Amer Zeidan:
Hi everyone. Good morning, good afternoon, good evening, wherever you are.
Welcome to our newest podcast series called Myeloid Monthly. My name is Amer Zeidan from Yale University, where I am a professor of medicine and the chief of hematologic malignancies division over there. And this series will have one episode every month where we talk about important subjects pertaining to anything related to myeloid malignancies. And we would love to hear from you about the subjects that you want us to cover. Now, our first episode is actually something that we are very, very excited about because it’s something that we have been discussing for several years now, which is about how to harmonize the classification systems for myeloid malignancies. And it’s a true pleasure to be joined today by two top experts in hematopathology who are very involved in the classification process that’s going on right now. Dr. Robert Hasserjan from MGH and Dr. Sanam Loghavi from MD Anderson. The three of us are actually on location live in Chicago for the Classification Advancement Meetings and those are advisory meetings that have been developed basically to try to advise on how to best harmonize the ICC and the WHO classifications. For those of you who are not very aware of what has been going on with the split on these classifications we’ll be providing an overview and discuss why it’s very important to have a unified harmonized classification.

But also importantly, you will hear a very, very updated overview of how these classifications will be recommended to be going forward. So Robert and Sanam, thank you so much for joining me today.

Sanam Loghavi:
Thank you so much for having us. It’s a pleasure to be here.

Amer Zeidan:
So Sanam, maybe I will start with you. Maybe you can tell us why classification in heme pathology is very important. Why don’t we just think about MDS and AML as like one single entity?

Sanam Loghavi:
Right. I think, you know. Well, historically, our classifications have been based on morphology because that was our best tool that we had in our armamentarium. But as the technologies have advanced and, you know, we’ve learned more about the biologic underpinnings of disease and what drives these different diseases, we know that, I mean, MDS and AML are examples, but none of these hematologic malignancies are really one entity. They’re heterogeneous in what really drives the disease and to really get the diagnosis right and be able to better guide therapeutic decision making and risk stratification has become very complicated, because you have to take into account the genetics, the immunophenotype, the morphology, and everything that drives it. And of course, this evolves with time as we learn more about these diseases. So we take it upon ourselves to update our classifications as we learn more about disease. But I think it’s very important because not only does it drive clinical care for individual patients, but also the decisions that regulatory bodies make in approving drugs, or in developing drugs – in decisions that pharmaceutical companies make in developing drugs. So it’s really where the ball starts rolling.

Amer Zeidan:
Thank you so much, Sanam. Robert, I think sometimes there’s often a confusion between classification, risk stratification, and prognosis, and sometimes the biological pathways that drive the disease. And I feel like each one of those has its own uses in terms of how we work with patients. But maybe you can give a sense of how classification differs from thinking about prognosis and biological pathways.

Robert Hasserjian:
Yeah, sure. I think that’s something that can be kind of confusing. But I think both actually have different functions in a way. I mean… Prognostication is just determining the aggressiveness of a disease or the outcome of a particular patient, the predicted outcome. And often it’s risk stratified as, say, a favorable, unfavorable, intermediate, or a score is given. It’s just surely a numerical grade to sort of assess median survival. Classification defines different disease categories, which often do have different prognoses as well, but really defines different biologic groups, which are usually mutually exclusive, so they’re separate disease categories. You could have, for example, two different diseases that may be very different in terms of their biologic origins, maybe even involve different systems, but have the same prognoses, just happen to have coincidentally the same prognosis and potentially vice versa. So they have different roles. That’s why I think if a patient is diagnosed with a myeloid neoplasm, we both give it the name that is telling you what is the biologic abnormality, what is the pathway that’s abnormal? What is the genetic underpinning of the disease? And then often a score, that’s the prognosis, that’s some kind of grade or score that’s more of a kind of quantitative assessment of the patient’s predicted behavior of that particular disease.

Amer Zeidan:
Yeah, and I think this is very important. So just to make sure our audience understands, we are not here in Chicago to replace, for example, the molecular IPSS or to think about the different way of the ELN 2022 or 2024 classification or risk stratification. This is primarily to understand how the diseases should be classified from a hematopathologic point of view, but it does inform our ability to put patients on clinical trials, to discuss the different therapies. And importantly, in my mind, it is how do we explore therapeutic vulnerabilities that might arise from certain biologic pathways, depending on the classification. So maybe, Sanam, can you talk to us about how the classification has evolved over the years in general? I’ll take a historic perspective from Rob as well, but maybe from your perspective as well, over the last 20, 25 years, how have we been looking at classification of myeloid malignancies, which is the focus of this meeting?

