Initial CHORUS data on HHT and ASH HematOmics Program

Summary

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Blood Podcast Episode Summary:

Initial CHORUS Data on HHT and ASH HematOmics Program
Date: July 23, 2026
Host: Dr. James Griffin (Dana Farber Cancer Institute)
Guests: Dr. Hani T. Alsamkari (Mass General Hospital), Dr. Jin Zhou (St. Jude Children’s Research Hospital)

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Episode Overview

This episode provides in-depth discussions of two major studies in hematology:

1. The Initial CHORUS Registry Data on Hereditary Hemorrhagic Telangiectasia (HHT): Dr. Hani T. Alsamkari discusses findings from the first prospective, federally funded US registry of HHT patients.
2. The ASH HematOmics (ASHOP) Program: Dr. Jin Zhou presents the development and future of a data-sharing platform enabling integrative analysis of genomic and clinical data in hematologic diseases.

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1. CHORUS Registry: The Clinical Spectrum of Hereditary Hemorrhagic Telangiectasia (HHT)

(Segment: 00:39–15:32)

Key Discussion Points & Insights

Background and Purpose (01:10)

• HHT is a progressive, inherited blood vessel disorder and the second most common inherited bleeding disorder globally and in the US, affecting about 80,000 people in the US (~1 in 4,000) and 1.6 million worldwide.
• Despite its prevalence, there has been a lack of long-term, prospective natural history data, with most previous studies being single-center and retrospective.
• The CHORUS registry is the first large, national, federally funded (US Congress) effort to systematically collect and analyze both retrospective and prospective data (over 2,400 data elements per participant).

Registry Methods and Cohort Description (03:30)

• Initial report covers first 600 patients (median age 53 [0–88 years], 60% women).
• Data collected via EMR abstraction and direct participant interviews, with follow-up visits.
• Comparable in scope to the Athen registry in hemophilia.

Findings: Disease Manifestations and Burden (04:47)

• Diagnostic Delay:
  • 60% experience recurrent spontaneous nosebleeds (epistaxis) by age 13, but 71% are not diagnosed until adulthood—delay often >20 years.
• Mucosal Bleeding:
  • 95% have recurrent spontaneous epistaxis, 60% of which is moderate-to-severe.
  • “Today’s mild is tomorrow’s moderate, and today’s moderate is tomorrow’s severe.” (Alsamkari, 05:38)
• GI and Menstrual Bleeding:
  • 1/3rd of patients have chronic GI bleeding, most requiring IV iron or transfusion.
  • Over 1/3 of postmenarchal women have heavy menstrual bleeding—a previously unreported figure.
• Iron Deficiency:
  • 70% have iron deficiency or iron-deficiency anemia.
  • 75% experience moderate-to-severe HHT-associated mucosal bleeding.
• Internal Bleeding and Organ Involvement:
  • 3% had intracranial hemorrhage; 2% had intrapulmonary hemorrhage.
  • Rates of intracranial hemorrhage similar to hemophilia A patients in the 1990s pre-prophylaxis.
  • 50% have pulmonary AVMs, 15% had brain AVMs, 75% (of those screened) have liver AVMs.
• Major Complications:
  • 7% each for pulmonary hypertension and heart failure.
  • 10% with severe cardiopulmonary disease; 4% with epilepsy; 35% suffer chronic migraines (a complication of pulmonary AVMs).
  • 1 in 6 have thromboembolism.
  • 1 in 5 have a serious CNS complication (hemorrhage or stroke).
• Takeaway:
  • “We previously underestimated the burden of this disease... It’s really high time that we continue to develop effective and licensed therapeutics for HHT.” (Alsamkari, 08:19)

Genetic Heterogeneity in HHT (09:05)

