new research on leukemia

Revumenib Shows Promise in Treating Advanced Acute Myeloid Leukemia

April 18, 2023 , by Sharon Reynolds

Revumenib blocks the interaction between the proteins MLL1 and menin. Disrupting the formation of this protein "complex" means the complex can't activate specific genes that fuel the development of leukemia cells.

A new type of targeted therapy shows promise for acute myeloid leukemia (AML), one of the most difficult leukemias to treat. The drug, revumenib, is part of a group, or class, of drugs known as menin inhibitors.

In an early-phase clinical trial called AUGMENT-101, treatment with revumenib caused about one-third of study participants’ cancers to completely disappear , known as a complete remission. All of the participants had previously received many other treatments, including in some cases a stem cell transplant .

The trial didn’t directly compare revumenib with any other drugs. But historically, “if patients’ cancers have progressed on that many lines of therapy, the chances of responding to anything else we [currently] have is less than 10%,” said Ghayas Issa, M.D., of the University of Texas MD Anderson Cancer Center, who helped lead the trial.

According to the most recent data from the study, published on March 15 in Nature , one participant was still in remission more than 16 months after starting treatment, and 12 more who had gone into remission went on to receive a stem cell transplant. Of this group, 9 continued to be in remission at the time of the last analysis, Dr. Issa and his colleagues reported.

Very few patients with recurrent leukemia can achieve remission—and stay healthy enough to receive a transplant—with current standard therapies, said Dr. Eytan Stein, M.D., of Memorial Sloan Kettering Cancer Center, who also helped lead the trial.

Several other menin inhibitors are also being tested in early-phase trials, said Eunice Wang, M.D., of Roswell Park Comprehensive Cancer Center, who was not involved in the study. “This could be the beginning of a new class of agents [for treating AML], which … is causing a lot of excitement,” she added.

Removing the key that starts the leukemia engine

Many new treatments that have been developed, such as ivosidenib (Tibsovo) and midostaurin (Rydapt) , target genetic changes thought to drive some forms of AML. But resistance to these drugs tends to develop relatively quickly. And each of the gene changes targeted by these drugs are found in only a minority of patients.

“About 50% to 60% of acute myeloid leukemias don’t have any of those mutations. And that leaves us with just toxic chemotherapy [for treatment],” said Dr. Wang.  

However, many AMLs do have one of two other common gene changes, KMT2A rearrangements and NPM1 mutations. These mutations cause blood cells to regress, or dedifferentiate, and behave like the stem cells they arose from. The result is the formation of leukemia cells instead of functional blood cells.

The cellular programs hijacked by both these gene changes require menin, which binds to the protein produced by KMT2A , called MLL1. The complex formed by these proteins in turn binds to chromatin (a tightly packed collection of DNA and proteins within the cell’s nucleus) and turns on the aberrant communication pathways triggered by the altered KMT2A or NPM1 .

Revumenib and other menin inhibitors work differently from other targeted therapies used in AML to date. Instead of blocking the activity of dysfunctional proteins, menin inhibitors stop the genes affected by the altered KMT2A or NPM1 from being expressed in the first place.

Dr. Issa describes the menin - MLL1 complex as the key that starts the engine of leukemia cell production.

“And [revumenib] creates a wedge between the key and the engine,” by binding to menin, which prevents it from binding to MLL1, he explained. When the menin - MLL1 complex can’t bind to chromatin, the cells that had acted like haywire stem cells either turn back into normal cells (a process called differentiation) or die.

What’s exciting about revumenib, Dr. Stein said, is not just the novel mechanism by which menin inhibition works, but that cancer-causing mutations that rely on menin are very common in AML.

“All told, menin inhibition may have a role in potentially 40% to 50% of all acute myeloid leukemias,” he said.

Pushing blood cells to behave

The phase 1 AUGMENT-101 trial—which was funded by Syndax Pharmaceuticals, the maker of revumenib—was the first to test the new drug in people. It was designed to test the drug’s safety and find the best dose for future, larger trials.

In total, 60 adults and 8 children with leukemia—most with AML—joined the trial. Participants had received a median of four prior treatments, and almost half had already undergone a stem cell transplant.