Sanam Loghavi:
Yeah, well, I just want to clarify that I haven’t been practicing for 25 years. I’m not that old. But no, no, no. You know, in all seriousness, I think the way the classification has evolved is really in essence that we’re relying a lot more on the genetics of disease because we’ve learned about the genetics of disease. And we know that, you know, for instance, I’ll give you an example of a de novo acute myeloid leukemia that is driven by an NPM1 mutation, is called acute myeloid leukemia. It has a very different biology and a very different clinical course than acute myeloid leukemia that arises from a background of MDS with myelodysplasia-related mutations. And now we know very well that these two diseases, even though they have the same overall name, they’re very two different biologies. So I think with our evolving knowledge about the molecular of disease, we’ve been able to do a better job in, you know, compartmentalizing the different subsets of these diseases that we had given a general broad name. And that is, you know, I think the gist of it. But I think Rob can probably give us a better overview of how it evolved because he’s been involved in several of these classifications.

Robert Hasserjian:
Sure. Yeah, unlike Sanam, I have been around for 20 years –

Yeah, I can speak to that. So I think I can, yeah, I completely agree with what Sanam said. And I think, and I can remember, I’m kind of saying that jokingly, but actually, truly, I remember in the early 2000s, when I was a practicing hematopathologist, and in the early 2000s is when the first, the third edition WHO introduced the concept of a genetically defined disease… leukemias with inversion 16. Before they had been defined mainly morphologically by say AML with eosinophilia, but then it was defined actually by the chromosomal translocation or the chromosomal inversion of 16. And this was an innovation. I remember a neuropathology colleague talking to me and congratulating me and saying, you guys really paved the way. And now we take for granted that many disease categories in other areas as well, in soft tissue tumors, in brain tumors, are defined by genetics. But it was really the hematologic or the myeloid classification that first developed the concept of defining a disease by a molecular driver rather than by the morphology. And now, of course, there are countless numbers, dozens of different molecular categories of AML. And I think this identifies diseases like promyelocytic leukemia that respond, as you mentioned, Amer to specific drivers, but also…
to also define specific different subgroups and allow us to understand the pathways by which these diseases develop. So I think, as Sanam said, our classification is moving more and more from morphologic to molecular while still retaining the morphologic features as either a clue to an underlying molecular abnormality or perhaps a categorizing case where we still don’t yet understand the molecular underpinnings of the disease.

Amer Zeidan:
So, Sanam, I think people always think about hematopathologists, you know, with a microscope, you know, it’s always something that always comes to our minds. And as both of you have evolved, kind of alluded to the importance of genetic testing, many of us who are like in medical school reading about Sudan Black stains and things like that. And the FAB classification, which I remember, you know, I still see it’s actually still mentioned up to date in some papers which predated even that WHO. But how do you think the morphology, how important is morphology still these days with all the advancements in flow cytometry and immunohistochemistry and genetic and molecular testing?

Sanam Loghavi:
Yeah, I think, you know, this is a very valid point and very important, but I do think that there is still value in the morphology of disease because, to put it simply, I think there’s a reason that things look the way they do, right? Sometimes we understand what that reason is and sometimes we don’t. And I’ll give you, you know, an example of… two different, very different diseases in the same maybe broad category that are driven by the same molecular driver, you know, essential thrombocythemia and primary myelofibrosis may both have a JAK2 mutation, maybe with different allele burdens. And we don’t really understand why they manifest in two different ways. But, you know, I can look at under the microscope and with relatively good confidence tell you that this is ET or PMF from the way the megakaryocytes look, from the way the megakaryocytes cluster. So I think, you know, even though we’ve learned a lot about the genetics of disease and we’re, you know, clinically looking at the genetics of disease, there’s a lot of things that we’re not looking at, including the epigenetic drivers of disease, you know, or other things that we don’t necessarily know are important, but actually have phenotypic manifestations and are associated with specific morphology. So a lot of these molecular drivers that we talk about are not specific to disease, right? You cannot just sequence someone’s blood, detect a JAK2 mutation, and say that they have ET or an early PMF. You really have to look at the bone marrow to know. And that’s just one example. I think, you know a great pathologist or hematopathologist is someone that can put together the morphology, the immunophenotype, the molecular drivers, and understand the clinical implications of disease. And in my mind, that’s the best way of doing it.