• Five genes implicated, most commonly endoglin and ACVRL1 (ALK1).
• Genetic subtype influences phenotype (e.g., endoglin mutations: more brain AVMs; ACVRL1: more liver AVMs; SMAD4: combined with juvenile polyposis and high GI cancer risk).
• “This is a genetically heterogeneous disease, and the genetics do matter… We recommend all patients with HHT get genetic testing.” (Alsamkari, 10:22)

Early Diagnosis and Awareness (11:12)

• Need for more HHT centers, leveraging existing hemophilia centers.
• Funding supports continuing medical education for earlier recognition.
• Simple clinical clues: recurrent nosebleeds (≥4/year), mucocutaneous telangiectasias.
• “If you have four or more nosebleeds a year, that is HHT… until proven otherwise.” (Alsamkari, 12:06)
• Family history is critical due to autosomal dominant inheritance.

Therapeutic Landscape and Future Directions (13:59)

• No licensed therapies for HHT yet, but several novel agents in development:
  • Vascular/angiogenesis-targeted drugs: small molecules, receptor agonists.
  • Coagulation-targeted approaches (e.g., siRNA against plasminogen).
  • Off-label antifibrinolytics and antiangiogenics have shown benefit—now moving toward disease-specific refinements.
• “It’s time to really refine that and develop therapies that are really honed in on this disease.” (Alsamkari, 15:20)

Notable Quotes & Memorable Moments

• “This disease is progressive. Both the bleeding and non-bleeding manifestations get worse over the lifespan.” (Alsamkari, 03:10)
• “The numbers were really eye opening... the incidence of intracranial hemorrhage found in CHORUS is similar to that in persons with hemophilia A in the 1990s.” (Alsamkari, 07:12)
• “We previously underestimated the burden of this disease… It’s really high time that we ultimately develop effective and licensed therapeutics for HHT.” (Alsamkari, 08:19)
• “If you have four or more nosebleeds a year, that is HHT… until proven otherwise.” (Alsamkari, 12:06)

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2. ASH HematOmics (ASHOP) Program: Integrative Genomic and Clinical Data Analysis

(Segment: 15:33–25:47)

Key Discussion Points & Insights

Origins & Purpose of ASHOP (15:57)

• Developed in partnership with the ASH Subcommittee on Precision Medicine.
• Designed to be an open-access, online platform aggregating large clinical and molecular (genomic, transcriptomic) datasets, initially focusing on leukemias, especially pediatric cases.
• Collaborative development with international experts from St. Jude, Children’s Research Hospital, and German leukemia labs.

AS HOP Platform Overview (17:00)

• Enables users from any scientific or medical background to:
  • Explore patient cohorts, survival differences, and genomic alterations.
  • Run integrative analyses, including UMAP visualizations and overlay clinical/genomic features.
  • Perform quick differential gene expression analysis (e.g., differences in NPM1-mutated vs. wildtype AML).
  • Access use cases and guided tutorials for various analyses.
  • “Through a couple of clicks, [the] user can launch this… under maybe 30 seconds and… see the differential gene expression analysis results.” (Zhou, 18:52)

Future Development and Expansion (20:12)

• Platform aims to expand to cover adult hematologic malignancies, classical hematology, and other omics (e.g., proteomics, metabolomics).
• Community engagement: researchers can propose new disease cohorts for inclusion; feedback will shape next development phases.
• Plans to include rare/classical diseases like HHT, leveraging registry datasets like CHORUS for integrative multisystem analyses.

Data Access and Utility (23:52)

• Portal accessible via the ASH hematology.org domain or by Googling “ASHOP”.
• Open-access after free sign-up; extensive user guides and YouTube tutorials available.
• Current data focus: predominantly pediatric/pre-treatment samples; future plans for relapse and survivorship samples.
• Efforts underway to diversify with more adult samples and include a broader array of diseases.