Trial participants took revumenib as a pill or, if unable to take pills, in liquid form twice a day, in escalating doses [see box], until their leukemia started growing again or they experienced unacceptable side effects.

Overall, 18 of the 60 patients who had a KMT2A rearrangement or NPM1 mutation experienced a complete remission with a full or partial recovery of the number of healthy blood cells, which lasted for a median of 9 months.

Twelve of these participants received a stem cell transplant after going into remission.

“Nearly all patients with [recurrent AML] are unable to get into remission with standard chemotherapy, and a successful transplant requires a patient to be in remission,” Dr. Stein said.

The side effect seen in the trial that helped the researchers identify the maximum tolerated dose for future studies was called QT interval prolongation, which is a problem with the heart’s electrical activity. Other serious side effects seen during treatment included a drop in the number of white and red blood cells. No participants had to stop taking revumenib permanently due to side effects, and no deaths were caused by the drug.

A potentially dangerous side effect of some leukemia treatments is called differentiation syndrome . This is caused by an immune-system reaction triggered when leukemia cells start to change back into normal cells. Although 11 patients developed differentiation syndrome, none of the cases were severe, and all disappeared with anti-inflammatory treatments.

During treatment, the trial investigators tracked gene expression changes in bone marrow cells taken from participants. As expected, they saw less activity of genes that drive leukemia and more activity of genes associated with healthy blood cell differentiation.

Tracking treatment resistance in real time

For some participants in AUGMENT-101, their cancers rapidly developed resistance to revumenib. In a companion study published in the same issue of Nature , a team led by Sheng Cai, M.D., Ph.D., and Ross Levine, M.D., of Memorial Sloan Kettering, and Scott Armstrong, M.D., Ph.D., of Dana-Farber Cancer Institute, teased out exactly what changes in leukemia cells were driving this resistance .

The team used multiple methods as part of this work, including x-ray crystallography to view the physical interactions of revumenib with the menin - MLL protein complex as well as whole genome sequencing .

Some patients whose AML initially responded to menin but then started growing again had new changes in the MEN1 gene, which encodes menin. Selection for these rare or new mutations happened as early as 2 months after starting treatment. In follow-up laboratory studies, the researchers saw that, without revumenib, cells with these new MEN1 changes were actually less likely to survive and thrive.

But that changed quickly once revumenib was added. The changes to MEN1 made it so revumenib could no longer disrupt menin from binding to MLL1. “So, the leukemia genes continue to be turned on, and that’s the basis of the resistance,” Dr. Cai said.

Although developing resistance presents a challenge, he added, it also confirmed the importance of menin to these types of AML. “The fact that [leukemia cells] have to mutate in order for them to escape this drug really means that we’re getting at the Achilles' heel of these leukemia subtypes,” he said.

Inhibiting menin with combination therapy, and earlier

The first generation of menin inhibitors shows promise in early trials. But Dr. Cai hopes that the structural information his team gathered may inform future drug development. “Seeing the way that the drug interacts with the protein gives us a lens to see where, strategically, we might be able to design newer menin inhibitors that work in other ways,” he said.

Revumenib is now being tested in a phase 2 study , with the goal of obtaining FDA approval for treating people with advanced AML with these specific gene alterations, Dr. Stein said. “And we have ongoing studies looking at combination therapies,” he added. For example, his team is now testing revumenib with venetoclax (Venclexta), another targeted therapy that has shown promise against AML .

Other potential strategies include combining menin inhibitors with standard chemotherapy, said Dr. Wang. “That way, maybe we could kill some of these [cells] that are becoming resistant by some other mechanism,” she said. The ongoing phase 1 AUGMENT-102 trial is looking at this type of combination in people whose leukemia has relapsed or not responded to at least two prior treatments.

Combinations of treatments that include a menin inhibitor may work best immediately after a diagnosis of leukemia, Dr. Wang added.

“To harvest the true benefit of [menin inhibitors], we may really need to move them up earlier in treatment, when we have the best chance at a cure,” she said.

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Researchers develop new method to remove blood cells in leukemia patients while building new blood system

by University of Basel

Researchers have developed an approach to "deleting" a blood system affected by leukemia while simultaneously building up a new, healthy system with donor blood stem cells. Writing in the journal Nature , the team reports on the promising results obtained in animal experiments and with human cells in the laboratory.