Amer Zeidan:
That’s great. Rob, maybe we can move to what happened in 2022, which I think what led us to be here. So the WHO was the primary classification that was used for many years and 2022, a different classification called the ICC was published and we had two classifications. And I think there was a lot of interest in the field to try to harmonize these two classifications. But maybe you can tell us about, you know, that particular period and what happened.

Robert Hasserjian:
Yeah, I think that was a period where there was division within the community. I think there were, I think, ideas of who should make the classification. There was disagreement about that, who should be in charge, whose role it was. So as a result, there were two groups that worked on developing a classification and published them simultaneously, resulting in two different classifications.
I think this has been a real problem for patients, for clinicians, for pathologists. It’s been confusing. The one, as I say, sometimes I say the silver lining of this is that these two groups, which did operate independently and had the two were kind of done confidentially, separately, in a sense came to the same conclusions for most entities. So there’s a very close agreement. So that validates that two independent groups can look at data and reach the same conclusions about most things in myeloid neoplasms. However, there were some differences. There are different ways to read data sometimes or to interpret data and expert opinion. So there were actually several significant differences as well. And this is what has been creating really the problems and the confusion. So this is why since the release of those two
two classifications, the hematopathology and the hematology community on the lymphoma side and the myeloid side have both been trying very hard to bring these back together again. And this is the purpose of this classification advancement meeting is to try to harmonize the two, or not necessarily harmonize, but at least reach a consensus on the two, and also incorporate new developments that have come out since 2022, because ,any studies that have interrogated the differences between the two and tried to say, well, this classification, this may be better, and for this aspect, the other classification may be better. So I think we have now more data to work with that can help clarify the differences and I think arrive at a consensus on going forward a single classification that would incorporate both the best of the ICC and the WHO and future and current advancements that have kind of advanced both classifications in a sense.

Amer Zeidan:
Yeah, and I would note here also that this is not like just an academic discussion. This is clearly something that affects the clinic. And as clinicians, we always had the ability to interpret kind of path report and recommend the treatment that we think is best with some flexibility. There are other aspects that are less flexible, such as clinical trial enrollment and potentially insurance authorizations for medications. But importantly, this actually in the U.S. coincided with a federal law that required the immediate release of any kind of path or any imaging immediately to patients. And what was happening is some of these reports were… like released immediately to patients before we even see them. And because many of these reports were reporting with the two different classifications, this created some confusion to patients as well. So I think there was a very strong sense that we really needed to have one unified for all of these different reasons. So Sanam, you were very involved in the process of trying to harmonize these two systems. There were some, you know, attempts here and there to try to kind of reconcile and find what are the areas that could be more amenable to putting together. But how did this very huge effort to put the two classifications together, come about. And I would note this probably almost four years now, and this has been in action for at least a couple of years.

Sanam Loghavi:
Yeah, I think, you know, I want to echo what Rob said in that I think the silver lining of having two classifications was really identifying the data gaps. Right. And saying, OK, this was the area where we didn’t have really solid data. And so it was maybe interpreted differently or we didn’t have any data at all. So people in this period of time tried to actually look at these differences and use evidence or data to either validate one or the other or you know give a different recommendation and I think that everybody in good faith really wanted to make in our community, wanted to make a unified and harmonized classification. And so the agreement was for everybody to come together from, you know, the WHO, ICC or people that were not affiliated with, either or, but were experts in their field to come together, form several different working groups and work on the different topics to try and come up with an up to date and harmonized classification. And I think the up to date part is also very important because in some areas there may have not been a difference in the two classifications, but we now know more about that topic, so we needed to update the classification. And the other thing I would, you know, emphasize, and I think Rob can speak better to this, is that, the CAM or the Classification Advancement Meeting is really a body of experts that is going to provide recommendations that will inform the next WHO recommendation, but it’s not, sorry, the classification, but it’s not the same thing, as the WHO classification, right? So we will put out the proceedings of the CAM as a series of recommendations. And then the WHO, the editorial board, will decide how they want to proceed with that.

Robert Hasserjian:

I think that’s a very important point because this was something – I just want to add to this that it’s a very important point that what we’re going to be releasing at the CAM are recommendations and people shouldn’t start using them right away as a classification because this then the it’s been timed well with the WHO editorial board that there will be a meeting. They’ll initiate the next classification and we’ll incorporate, I think, and we’ll use the hopefully the recommendations of the CAM, which are our leading experts in the field. And there’ll be many overlap, I would think, between the people who developed the WHO and people who participated in the CAM. But it’s important that it’s an independent group that actually will produce the classification. I think that’s important. So the purpose of the CAM is to gather evidence, develop recommendations from experts, proposal of guidelines for a classification and recommendations, in some cases very detailed, or maybe saying for these there was no consensus, we couldn’t reach an agreement. And then perhaps that might, again, stimulate some studies that would try to look and maybe in the year that ensues before the actual final classification release, maybe that can be resolved.