Notable Quotes & Memorable Moments

• “The goal is really to allow the broad community... to come into this portal and ask a question.” (Zhou, 17:11)
• “We built all of these and we talk about a few use cases… These only serve as examples how anyone might utilize ASHOP to interrogate this large result.” (Zhou, 19:16)
• “We absolutely hope… to get the feedback from the broad ASH community and... collect additional disease types from diverse population backgrounds.” (Zhou, 25:43)

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Timestamps for Important Segments

• 00:39–15:32: CHORUS Registry and HHT (Dr. Hani T. Alsamkari)
• 09:05: Genetic Heterogeneity in HHT
• 13:59: New Therapeutics in HHT
• 15:33–25:47: ASHOP Program Overview and Future Directions (Dr. Jin Zhou)
• 17:00: ASHOP Platform Capabilities and Use Cases
• 20:12: Expansion Plans for Platform and Data Types
• 23:52: Accessing the AS HOP Platform

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Takeaways

• CHORUS is revolutionizing understanding of HHT: The registry’s findings underscore a higher disease burden and complexity than previously understood, with urgent need for earlier diagnosis and targeted therapies.
• ASHOP is democratizing data-driven hematology research: With extensive clinical and genomic datasets, robust analytical tools, and a vision for broad disease and ‘omics’ inclusion, the platform is set to drive discovery and precision in hematologic disease research.

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For full articles and platform access, visit bloodjournal.org and search for “CHORUS HHT registry” or “ASHOP HematOmics Program”.

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Transcript

[A]

Welcome to the American Society of Hematology Conversations with Blood Authors Podcast this blood podcast episode is hosted by Dr. James Griffin from the Dana Farber Cancer Institute in Boston. He discusses clinical spectrum of Hereditary Hemorrhagic Telangiectasia data from the Comprehensive HHT Outcomes registry of the US with Dr. Hani T. Alsamkari. He also talks with Dr. Shin Jo regarding his article. The ASCH hematology program supports integrative analysis of genomic and clinical data in hematologic diseases.

[B]

Hello everyone, My name is Jim Griffin. I'm at the Dana Farber Cancer Institute and I have the pleasure of introducing two excellent blood papers that are going to be presented by their authors. The first paper is entitled Clinical Spectrum of Hereditary Hemorrhagic Telangiectasia Data from the Comprehensive HHD Outcomes registry of the US or chorus. This paper is going to be discussed by Dr. Hani Al Samkari at the Mass General hospital and colleagues.

[C]