In aggressive cases of leukemia, the only chance for a cure is to replace the diseased blood system with a healthy one. Although the transplantation of donor blood stem cells is a well-established form of treatment, it is an onerous process for patients.

First, chemotherapy is used to remove the body's own blood stem cells as well as most of the blood cells. Only then do the attending physicians intravenously administer the stem cells from a suitable donor to the patient. This procedure is associated with side effects and potential complications.

The team led by Professor Lukas Jeker from the Department of Biomedicine at the University of Basel has taken a different approach. In their article, the team describes how all blood cells can be removed from a leukemia sufferer in a targeted manner while a new blood system is built up at the same time.

Mixing console for blood systems

The system established by the researchers in Jeker's team can be imagined as a mixing console, where a DJ gradually fades down the level of the first song while raising the volume of the second until the first track dies away completely and only the second is audible.

The fading-down process works as follows: Specific antibodies coupled to a cytotoxic drug recognize all blood cells in the patient's body based on a surface structure . This marker is common to all the different types of blood cell (both healthy and diseased) but does not appear on other cells of the body. Bit by bit, the antibody-drug conjugate therefore recognizes and destroys all cells of the diseased blood system.

While this is taking place, the second song also starts—that is, the patient receives a transplant of new, healthy blood cells from a suitable donor.

To prevent the antibody-drug conjugates from also attacking the new blood stem cells, or the blood cells they produce, the researchers use genetic engineering techniques to modify the donor stem cells in a targeted manner. Specifically, they introduce a small change in the surface molecule so that the antibodies don't recognize the new blood cells.

The researchers refer to this targeted modification of the donor stem cells as "shielding," because it acts like a protective shield against the cancer treatment.

Elaborate search for suitable regulators

The two first authors of the study, Simon Garaudé and Dr. Romina Matter-Marone, worked with an interdisciplinary team of bioinformaticians, biochemists, genetic engineering specialists, and clinicians from academia and industry to select the best-suited target structure—and the best protective modification for the fading-down process—from the multitude of surface molecules on blood cells. The chosen molecule, known as CD45, proved extremely promising in trials on mice and human cells in the laboratory.

"We needed a surface molecule that appeared with approximately the same frequency on all blood cells if possible, including the leukemia cells, but that wasn't present on other cells in the body," explains Jeker.

CD45 met this requirement and, at the same time, was also suitable for "shielding"—in other words, it could be modified on the donor blood stem cells in such a way that these cells were protected from the cancer treatment but the function of CD45 remained completely normal.

Applications beyond cancer

"The new approach could pave the way for new treatment options for patients whose state of health is incompatible with the chemotherapy needed for stem cell transplantation," says joint first author Romina Matter-Marone. Although further tests and optimization are needed, the aim is for initial clinical trials to begin in just a few years' time.

The "mixing console for blood systems" also opens up further possibilities, as joint first author Simon Garaudé explains. "We show how cells that are 'invisible' to a blood cell remover can be used to swap out the entire blood system."

This, he says, is an important step toward a programmable blood system that could also assume functions on demand—for example, to correct a serious genetic defect or to impart resistance to specific viruses such as HIV.

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The Leukemia & Lymphoma Society is Accepting Applications for up to $2.5 Million in Funding Through its Equity in Access Research Program 

Rye Brook, NY, May 22, 2024 – Today, The Leukemia & Lymphoma Society’s (LLS) Equity in Access Research Program announced the opening of its application process for the 2025 funding cycle. Now through September 12, 2024, researchers are invited to submit Letters of Intent for studies that align with the topic of “Building Evidence for Effective Interventions to Increase Therapeutic Cancer Clinical Trial Accrual: Promoting Access for Patients from Underrepresented Groups.”  LLS’s Equity in Access Research Program will review submissions to allocate up to $2.5 million per funded study, with awards to begin next summer.  

