Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/s41409-025-02518-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The bispecific innate cell engager AFM28 eliminates CD123 leukemic stem and progenitor cells in AML and MDS.
Nat Commun
August 2025
Department of Hematology and Oncology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Strategies targeting leukemic stem and progenitor cells (LSPCs) are needed for durable remissions in acute myeloid leukemia (AML) and high-risk myelodysplastic neoplasms (MDS). While CD123 constitutes a promising target on LSPCs and leukemic blasts, previous CD123-targeting approaches showed limited efficacy and challenging safety profiles. Here, we describe the preclinical efficacy and safety of the bispecific CD123/CD16A innate cell engager "AFM28", demonstrating superior activity against AML and MDS patient-derived LSPCs and blasts in vitro compared to an Fc-enhanced CD123-targeting antibody, especially towards CD123 and/or CD64 leukemic cells.
View Article and Find Full Text PDFVenetoclax combined with azacitidine in elderly acute myeloid leukemia: A retrospective comparison of 14-day vs 28-day dosing regimens.
Medicine (Baltimore)
August 2025
Department of Hematology, The Affiliated People's Hospital of Ningbo University, Ningbo, China.
However, this study has several limitations that must be acknowledged. First, the non-randomized allocation of treatment duration introduces potential selection bias, particularly as frailer patients were more likely to receive shorter therapeutic cycles, which may have confounded outcome assessments. Background: Although the standard 28-day venetoclax (VEN) regimen combined with azacitidine (AZA) improves outcomes in elderly patients with acute myeloid leukemia, emerging evidence suggests that shorter VEN cycles may maintain efficacy with enhanced safety.
View Article and Find Full Text PDFScreening for Antileukemia Agents in FMS-like Tyrosine Kinase 3 (FLT3)-Mutated Acute Myeloid Leukemia Cells.
ACS Pharmacol Transl Sci
August 2025
Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, São Paulo, CEP 05508-900, Brazil.
Acute myeloid leukemia (AML) remains a challenging hematological malignancy due to its genetic heterogeneity, high relapse rates, and limited therapeutic options for refractory cases. FMS-like tyrosine kinase 3 (FLT3)-internal tandem duplication (FLT3-ITD) mutations are among the most frequent genetic alterations in AML, associated with poor prognosis and treatment resistance. In this study, we investigated the antileukemic potential of compound HI042, identified from a library of 78 molecules, focusing on its effects on FLT3-ITD-mutated AML models.
View Article and Find Full Text PDFMechanism of action of decitabine in treating acute lymphoblastic leukemia.
Front Med (Lausanne)
July 2025
Department of Hematology, The Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Purpose: This study aimed to evaluate the underlying mechanisms of decitabine (DAC) in inhibiting acute T-acute lymphoblastic leukemia (T-ALL) cell proliferation and promoting apoptosis.
Methods: Human T-ALL cells (CCRF-CEM) were treated with varying concentrations of DAC, and cell proliferation was assessed using a CCK-8 assay. Flow cytometry was used to detect apoptosis and cell cycle alterations.
Sodium Caseinate Induces Apoptosis in Cytarabine-Resistant AML by Modulating SIRT1 and Chemoresistance Genes, Alone or in Combination with Cytarabine or Daunorubicin.
Int J Mol Sci
August 2025
Hematopoiesis and Leukemia Laboratory, Research Unit on Cell Differentiation and Cancer, Faculty of High Studies Zaragoza, National Autonomous University of Mexico, Mexico City 09230, Mexico.
Resistance to cytarabine (Ara-C) remains a major obstacle to the successful treatment of acute myeloid leukemia (AML). Therefore, modulating Ara-C resistance is indispensable for improving clinical outcomes. We previously demonstrated that sodium caseinate (SC), a salt derived from casein, the principal milk protein, inhibits proliferation and modulates the expression of Ara-C resistance-related genes in chemoresistant cells.
View Article and Find Full Text PDF