Amer Zeidan:
Yeah, I was saying that one of the, I guess, silver linings is because of the differences between the two classifications. There has been a number of kind of analyses and data sets trying to look at the specific differences between the two classifications in the last year. So that provided extra evidence in the areas of controversy to try to unify them. But please go ahead, Sanam.

Sanam Loghavi:
Yeah, you know, the other thing I wanted to emphasize about the CAM and the process is that, you know, for those unfamiliar with this process, this is not just a three-day meeting where we’re coming together and making decisions here. This has been a lengthy process with, you know, several different working groups with clinical, genetic, pathology representatives for each disease entity or each disease group that have met on a weekly, sometimes twice weekly basis for several months now, trying to reconcile these differences, gather the data, come up with recommendations. Sometimes, you know, we’ve had very heated discussions over controversial topics. So this has been a really, you know, dedicated effort in trying to get this right. And I think that’s important. It’s not just that we’re here for three days and we’re going to resolve everything, right?

Amer Zeidan:
100%. Rob, you have a very important role in the American Society of Hematopathology, and the American Society as well as the European societies have played a very important role in the classifications in general. And I think one of the criticisms I hear often is the WHO has more of a global view in countries where they have more somewhat limited resources, they might not have access to a lot of the genetic testing or some of the kind of more advanced flow cytometry techniques, etc. And one of the struggles has been always is how do you come up with a classification that helps advance the treatments and inform kind of the disease therapeutic development, but at the same time can be used globally, which is something the WHO kind of thinks about a lot. So how do you reconcile these two different aspects as you come up with a new classification?

Robert Hasserjian:
Yeah, I think that is a valid point. And I want to emphasize, although the CAM is being organized by the societies, by the American Society for Hematopathology, it’s based in the U.S., and the European Association for Hematopathology, we do have people from all over the world that are participating in the CAM, from Asia, from Africa, from all continents who are contributing. But I think the point is still well taken. And I think one thing that we have been endeavoring to do is provide, for example, surrogates that could be done. Like in some cases, if a molecular test is not available, an immunostain could be helpful in places that don’t have the resource for molecular testing. But also one thing we have heard, and the clinicians have validated this, at least in the MDS group, is if we say that these molecular testing are required, it can often help countries that may not, the government may not pay, for example, for some molecular testing. It may actually help increase the likelihood that these tests will eventually become available in those countries. So we’ve heard sometimes we want you to make more stringent criteria so that we can actually have these tests approved by our government or paid for because they are.
really important. And as Sanam said, as you discussed at the beginning, these molecular markers are things that can influence treatment and can make the difference between getting a life-saving targeted therapy and dying of the disease that may have a targetable agent. And if you don’t look for it, you’re not going to find it. So I think we don’t want to shortchange those patients because of the fact that the test may not be available. We want to try to make sure that testing becomes available wherever it’s needed to save patients’ lives because it’s so critical to accurately diagnose these diseases.

Amer Zeidan:
Yeah, and this is, I think, a very important point. Now, I think I would actually note here that we are in the morning of the very first day, so the meeting is still to take place, so we cannot kind of discuss a lot of kind of conclusive recommendations, but maybe we can discuss some of the highlights of the main items of discussion, starting with MDS with you, Robert, about what are the main things, the main themes that will be discussed over the next couple of days in terms of MDS classification.