“For LLS, a key part of advancing health equity is a commitment to reducing and ultimately eliminating health disparities that impact patients with and survivors of a blood cancer,” said Eric Cooks, Ph.D., Senior Program Director of LLS’s Equity in Access Research Program.  “This program is designed to generate evidence that will guide changes in healthcare policy and practice to ensure that all individuals affected by blood cancer can access and utilize the treatment, care, and resources necessary to optimize their quality of life and outcomes, throughout their journey from diagnosis to survivorship.” 

LLS’s Equity in Access Research Program Key Dates & Deadlines: 

• May 22, 2024: Application period begins 
• June 18, 2024 (12:00 p.m. ET): Webinar for prospective applicants (register here)  
• September 12, 2024 (3:00 p.m. ET): Deadline to submit Letters of Intent 
• November 1, 2024: LLS notifies applicants whether they are invited to submit a full proposal  
• January 30, 2025 (3:00 p.m. ET): Deadline for invited applicants to submit full proposals and associated documents  
• April/May 2025 : Notification of awards 
• July 1, 2025: Grant start date 

To learn more about LLS’s Equity in Access Research Program, including how to apply, study criteria, key dates and deadlines, award amounts, and more, visit https://www.lls.org/research/equity-access-research-grants .   

Since its launch in 2022, LLS’s Equity in Access Research Program has awarded more than $5 million in funding to health services researchers across the US. The work funded through the program is making an impact and gaining recognition – earlier this year, an article co-authored by Dr. Stacie Dusetzina, a health policy researcher at Vanderbilt University, and Dr. Lauren Nicholas, a health economist at the University of Colorado Anschutz, titled “Comparing Medicare plan selection among beneficiaries with and without a history of cancer,” was selected as an “Editor’s Choice” article by Health Affairs Scholar .  

LLS proudly and gratefully acknowledges the leadership support of Royalty Pharma and AstraZeneca for their support of the Equity in Access Research Program and other initiatives focused on reducing healthcare disparities in blood cancer care and treatment. 

This year, LLS’s Equity in Access Research Program team will be onsite in Chicago at the 2024 ASCO Annual Meeting from June 1 – 3. To learn more about the program and the current Request for Proposals, please stop by booth #10005 to speak with an LLS representative. 

#     #     #

For questions about this RFP and the application process, please contact  [email protected] .

For media inquiries, please contact [email protected].

About The Leukemia & Lymphoma Society  The Leukemia & Lymphoma Society® (LLS) is the global leader in the fight against blood cancer. The LLS mission: Cure leukemia, lymphoma, Hodgkin's disease, and myeloma, and improve the quality of life of patients and their families. LLS funds lifesaving blood cancer research around the world, provides free information and support services, and is the voice for all blood cancer patients seeking access to quality, affordable, coordinated care.    Founded in 1949 and headquartered in Rye Brook, NY, LLS has regions throughout the United States and Canada. To learn more, visit www.LLS.org . Patients should contact the Information Resource Center at (800) 955-4572, Monday through Friday, 9 a.m. to 9 p.m. ET.    For additional information, visit lls.org/lls-newsnetwork . Follow us on Facebook , Twitter , and Instagram . 

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Research articles

Inhibition of NOTCH4 sensitizes FLT3/ITD acute myeloid leukemia cells to FLT3 tyrosine kinase inhibition

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Increased coexpression of PD-L1 and IDO1 is associated with poor overall survival in patients with NK/T-cell lymphoma

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Niclosamide combined to Azacitidine to target TP53 -mutated MDS/AML cells

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The gray area of RQ-PCR-based measurable residual disease: subdividing the “positive, below quantitative range” category

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Asciminib monotherapy in patients with chronic-phase chronic myeloid leukemia with the T315I mutation after ≥1 prior tyrosine kinase inhibitor: 2-year follow-up results

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Repurposing pexmetinib as an inhibitor of TKI-resistant BCR::ABL1

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Chimeric antigen receptor T-cell infusion for large B-cell lymphoma in complete remission: a center for international blood and marrow transplant research analysis

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Clinical implications of CSF-ctDNA positivity in newly diagnosed diffuse large B cell lymphoma

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Molecular subgroups of T-cell acute lymphoblastic leukemia in adults treated according to pediatric-based GMALL protocols

• Martin Neumann
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Analysis of measurable residual disease by IG/TR gene rearrangements: quality assurance and updated EuroMRD guidelines