Dr. Al Samkari, thank you so much Dr. Griffin. It's really my pleasure to talk on our paper on the first report from the Korus Registry. I think before we do that it'll be important to just take everyone back to what is HHT and why is HHT important? HHT is a progressive multi system inherited bleeding disorder caused by abnormal blood vessel formation with numerous morbid and potentially fatal manifestations. This is the second most common inherited bleeding disorder worldwide and in the US with about 80,000 patients in the US and about 1.6 million worldwide. Despite that and being as the second most common inherited bleeding disorder, twice as common as hemophilia, we have very little overall long term prospective data on the natural history of hht. Most of the data in HHT before QORUS came from retrospective single center reviews and reports and qoris is really the first of its kind. It's a national United States registry, prospective and retrospective registry funded by the US Congress explicitly to try to address this gap in knowledge about HHT. We recognize that HHT is about 1 in 4000 individuals that it occurs both in men and women. It's autosomal dominant. In addition to being the second most common inherited bleeding disorder, it's the most clinically significant and morbid inherited bleeding disorder of women and in fact tends to have more severe overall manifestations in female patients, though both males and females can have severe manifestations of hht. This is a progressive disease. Both the bleeding and non bleeding manifestations get worse over the lifespan and so QORIS really this report from Chorus is the first 600 patients enrolled and QORUS is really comprehensive registry with over 2,400 data elements collected. The data is collected at each site by trained research coordinators through the electronic medical record, as well as direct interviews with participants and participants have follow up visits and so on. It's analogous in many ways to the Athen registry in hemophilia. The results of this showed a number of really important things that we recognize now about hht. Just to take a step back, the median age of patients was about 53 years. Patients aged from 0 to 88 years. 60% were women. In this initial report, despite 60% of participants developing recurrent spontaneous epistaxis, which is sort of the CYNO of HHT, but by no means the only manifestation by age 13. The vast majority, or about 71% of patients were only diagnosed as adults and generally in middle to late adulthood. So the delay in diagnosis from initial manifestation, which could have been recurrent epistaxis or stroke, was over two decades. Really representative of the fact that this is a progressive disease and we typically think of bleeding disorders as, you know, very obviously progressing in small children. And that's not the case with hht. In many patients, the manifestation of mucosal bleeding, which is what this disease is really most well known for, we found that 95% of patients had recurrent spontaneous epistaxis, of which 60% was in the moderate to severe category. We know that this is a progressive disease. So today's mild patients are tomorrow's moderates and today's moderates are tomorrow's severes. About a third of patients had chronic gastrointestinal bleeding. Most of these patients required parenteral support with intravenous iron and or red cell transfusion. Because of this significant burden of chronic GI bleeding, we found the incidence of heavy menstrual bleeding in post medical age females was over a third of women hht, which is something that's never been described before and something that is definitely in need of further evaluation. Overall, 70% of patients had iron deficiency or iron deficiency anemia. Three quarters of patients had moderate to severe HHC associated mucosal bleeding, numbers that again had never been described in the past and greater than the burden of disease that was believed to occur. And then with regards to internal bleeding, 3% of patients had reported intracranial hemorrhage and 2% had reported intrapulmonary hemorrhage from ruptured brain or pulmonary arteriovenous malformations. These numbers were really eye opening and the incidence of intracranial hemorrhage found in Chorus is actually similar to the incidence of intracranial hemorrhage in persons with hemophilia a in the 90s, right before routine factor prophylaxis. The most recent report from Athens puts that incidence at around 0.5% now in patients with hemophilia. So with our modern advances in therapy, so definitely a long way to go with regards to HHT and a really significant burden of both mucosal bleeding that causes major quality of life and anemia and iron deficiency related complications as well as significant and potentially fatal internal bleeding complications. On top of that, half of patients had pulmonary arteriovenous malformations, about 15% had brain arteriovenous malformations, and about 75% of those screened had liver arteriovenous malformations. And These internal organ AVMs led to a really major burden of other severe disease complications like pulmonary hypertension, heart failure, both of which occurred in 7% of patients. 1 in 10 patients with severe cardiopulmonary disease, 4% with epilepsy, 35% with chronic migraines. That's actually a complication of pulmonary AVMs. 1 in 6 patients developing thromboembolism, either venous or arterial thromboembolism, which makes HHT inherited bleeding disorder that also has an elevated risk of thromboembolic complications. And ultimately one in five patients total developing some serious CNS complication, whether that's a intracranial hemorrhage or a stroke, complications of brain AVMs, so on and so forth. I really think that the main take home from Chorus registry initial report is we previously underestimated the burden of this disease. We recognize it now. It's really high time that we ultimately develop effective and licensed therapeutics for hht. Given that there still remain no licensed therapies for HHT anywhere in the world. Thankfully there are now HHT specific drugs that are in development that will hopefully address this really dramatic unmet need.

[B]

Thank you very much for that nice discussion. Just a couple of questions. Your paper also talks a little bit about the genetic events that have led to the diagnosis of HHT and specifically mentions about five different genes that sometimes have a mutation. Does the syndrome that results from these mutations, from the five different possible mutations all look about the same or are there some differences?