Robert Hasserjian:
Yeah, I think so. The main issues that are difficult in MDS, and this is true for both WHO and ICC, I think struggled is, first of all, how to define MDS, which is a malignant disease. And we know that MDS has certain mutational signatures or genetic signatures that also can happen in benign, well, diseases that are thought to be benign or clonal disorders that are not considered to be equivalent to MDS. So deciding when to call a patient having to have MDS, which is a myeloid neoplasm. And so traditionally, this has been based on morphologic dysplasia. But one thing that has been recommended is to now allow certain mutation profiles to allow a diagnosis of MDS, even if the pathologist can’t see sufficient morphologic dysplasia in patients who have cytopenia that may require treatment. This would open potentially more patients, would open availability for these patients to be treated, even if the dysplasia is not there, at least initially. The other has introduced new genetically defined groups of MDS based on recent evidence. Some of this is based on molecular clustering studies showing that their particular
genetic subgroups that seem to form a true entity. And this is, of course, validated by either differences in prognosis or morphology or even gene expression profile for some diseases. So this is also another thing that’s being recommended is the addition of some new genetically defined entities. For example, an MDS with DDX44 mutation, which is a germline mutation that can give rise to MDS or AML and has some unique features and potentially treat an implication. So I think that’s an example of one of the new entities that’s added. So I think those are some of the most important changes is, of course, incorporating more genetics in the diagnosis of MDS that impacts both its definition and also in its classification.

Amer Zeidan:
Yeah, and Sanam, I think you’re a member of both MDS and the AML kind of side of things. And as you mentioned, we had, to put it mildly, some heated discussions and some aspects of MDS. So how did it go with AML and what will be kind of the primary focus of discussion?

Sanam Loghavi:
Yeah, I think…You’re right. I’m MDS/AML. But so, you know, I think for the most part, there’s broad agreement in the AML group on things that have been decided on, which is really nice. The major changes, I think, you know, one of the differences between the WHO and the ICC was in the AML-defining genetic categories, such as, you know, NPM1, KMT2A, NUP98, there was a different blast threshold. I believe that, you know, I’m not going to say what the recommendation is. I don’t want to give it away. But there is a, you know, we’ve agreed upon a uniform or unified recommendation, which is good. I think the other is the definition of TP53 mutated in, this is both in MDS and AML, the definition of biallelic inactivation or, you know, multi-hit is going to become much more stringent in the hopes of, you know, better identifying the ones that have actually biallelic status and may have a different biology. That’s one thing. And then a true confirmed monoallelic TP53 will be distinct category in AML. And I think finally, there’s been some resolution, you know, there was some subtle differences in both the gene mutations and the cytogenetic alterations that were considered myelodysplasia related in the two classifications, and those have been resolved. I think there’s broad agreement on what constitutes cytogenetic myelodysplasia related changes as well as gene mutations. And I think for the most part, oh, and of course, the contentious area that still remains is the cases that have between 10 to 20 percent blasts is whether to retain the MDS/AML category that was introduced by the ICC or go back to having MDS with increased blasts. And I think this is still very much in debate. This is going to be discussed and hopefully, you know, we’ll come to a resolution. But I have a sense that it’s going to be driven by the genetics of the disease. You know, the decision is going to be made by the genetic drivers, not necessarily the blast count. So that’s where we are in AML.

Amer Zeidan:
Yeah, and I think, again, there has been a very nice kind of bi-directional process between, you know, the lab or the classification and the treatments. For example, with the menin inhibitors, we know NPM1 and KMT2A rearranged kind of leukemias. And I think these getting categories, that makes it kind of straightforward in terms of the treatments. That’s on the success part. But of course, on the downside, the TP53, which has been very difficult, no therapeutic has worked. And my own belief, actually, part of the failures have been, as you alluded to, is probably we lacked a very stringent definition of TP53 mutated myeloid neoplasms. And we also separated them into MDS and AML, which made it very difficult to enroll on these trials because it’s already relatively rare entity and you are dividing it between diseases. So you cannot do like big phase three trials, but also how we define TP53 varied a lot. As you mentioned, there are multiple different ways and they might not be all leading to or kind of describing the same biologic underpinning of the real TP53 mutations. So I think some of these aspects would be very important for
for drug development.

I know the three of us have to run to to the meeting soon to start the proceedings but maybe we can in the last few minutes talk about the MDS/MPN overlap and maybe MPN, maybe Rob, do you want to talk a little bit to this about what will be discussed in the meeting?

Robert Hasserjian:

