow transplant and still have their disease raging on. As well as lymphomas and now multiple myeloma. And today, CAR T-cells, this technology, this therapy is commercially available for patients with acute lymphocytic leukemia, acute lymphoblastic leukemia as well as lymphoma. And we do it all the time here at the Cleveland Clinic.

Nada Youssef:   Then CAR T-cell is removing the cell and fixing it and then getting a bunch of them and putting it back into the body.

Aaron Gerds:     Not the cancer cell, but an immune cell.

Nada Youssef:   Okay, an immune cell.

Aaron Gerds:     And basically, yeah, we're taking this immune cell that has failed to kill the cancer cell. It's failed to kill the leukemia cell, the lymphoma cell. We're taking it out, we're reprogramming the inner bits to make it be this little killer robot. And we grow a whole bunch of them and we put them back in the patient. They go around and they kill all these cancer cells, which is pretty amazing.

Nada Youssef:   And then you were talking about a bone marrow transplant. Can you explain what that looks like and where do you get the bone marrow from? Does it have to be family member? How complicated is it?

Aaron Gerds:     There are two types of bone marrow transplant autologous and allogeneic. Autologous, you're getting your own cells back. You donate your own cells, we freeze them down and then we give them back. Really the whole thing of that is we can give high doses of chemotherapy and then give you stem cell rescue. Chemotherapy that would normally kind of kill off your bone marrow and help you protect you against that effect. That's really used for lymphoma and myeloma. With leukemias we generally use something called an allogeneic transplant where we take someone else's bone marrow and give it to the patient. That's because we really need someone else's immune system to go into the patient, look at the cancer and say, "This leukemia is foreign, I got to go kill it." Because the patient's own immune system isn't doing that.

Yeah, we often look to family members first. Each sibling of a patient will be a one in four chance of being a match. And we're not looking at blood type, we're actually looking at immune type or it's the fancy term is called human leukocyte antigen or HLA. It's like immune type. We have blood type A, B, O where we can type red blood cells and find matches. But this is like we're typing the immune system really. A sibling will have a one in four chance of being a match. If we can't find, if none of the siblings for a patient are the match, we'll look in the registry. In the registry there are over 20 million patients worldwide that have agreed to donate their blood and bone marrow. And we can tap not only the US registries but European registries and other registries around the world and find matches for patients.

But that doesn't always work. And then we look to other sources to get these stem cells. We can actually, we've now developed methods of using half match transplants. Each sibling be a one in two chance of being a half match, a parent or a child would be a half match. And then also umbilical cord blood. We use umbilical cord blood to do these transplants because umbilical cord blood is so naive, it's so not exposed to the world that it can actually tolerate more mismatching when we look to type the immune system. It's more permissive if you will. And so we can use cord blood as well. This day and age we say everyone has a match of some variety and that the door to transplant shouldn't be closed because we can't find a potential donor.

Nada Youssef:   I'm curious about that cord blood. How are you getting that? Does it have to be a family member again that's pregnant? Or is it just pregnant woman can just...

Aaron Gerds:     Yeah, so anybody can donate their cord blood when they have a child. Here in Cleveland we have a very robust cord blood bank actually. One of the, personally, I think one of the better ones in the nation. But I'm biased of course. And so when you deliver your child at the hospital, you can say, "Yes, I'd like to donate my cord blood." Here again in the Cleveland area would donate to the cord Cleveland Cord Blood Bank and then they would come in, they would check it and they would collect it all and take it off and freeze it down and then give it to someone they need. Someone in need.

I think this is different than some of the for profit cord blood banks where you pay to store your own cord blood. To date there's only been one case report of a person using their own cord blood back. I think, I would be wary of some of these things and certainly I think there's something about paying it forward, donating your cord blood to the greater good and hopefully someone can use it for a positive thing in the future. In fact, when my first son was born, we donated his cord blood to the Cleveland Cord Blood Bank. And about a year later the cord blood was actually used to do a transplant in another young child.

Nada Youssef:   Nice. Good for you.

Aaron Gerds:     We're not privy to what happened, but I'd like to think that it did help some other child out.

Nada Youssef:   Very, very well said. Thank you. Is there a cure? And I know there's a million different types, so it's a really heavy question. But you say it's curable.

Aaron Gerds:     It is a heavy different. It is definitely curable, meaning that there are therapies that exist that can lead to longterm maintenance free remissions. Bone marrow transplant's certainly one of them for a lot of patients. There are some patients with CAR T-cells where we think we can maybe cure them. Certainly the story with an imatinib and CML, we're curing people with just a pill, which is pretty amazing. And actually now we're starting to think about stopping the imatinib in some patients who have been really, really good missions. They may not even need lifelong treatment, which is exciting. Definitely a curable disease.

Nada Youssef:   That's excellent. Thank you so much for your time. Appreciate it.

Aaron Gerds:     My pleasure.

Nada Youssef:   Thank you. And thank you so much for joining us. It's been a pleasure and thanks again for listening and we hope you enjoyed this podcast. For questions about leukemia or to make an appointment, please call our cancer answer line at (866) 223-8100. For more information, please download our leukemia treatment guide at clevelandclinic.org/leukemiaguide and to listen to more of our Health Essentials podcast where some of our Cleveland Clinic experts come and talk about topics, make sure you go to clevelandclinic.org/hepodcast. And for more health tips, news, and information from Cleveland Clinic, make sure you're following us on social media, Facebook, Instagram, and Twitter @ClevelandClinic. Just one word. Thank you. We'll see you again next time.