[C]

There are differences. There are about five different genes that can be mutated that cause HHT or known HHT like syndromes. The most common are mutations in endoglyns and ACVRL1 or ALK1 that's a different ALK than the anaplastic lymphoma kinase. This is the activin like receptor kinase. And these are both really important endothelial cell surface receptors that are involved in vascular quiescence and maintaining vascular quiescence. And so they become mutated. And then ultimately downstream you have overactive angiogenesis, dysregulated angiogenesis, a lack of normal blood vessel maturation, and this results in the telangiectasias and the AVMs of HHT. But one thing Cora showed and confirmed as well are that there are some differences in the various manifestations that we see. HHT patients are unified by mucosal bleeding, but beyond that, there's a lot of heterogeneity and who develops what. And patients, for example, with endoglyn mutations are more likely to develop brain AVMs, patients with ALK1 mutations more likely to develop liver AVMs, patients with a rare subtype called SMAD4. Mutated HHT causes HHT juvenile polyposis syndrome, where patients have all of the manifestations of hht, but also juvenile polyposis and a very high risk for intestinal cancers. This is a genetically heterogeneous disease and the genetics do matter. So while we diagnose patients with HHT in clinic using the Curacao clinical criteria, we recommend that all patients with HHT get genetic testing to figure out the underlying mutation.

[B]

You mentioned that epistaxis is extremely common in this disease and that a fair number of patients actually show severe epistaxis by the age of 13. But that diagnosis typically doesn't take place for another 10 or 20 years. How can we improve this? Is it possible to develop education plans that will accelerate the diagnosis of this disease at a much earlier age?

[C]

I absolutely think so. There's a multi pronged effort to try to improve this number one, more HHC centers of Excellence. Right now we have, for example, 28 hhc centers in the United States, and that doesn't even add up to one in each state. And large states like Texas, for example, only have two centers. So we need more HHT centers. And the one definite way to develop more HTC centers is for hemophilia treatment centers, which there's an obvious synergy there to expand and add HHT and become an HHT center of Excellence. Many of our newest centers have taken that route, and we strongly encourage that. Beyond that, we have funding from HRSA and the US Government in the US Part of that funds continuing medical education, education of community providers. I always say nosebleeds are common in kids, but they're not really all that common in teenagers, and they're not common in adults. And if you have recurrent nosebleeds, which we define very, very liberally as four or more per year, most patients HHT have nosebleeds every week or multiple a day, right? But if you have four or more nosebleeds a year, that is HHT in adult or a young adult, that's HHT until proven otherwise. It's easy enough to rule out von Willebrand disease. The thing that recurrent nosebleeds can be hiding, that can really be deadly or really cause major complications if it's missed is hht. And it's easy enough to look at the tips of their fingers, look at their face, their lips, their tongue, their ears. They don't have to disrobe. You can look at all of these things in a minute in the office. And, and if they have any red spots, any little red dots that are consistent with telangiectasias, and if you're not sure what they look like, Google them, you can tell, wait a minute, this might be a patient with HHT. I care for over 500 families with HHT at the MGH HHT center of Excellence, which I co direct. And I have never met a patient that has mucocutaneous telangiectasias in these typical locations and recurrent epistaxis that didn't ultimately have a diagnosis of hht. So yes, there is a lot more we can do and we should do, but one of the things we recognize, right, because it's a progressive disease, kids may not have obvious manifestations, they may not have the mucocutaneous telangiectasias, yet they may have mild epistaxis. Look at the parents, right? This is autosomal dominant. This disease runs in families. So ask the parents, ask about family history of nosebleeds, and you can pick up on it.

[B]

One last question. You mentioned that new treatments may be coming. And of course, one of the big problems with HHT is that there hasn't been good treatments to reduce the incidence of bleeding. What's the basis of these new treatments and when can we expect to know whether they work?