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Integrated proteogenomic analysis for inherited bone marrow failure syndrome

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DNA damage response genes as biomarkers of therapeutic outcomes in acute myeloid leukemia patients

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Context-dependent role of trisomy 6 in myelodysplastic neoplasms and acute myeloid leukemia: a multi-omics analysis

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TIF1β activates leukemic transcriptional program in HSCs and promotes BCR::ABL1-induced myeloid leukemia

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Kinomica to present research abstract on a multi-drug biomarker signature to predict best first-line treatments for acute myeloid leukemia (aml) at the 2024 asco annual meeting.

Predicting patient response to first-line AML treatment using phosphoproteomic data from routine diagnosis samples

LONDON , May 29, 2024 /PRNewswire/ -- Kinomica Ltd., a developer of KScan® precision oncology diagnostics, today announces that it will be presenting data on a multi-drug biomarker signature for accurately predicting best first-line treatments in newly-diagnosed acute myeloid leukemia patients at the American Society of Clinical Oncology (ASCO) annual meeting, which will be held May 31 – June 4 , in Chicago, IL.

"AML is a heterogeneous malignancy with poor prognosis. Several treatments are approved for AML, but clinical trials have shown that current stratification approaches to determine patients' eligibility produce false positives and negatives," said Arran Dokal PhD, CTO of Kinomica. "Here, we used phosphoproteomics to build signatures that accurately predict which of the approved therapies venetoclax plus azacitidine, intensive chemotherapy (IC), or IC plus midostaurin may be more efficacious for a given patient."

Details of the poster presentation are as follow:

Poster Title : Multi-drug algorithm to accurately predict best first-line treatments in newly-diagnosed acute myeloid leukemia (AML)

Presenter : Pedro Rodriguez Cutillas at Barts Cancer Institute

Authors : Pedro Rodriguez Cutillas [1] , Weronika E. Borek [5] , Josie A. Christopher [5] , Luis Veiga Nobre [5] , Amy Campbell [5] , Janet Kelsall [5] , Federico Pedicona [5] , Nazrath Nawaz [5] , David N. Perkins [5] , Pedro Moreno Cardoso [5] , Andrea Arruda [2] , Alexander Joseph Ambinder [3] , Sayantanee Dutta [4] , Paolo Gallipoli [1] , Heinz Sill [4] , Gabriel Ghiaur [3] , Mark D. Minden [2] , Andrew Williamson [5] , John G. Gribben [1] , Arran David Dokal [5]

Organizations :  [1] Barts Cancer Institute,  [2] Princess Margaret Cancer Centre,  [3] Johns Hopkins University,  [4] Medical University of Graz,  [5] Kinomica Ltd

Poster Session : Hematologic Malignancies—Leukemia, Myelodysplastic Syndromes, and Allotransplant

Session Date and Time : Monday June 3, 2024 , 9:00 AM - 12:00 PM CDT

Poster Board Number : 84

Abstract Presentation Number : 6525

The Abstract is available on the ASCO online itinerary planner here .

About Kinomica

Kinomica is a developer of precision oncology diagnostics. The company has developed KScan®, a phosphoproteomic diagnostic platform to help clinicians better realize the full potential of precision medicine by predicting which of the drugs currently approved to treat a disease a particular patient will respond best to, thereby aiding clinical decision making. Learn more at www.kinomica.com and follow us on LinkedIn .

Logo - https://mma.prnewswire.com/media/2422786/4729421/Kinomica_Logo.jpg

View original content to download multimedia: https://www.prnewswire.com/news-releases/kinomica-to-present-research-abstract-on-a-multi-drug-biomarker-signature-to-predict-best-first-line-treatments-for-acute-myeloid-leukemia-aml-at-the-2024-asco-annual-meeting-302157990.html

SOURCE Kinomica Ltd.

Gentler cell therapies for blood cancer

Researchers have developed an approach to "deleting" a blood system affected by leukemia while simultaneously building up a new, healthy system with donor blood stem cells. Writing in the journal Nature , the team reports on the promising results obtained in animal experiments and with human cells in the laboratory.

