Newsletters
Inhibition of Nucleoporin 214 Depletes Leukemia Stem Cells by Promoting Heme Catabolism and Lipid Peroxidation
[Blood] By screening the nucleoporin (NUP) family, scientists identified NUP214 as a frequently overexpressed gene and a critical fitness determinant in leukemia stem cells (LSCs). NUP214 acts as a conserved driver of LSC survival by restricting heme catabolism, limiting Fe²⁺ accumulation, and suppressing lipid peroxidation.
PTBP1 Controls Oncogenic Transcript Processing and Maintenance of Acute Myeloid Leukemia
[Leukemia] Researchers identified the RNA splicing factor PTBP1 as a key dependency in acute myeloid leukemia, sustaining leukemia by controlling the processing of essential oncogenic transcripts.
Single-Cell Architecture of Purinergic Signaling in Human Cord Blood Hematopoietic Stem and Progenitor Cells
[Leukemia] Investigators mapped purinergic signaling at single-cell resolution in human cord blood stem and progenitor cells, revealing how ATP and adenosine pathways are organized across early blood cell development.
The Role of the Adenosinergic Pathway in Resistance to Hypomethylating Agents in Patients with High-Risk Myelodysplastic Syndromes
[British Journal of Haematology] The authors investigated the expression of CD39, CD73 and related adenosinergic pathways and their clinical associations in T cells of higher-risk myelodysplastic syndromes patients undergoing hypomethylating agent therapy.
Chemotherapy-Related Anaemia Is Regulated through Caspase-1 Mediated ROCK1 Activation
[Blood Advances] Scientists showed that chemotherapy-induced anemia is driven by Caspase-1–mediated ROCK1 activation, which suppresses red blood cell production and reveals a potential therapeutic target for improving erythropoietic recovery.
Epigenetic Markers Expand Genetic Risk Estimation in Acute Myeloid Leukemia
[Blood] Researchers assessed whether DNA methylation patterns in AML patients can augment risk assessments provided by genetic and other markers to better predict outcomes
Histone Deacetylase Inhibitors As Venetoclax-Sensitising Partners in Acute Myeloid Leukaemia: Mechanisms, Pharmacology, and Translational Perspectives
[British Journal of Pharmacology] The authors discuss the rationale and evidence for combining histone deacetylase inhibitors with venetoclax in AML, including mechanisms of action, resistance pathways, and preclinical and clinical data
FDA Approves PharmaEssentia’s BESREMi® (ropeginterferon alfa-2b-njft) for Adults with Essential Thrombocythemia, A Rare Blood Cancer
[PharmaEssentia USA Corporation (Business Wire)] PharmaEssentia USA Corporation announced the US FDA has approved BESREMi® for the treatment of adults with essential thrombocythemia (ET), making it the first new FDA-approved treatment for ET in nearly three decades.
Cancer Center Physician Receives $150,000 New Investigator Research Grant to Study Treatment-Resistant Leukemia
[University of Cincinnati] The University of Cincinnati Cancer Center’s Dr. Sarah Skuli, has received a two-year, $150,000 New Investigator Research Grant from the Leukemia Research Foundation. The funds will go toward a project that focuses on leukemia carrying mutations in the TP53 gene, which leads to very poor outcomes for patients.
Ex Vivo Live Macrophage Engineering Strategies in Immunotherapy
[Biotechnology Advances] Successful macrophage immunotherapy requires solving two central in vivo determinants: preserving a therapeutically favorable functional state despite suppressive cues, and achieving robust, disease-selective localization and engagement.
T Cell Immunosenescence Limits CD19 CAR T-Cell Function in Chronic Lymphocytic Leukemia
[Blood] Investigators identified immunosenescence as a measurable and functionally consequential barrier to CAR T-cell efficacy in chronic lymphocytic leukemia and a candidate for therapeutic modulation.
Tisa-Cel and Axi-Cel CAR Structure Influences the Development of Resistance to CD19-CAR-T Therapy
[Leukemia] Researcher showed that CAR structure is a critical determinant of CD19 loss in tumor B cells. Specifically, repeated exposure to CD19–4-1BB-based CAR-T cells, but not CD19–CD28-based counterparts, drives FMC63-epitope and total CD19 protein loss.

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