yeah this is an area, so, we’re talking, you’ve been talking mostly about MDS, which is a disease associated with cytopenia and ineffective hematopoiesis. And the patients get anemia as the most common cytopenia. And this often requires treatment and patients are very symptomatic. MPN, in contrast, is a proliferative process where there’s an overproduction. The cells mature, but they’re producing too many cells of one type, as you know. And then for decades now, it’s been recognized an overlap group where there’s both proliferative and dysplastic features. An example would be chronic myelomonocytic leukemia, where there’s overproduction of monocytes, but at the same time, some dysplasia and usually a cytopenia. So this latter group is particularly difficult to define because there are those mixed features and how do you combine them? How do you define them? Proliferation has been traditionally defined by blood counts, increased monocytes, increased white count, but we have to apply a level. What is increased? And that’s somewhat arbitrary, right? We have these arbitrary thresholds, which may or may not define certain categories. We can try to use genetics. Proliferation is often driven by, as Sanam mentioned earlier, like JAK-STAT pathway mutations, like JAK-2 or RAS pathway mutations. But what do you do if you have those mutations, but the counts are not elevated or vice versa? So it’s, again, the question of, is proliferation defined by blood counts, by genetics, what we see under the microscope? And so this is why in defining this overlap disease, this is particularly controversial. And I think I’ll turn it over to Sanam, who’s been involved a little more in those discussions, but it’s a particularly difficult group to define because you have kind of different things you could weigh more or less in terms of defining what is truly a mixed proliferative and dysplastic disease.

Sanam Loghavi:

Yeah, I agree. I think that’s, you know, that was one of the major topics of discussion on the MDS/MPN overlaps. I think the other is, you know, the newer definition of chronic myelomonocytic leukemia in both the WHO
the ICC had lowered the absolute monocyte count that was required for this diagnosis to 500 in the presence of clonality, of course, but really without specifying what type of clonality. Now, I think the ICC had built in a morphologic criterion, which was very helpful in, you know, teasing out some of the MDSs that had borderline monocytosis. But I think, you know, from several papers that have been published in the interim, we know that, you know, the genetics also help. So there are several, you know, there are various specific genetics that are associated with borderline monocytosis, like deletion 5Q, like biallelic TP53, like SF3B1 mutated MDS, and then other genetic signatures that are really, you know, typical for CMML, like a biallelic TET2 mutation, like a TET2 SRSF2 mutation. And so, you know, the attempt has been really to combine all of these to come up with a refined diagnostic criteria for CMML that really helps us avoid over-diagnosis and under-diagnosis of CMML and to be able to tease out MDS and CMML a little bit better.

Amer Zeidan:
Yeah, thank you so much. So maybe we can conclude by what are the next steps, as I think both of you have alluded, this is a three-day kind of culmination of multiple months of active discussions, and there will be kind of a consensus establishing process that will come out of this meeting. There will be probably some areas that will not reach consensus, but what happens after this? Maybe, Rob, you can talk to us about this. When do we expect the new, I guess, unified classification to come out?

Robert Hasserjian:

I can’t give a specific timeline, but the plan is, as Sanam said, just as before the meeting, there was a lot of work, there’ll be a lot of work after the meeting too, right? The groups will reconvene, there’ll be some, there’ll be votes taken, there’ll be some consensus achieved, and there might be reworking some entities, you know, taking some input from the discussions that happen at this meeting. And then there’ll be publications of the proceedings of the meeting, you know, in both the lymphoid and the myeloid that will give the details of what the recommendations are. These will be published, but importantly, these won’t be actually a final classification, right? These will be recommendations to, you know, the WHO that will then, the plans are probably in either, you know, later to 2026, the process will start early 2027, and the WHO will convene an editorial board, will develop authors, and then will actually finalize the classification will develop the final classification, presumably taking the recommendations of the CAM, at least the conclusions that are reached. Particularly ones that have strong consensus will kind of adopt those, but again it’s a separate process so that is the process we’re expecting, you know, I can’t give a specific date, but sometime in 2027, hopefully, is when we’ll have the next final classification that we can use. But in the meantime, the CAM is kind of a stepping stone, is an initial step to move towards that consensus final classification. There’ll be one classification that we all will accept what the WHO finally publishes again in 2027, hopefully.

Amer Zeidan:
Yeah, and I think this is something that many of us kind of look forward to. I mean, this clearly was, I think, a very well-taught process and required a lot of discussions and delegations. And, you know, especially these days, someone, you know, wonder if politicians can do that to sort out their issues as well. But this is great. Thank you so much both for this excellent discussion. Any final words, Sanam?

Sanam Loghavi:
No, thank you so much for having us. I think this was a great opportunity to discuss. And then I think, you know, good luck to all of us and the heme community in reaching a consensus and, you know, coming up with a classification that is most helpful to our patients above everybody.

Amer Zeidan:
And hopefully we’ll have a subsequent podcast in the future once things are kind of more finalized to discuss some of those kind of final recommendations. Thank you so much to our audience for listening in. Again, we are here reporting from Chicago from the Classification Advancement Meeting. And thank you so much for listening.