In aggressive cases of leukemia, the only chance for a cure is to replace the diseased blood system with a healthy one. Although the transplantation of donor blood stem cells is a well-established form of treatment, it is an onerous process for patients. First, chemotherapy is used to remove the body's own blood stem cells as well as most of the blood cells. Only then do the attending physicians intravenously administer the stem cells from a suitable donor to the patient. This procedure is associated with side effects and potential complications.

The team led by Professor Lukas Jeker from the Department of Biomedicine at the University of Basel has taken a different approach. Writing in the journal Nature , the team describes how all blood cells can be removed from a leukemia sufferer in a targeted manner while a new blood system is built up at the same time. The results represent the successful completion of a project funded by the European Research Council with a Consolidator Grant of EUR 2.4 million.

Mixing console for blood systems

The system established by the researchers in Jeker's team can be imagined as a mixing console, where a DJ gradually fades down the level of the first song while raising the volume of the second until the first track dies away completely and only the second is audible.

The fading-down process works as follows: Specific antibodies coupled to a cytotoxic drug recognize all blood cells in the patient's body based on a surface structure. This marker is common to all the different types of blood cell (both healthy and diseased) but does not appear on other cells of the body. Bit by bit, the antibody-drug conjugate therefore recognizes and destroys all cells of the diseased blood system.

While this is taking place, the second song also starts -- that is, the patient receives a transplant of new, healthy blood cells from a suitable donor. To prevent the antibody-drug conjugates from also attacking the new blood stem cells, or the blood cells they produce, the researchers use genetic engineering techniques to modify the donor stem cells in a targeted manner. Specifically, they introduce a small change in the surface molecule so that the antibodies don't recognize the new blood cells. The researchers refer to this targeted modification of the donor stem cells as "shielding," because it acts like a protective shield against the cancer treatment.

Elaborate search for suitable regulators

The two first authors of the study, Simon Garaudé and Dr. Romina Matter-Marone, worked with an interdisciplinary team of bioinformaticians, biochemists, genetic engineering specialists, and clinicians from academia and industry to select the best-suited target structure -- and the best protective modification for the fading-down process -- from the multitude of surface molecules on blood cells. The chosen molecule, known as CD45, proved extremely promising in trials on mice and human cells in the laboratory.

"We needed a surface molecule that appeared with approximately the same frequency on all blood cells if possible, including the leukemia cells, but that wasn't present on other cells in the body," explains Jeker. CD45 met this requirement and, at the same time, was also suitable for "shielding" -- in other words, it could be modified on the donor blood stem cells in such a way that these cells were protected from the cancer treatment but the function of CD45 remained completely normal.

Applications beyond cancer

"The new approach could pave the way for new treatment options for patients whose state of health is incompatible with the chemotherapy needed for stem cell transplantation," says joint first author Romina Matter-Marone. Although further tests and optimization are needed, the aim is for initial clinical trials to begin in just a few years' time.

The "mixing console for blood systems" also opens up further possibilities, as joint first author Simon Garaudé explains: "We show how cells that are 'invisible' to a blood cell remover can be used to swap out the entire blood system." This, he says, is an important step toward a programmable blood system that could also assume functions on demand -- for example, to correct a serious genetic defect or to impart resistance to specific viruses such as HIV.

• Hypertension
• Immune System
• Brain Tumor
• Blood Clots
• White blood cell
• Adult stem cell
• Embryonic stem cell
• Bone marrow

Story Source:

Materials provided by University of Basel . Original written by Angelika Jacobs. Note: Content may be edited for style and length.

Journal Reference :

• Simon Garaudé, Romina Marone, Rosalba Lepore, Anna Devaux, Astrid Beerlage, Denis Seyres, Alessandro Dell’ Aglio, Darius Juskevicius, Jessica Zuin, Thomas Burgold, Sisi Wang, Varun Katta, Garret Manquen, Yichao Li, Clément Larrue, Anna Camus, Izabela Durzynska, Lisa C. Wellinger, Ian Kirby, Patrick H. Van Berkel, Christian Kunz, Jérôme Tamburini, Francesco Bertoni, Corinne C. Widmer, Shengdar Q. Tsai, Federico Simonetta, Stefanie Urlinger, Lukas T. Jeker. Selective haematological cancer eradication with preserved haematopoiesis . Nature , 2024; DOI: 10.1038/s41586-024-07456-3

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Join 7News' Eileen Whelan in fundraising for Leukemia and Lymphoma Society

by Joy Wang

ARLINGTON, Va. (7News) — Five days a week, you’ll find First Alert Meteorologist Eileen Whelan forecasting the weather and preparing you for your day. A couple of hours later, there she is again, this time hosting Good Morning Washington.