[C]

Fantastic question. There are already two new treatments that are in clinical trials. Actually now three. As of just recently, there are six in development. These novel therapies in HHT take advantage of either two pathways to treat the disease. Either they're vascular acting, they act on this dysregulated angiogenesis, either by targeting important downstream nodes of the lesion alk1 endoglin, bmpr2 pathway like for example akt or a receptor called apelin or they involve antibodies that agonize ALK1 itself. That's one modality that is being used to treat and these several drugs are already in clinical trials in the clinic. The other modality is coagulation system going directly after hemostasis. This involves small interfering RNA targeted at plasminogen to drop plasminogen levels drastically and therefore treat mucosal bleeding wherever it happens, whether that's epistaxis, GI bleeding or heavy menstrual bleeding. Both of these approaches have demonstrated either affecting the plasminogen, for example with off label antifibrinolytics or affecting angiogenesis with off label antiangiogenics. We have shown efficacy with those approaches with off label drugs and now it's time to really refine that and develop therapies that are really honed in on this disease. And that's exactly what's happening now.

[B]

Thank you very much.

[D]

Thank you.

[B]

We're going to go on to the next paper in the podcast. The title of the paper is the American Society of Hematology Hematomics Program Supports Integrative Analysis of Genomic and Clinical Data in Hematology Hematologic Diseases. The podcast will be presented by Dr. Jin Zhou from the Department of Computational Biology at St. Jude Children's Research Hospital in Memphis, Tennessee.

[D]

Dr. Zhou, thank you so much. Dr. Griffin, the backdrop of our study is we all know the power of the quote unquote big data. If I can give a very quick history of this project in that we started working with the American Society of Hematology Subcommittee on Precision Medicine on possibly to build up a online resource for worldwide researchers to access the large data sets that has been generated for hematology or could be in specific for the hematological malignancies or leukemias. It has been a long time interest of my own research field and I jumped into this opportunity and worked with the Subcommittee on Precision Medicine as well as our local experts on childhood leukemia, that is Dr. Charles Mulligan from Central Children's Research Hospital and his laboratory staff as well as Dr. Thorsten Hafalach from Unique Leukemia Laboratory from Germany. I had the huge privilege to be able to work with these domain experts. We first curated and harmonized large scale of both clinical as well as molecular characterization profiling results for both pediatric as well as adult leukemia cohorts. The current cohort has a bigger emphasis on the pediatric side and it is our wish to later generalize the to adult broad hematological malignancy as well as classical hematology, which I can touch on later. Long story short, we launched this ASH HOP platform as a convenient place for anybody who's interested in finding out about these leukemia studies, any characteristics about these cohorts, these patients, and see their survival differences and to look at their genomic characterization that includes their somatic genomic alterations and the transcriptome profiling results. So we generated this online platform we branded on as ashop. Through a very close collaboration between my institution, the Central Children's Research Hospital with ash, we launched this platform and produced this manuscript to discuss this pilot phase of this project. I'm very happy, I'm very grateful for this being selected, not only being accepted as article in the journal Blood, but also being featured on this podcast. You can see that it is a resource that we generate here and the goal is really to allow the broad community, whether you are in the hematology or even just from the general cancer field or medicine field, you could come into this portal and ask a question. So this portal is designed really to be open ended. In order to engineer the portal to answer some typical questions, especially related to the leukemia studies, we also built in advanced genomic and transcriptomic integration analysis features that include transcriptome UMAP projection that shows at a very high level, we compare these leukemia transcriptomes and how they are different and how their similarities are. And then we allow user to overlay any feature of interest, whether they are clinical, demographic or any kind of a molecular feature. They can overlay on that and see whether these features can correlate with their transcription differences. Following on that, the user can stratify the cohort into arbitrary groups. Whether you stratify, you see there's the separation in the transcription embedding, you see the separation into two different groups and you can select these two groups or such as I can say I'm interested in this particular genomic loci or particular gene. I ask the question what is the transcription difference? It might be that may be caused by this highly mutated gene in acute myeloid leukemia, which is npm1. What are the transcription differences for the npm1 altered versus npm and wild type. And then user can just through a couple of clicks user can launch this quote unquote differential gene expression analysis under maybe 30 seconds and user will see the differential gene expression analysis results and then interpret that through the subsequent gene set enrichment. We built all of these and we talk about a few use cases that have either been already noticed in the prior leukemia studies or has been so much look at through at a large cohort scale and we discussed these as use cases in our manuscript. These only serve as examples how anyone might utilize as HOP to interrogate this large result that is the very simple introduction of that. On top of this existing palette phase which has been completed and launched, there are far more exciting work that we could do. I listened to Dr. Al Samkari's study of HHT which is fascinating. I immediately think that data set it could be a candidate that we can include in R shop because we want to expand to classical hematology to capture these clinical features for this separate group of patients will capture their clinical features and their genetic alteration genetic providing results so that these patients will be available in addition to any other patient cohorts disease cohort that's already on the ASH hub. We can do aggregate study and maybe we can notice something new. We are planning for the next phase of the ASH hop. We will be opening to the broad ASH community and let the community propose what disease cohorts that they already have ready and they want to be included in the Azure platform. We'll be very open to that. Not only we're expanding on the cohort wise, but also the other orthogonal dimension will be providing results because the providing result doesn't stay on the DNA or RNA level. We can go with single cell level, go with proteomics, metabolomics or epigenetic, etc. Etc. We're open for accepting the community to tell us what they are interested in most and we're open to that and we want to collect the feedback and then prioritize to steer the next phase of ashop. I'm really excited. I hope the listeners and readers of our paper will be happy to check it out and give us a feedback how this might help with our research.