It’s fair to say that informing, participating, and trying to improve this community is what she’s all about.

But this story isn’t about all the work on camera. In fact, Eileen is the same person behind the scenes. This year, she’s campaigning in the Visionaries of the Year Fundraiser for the Leukemia and Lymphoma Society.

“We’re hoping to make a massive difference,” she said.

It was 2014 when Eileen lost her mother-in-law, Terri Biss, to leukemia.

“I was fortunate to know her for about six months, but I know she underwent chemotherapy, a bone marrow transplant,” described Eileen. “I just saw how it affected my husband and his family.”

Terri never got to meet her grandson Charlie.

“He doesn’t get to grow up with his other grandmother. So it’s really important for us to raise this money so that more families don’t have to go through this,” she said.

Funding for blood cancer treatment has led to game-changing insights for patients with other cancers and diseases. Money raised from this campaign stays right here in the DMV.

SEE ALSO: More young adults need to be tested for cancer

Mike Litterst, who you often see on 7News, especially during cherry blossom season, is also helping to raise money for this campaign.

He brought his son Jeffrey to our 7News studios to share their story.

“The summer before my senior year (I) had a growth on my leg and, you know, it didn’t really go away,” said Jeff.

The summer before his senior year, he learned that this baseball-sized growth was lymphoma.

“The doctor came out after you know an hour or so and took us aside and you know said to us it's cancer,” said Mike. “I distinctly remember the words alone, literally, knocked my wife back a couple of steps. You know, it’s that sort of blow.”

“It was shocking. It was panic-inducing,” remembered Jeff. “You know, this moment of like, oh my god, this isn’t supposed to happen to me. I’m only 16 years old.”

Jeff spent the rest of high school going through chemotherapy.

“I did a lot of school theater, and just kind of like you know, cancer and chemotherapy and everything else, it just makes you lethargic, so tired,” described Jeff. “You can’t stay up.”

But thanks to new treatment protocols, Jeff not only finished high school, but he also graduated on time, went to college, and has been in remission ever since.

SEE ALSO: D.C. team named 2024 Student Visionaries of the Year by Leukemia and Lymphoma Society

“The research is working. The researchers are winning the type of lymphoma Jeff had. If he had it when I was his age, the five-year survival rate was only 46%. It’s up to almost 80% now, and that is directly because of ongoing research,” said Mike.

With your help, more money can go towards that research.

“All of the money that we're raising is going to research for new treatments,” said Eileen. “What's really encouraging is a lot of the research that is being done for blood cancer is then paving the way for other treatments for other cancers.”

From educational supplies to volunteer training, lab materials, and clinical trial research — every dollar counts.

“Not a day goes by that we don't think about his care team of doctors and nurses,” said Mike. “But I would like nothing better when this is all over than to put all the amount of work that they don't have anything to do.”

“Don't give up,” said Jeff. “There’s definitely hope.”

You can read more about Jeff's journey here and Eileen's story here .

If you’d like to help Team Dunkin’ Cancer, named after Eileen’s mother-in-law’s love for Dunkin’ Donuts, you can do that and learn more about her story here . The last day to donate is June 8.

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Dr. Paul Parkman, Who Helped to Eliminate Rubella, Dies at 91

He also identified the virus, which can cause infants to be born with severe physical and mental impairments as well as causing miscarriages and stillbirths.

By Sam Roberts

Dr. Paul D. Parkman, whose research was instrumental in identifying the virus that causes rubella and developing a vaccine that has prevented an epidemic of the disease in the United States for more than 50 years, died on May 7 at his home in Auburn, N.Y., in the Finger Lakes region. He was 91.

The cause was lymphoblastic leukemia, his niece Theresa M. Leonardi said.