[B]

Thank you very much. You mentioned that the data set so far is somewhat enriched for younger patients, pediatric patients in particular. When do you think more adult diseases like myeloma, lymphomas and so forth might be added to the database?

[D]

I couldn't just directly give the timeline yet, but hopefully later this year we will start to reach out to the broad hematology community. We have already demoed our data portal to some ASH members and immediately there are already feedback high interest of adding in the myeloid malignancies, the multomyeloma, etc. Etc. There will be a lot of data set that could be immediate candidate to be included in the ashrap.

[B]

If you would just mention to the listener how they can access this right now. Where do they find the portal that you use? And I think one thing you might also emphasize is that when I went to that site to have a look at it, there were some really excellent examples and walkthroughs of how to use this site effectively.

[D]

There is a direct URL to access. It's called ASHOP A S H O P under hematology.org domain name. Or you can just simply Google ASH hop. It should pop up right now. You do have to sign up and log in to access it. All the data are open access right now and we could possibly later on expand to have this access control layer which is under discussion right now. But now all data is open access. Still you do need a single sign on to be able to access it while you are on the site. We also provide several user guides, such as written guides or YouTube tutorials.

[B]

Just a couple of other questions for you. Were all the samples that are there so far pre treatment samples, diagnostic samples, and are there any plans to look at relapse samples, at least in some diseases like the acute leukemia?

[D]

I believe right now most if not all the samples are pretreatment. They are diagnostic. We definitely want to be able to include the relapse or even the survivorship.

[B]

That would be terrific. Do you have plans to increase the number of adult patients in particular with the diseases you're already studying? Because as you mentioned, this is particularly enriched for diseases like B cell all in terms of just the numbers of samples that are in the base.

[D]

It is a little bit skewed for the pediatric B cell leukemia. It's just in part because there's a lot of progress has been made based on the disease's higher occurrence. And again, we will absolutely hope to begin the second phase of the ASH hop. A primary objective of that will be to get the feedback from the broad ASH community and we want to collect additional disease types from diverse population backgrounds to get them included in the ASH hub.

[B]

I'd like to thank both of the presenters for really excellent discussions and for contributing such interesting papers. I'm glad that we had the opportunity to cover these in our podcast.

[A]

Thank you for listening to this episode of Conversations with Blood Authors. To read the articles, visit bloodjournal.org this episode is copyrighted by the American Society of Hematology.