Rubella, also known as German measles because German scientists classified it in the 19th century, is a moderate illness for most patients, identified by a spotty and often itchy red rash. But in pregnancies, it can cause infants to be born with severe physical and mental impairments and can also cause miscarriages and stillbirths.

When Dr. Parkman was a pediatric medical resident in the 1950s at the State University Health Science Center (now the SUNY Upstate Medical University) in Syracuse, he once recalled, he anguished over showing a new mother her stillborn baby whose rash, he would learn later, probably resulted from the mother’s infection with rubella during pregnancy.

In 1964 and 1965, rubella — an epidemic that struck every six to nine years — caused about 11,000 pregnancies to be miscarried, 2,100 newborns to die and 20,000 infants to be born with birth defects.

That was the worst outbreak in three decades — and the last rubella epidemic in the United States. The disease was declared eliminated in the Americas in 2015, although the virus has not yet been eradicated in Africa or Southeast Asia.

The rubella virus was identified and isolated in the early 1960s by Dr. Parkman and his colleagues at the Walter Reed Army Institute of Research in Silver Spring, Md., and a team of researchers at Harvard University led by Thomas H. Weller.

In 1966, Dr. Parkman, Dr. Harry M. Meyer Jr. and their collaborators at the National Institutes of Health, including Maurice R. Hilleman , disclosed that they had perfected a vaccine to prevent rubella. Dr. Parkman and Dr. Meyer assigned their patents to the N.I.H. so that the vaccines could be manufactured, distributed and administered promptly.

“I never made a nickel from those patents because we wanted them to be freely available to everybody,” he said in an oral history interview for the N.I.H. in 2005.

President Lyndon B. Johnson thanked the researchers, noting that they were among the few who could “number themselves among those who directly and measurably advance human welfare, save precious lives, and bring new hope to the world.”

Still, after Dr. Parkman retired from the government in 1990, as director of the Food and Drug Administration’s Center for Biologics Evaluation and Research, he expressed concern about what he called the unfounded skepticism that persisted about the value of vaccines.

“With the exception of safe drinking water, vaccines have been the most successful medical interventions of the 20th century,” he wrote in 2002 in Food and Drug Administration Consumer, an agency journal .

“As I look back on my career, I have come to think that perhaps I was involved in the easy part,” he added. “It will be for others to take on the difficult task of maintaining the protections that we struggled to achieve. We must prevent the spread of this vaccine nihilism, for if it were to prevail, our successes could be lost.”

Paul Douglas Parkman was born on May 29, 1932, in Auburn and raised in Weedsport, a nearby village of about 1,200. His father, Stuart, was a postal clerk who served on the village Board of Education and raised poultry to support his son’s education. His mother, Mary (Klumpp) Parkman, managed the household.

In 1955, Paul married a former kindergarten classmate, Elmerina Leonardi. She is his only immediate survivor. His brother, Stuart, and his sister, Phyllis Parkman Thompson, died earlier.

Enrolled in an accelerated degree program, he received his bachelor’s degree in pre-medicine from St. Lawrence University in Canton. N.Y., and his medical degree from the State University Health Science Center, both in 1957.

In 1960, he enrolled in the Army Medical Corps as a captain. After serving at Walter Reed as a researcher, he was chief of general virology for the N.I.H. from 1963 until the department was absorbed by the Food and Drug Administration in 1972. There, as director of the biologics center, he oversaw policies on H.I.V./AIDS testing and the approval of a vaccine for the most common cause of bacterial meningitis and imposed greater scrutiny of blood banks. He retired in 1990 as director of the Center for Biologics Evaluation and Research.

Dr. Parkman was trained as a pediatrician. That he came to specialize in viruses was both serendipitous and inauspicious.

While stationed at Fort Dix in New Jersey, he was assigned to study the seasonal flood of head cold and flu cases among new recruits.

“A runny nose isn’t too much to look at,” Dr. Parkman said in the oral history interview. He became hooked on virology, but he returned to Washington hoping for a subject more challenging than the common cold. He found it.

Sam Roberts is an obituaries reporter for The Times, writing mini-biographies about the lives of remarkable people. More about Sam Roberts