Acute Myeloid Leukemia Research

This study identifies ATM-driven DNA repair and ROS addiction as mechanisms of resistance to FLT3 inhibitors in AML and shows ATM inhibition can overcome resistance in vitro and in vivo.

This study shows that NPMc+ and Flt3-ITD cooperate to create a new quiescent HSC state that supports leukemia transformation and stem cell maintenance.

The paper identifies ferritinophagy as a therapeutic target in quiescent leukemic stem cells, showing that inhibiting NCOA4 reduces leukemia.

This study shows that PHF6 loss increases AML aggressiveness by enhancing leukemia stem cell self-renewal through context-specific transcriptional changes.

This study uses serial blood samples to analyze pre-cancerous evolutionary dynamics in acute myeloid leukaemia, showing how driver mutations accumulate and drive clonal expansion over decades.

This study shows that the CXCL12 gradient, regulated by DPP4 and GPC3, determines leukemia stem cell (LSC) localization and behavior, influencing leukemia progression.

This study identifies mitotic vulnerabilities in AML cells induced by therapeutic agents, showing increased cytotoxicity during mitosis compared to S/G2 phase arrest.

This study investigates the combination of artesunate and arsenic trioxide to treat AML with reduced off-target effects on normal hematopoietic stem cells.

This study uses multi-omics analysis to identify genetic and epigenetic changes in AML progression and relapse.

This study uses single-cell RNA-sequencing to analyze the individual and combined effects of Trisomy 21 and GATA1s on hematopoietic progenitor cells, revealing their impact on lineage skew and proliferation.

This study shows IRF2BP2 counteracts the ATF7/JDP2 AP-1 heterodimer to prevent excessive inflammation in AML cells, revealing a potential therapeutic target.

The paper develops machine learning models to identify clonal hematopoiesis driver mutations, outperforming existing methods and applying them to UK Biobank data to confirm known associations.

The paper estimates mCA fitness in the NHLBI TOPMed cohort and identifies genetic variants associated with clonal expansion rates.

The paper characterizes NPM1-mutated AML subtypes using epigenomic and transcriptomic data, revealing distinct clinical and molecular features based on H3K27me3 levels at the HIST1 cluster.

UNISOM improves CHIP detection from low-coverage sequencing data by combining variant calling with machine learning classification, identifying low-VAF mutations with high sensitivity.

This study identifies a synergy between hypomethylating agents and SUMOylation blockade in MDS/AML using CRISPR-Cas9 screening, showing improved therapeutic outcomes in xenograft models.

This study identifies proteomic differences between AML patients at low and intermediate altitudes after chemotherapy, highlighting variations in metabolic and signaling pathways.

The paper introduces a cost-effective CHIP assay, identifies 101 CHIP cases in a cohort, and finds heterogeneity in clonal expansion rates by driver gene and individual.

This study investigates plasticity and dynamics of hematopoietic cells in leukemia using scRNA-seq and identifies cell transitions and correlations between B- and T-cell leukemias.

This study profiles single-cell multiomic data from clonal hematopoiesis patients and controls, revealing pro-inflammatory profiles in monocytes and T cell dysfunction.

The paper uses multiomic analysis of leukemic clones in a mouse model to identify growth regulators and validate their roles in AML.

This study investigates miR-155 expression in leukemic stem cells and finds it regulates self-renewal and quiescence.

This paper uses machine learning to predict drug sensitivity in AML patients using the BeatAML dataset, finding RNA sequencing data provides better predictive power than whole exome sequencing or clinical data.

The paper identifies monocyte-endothelial interaction alterations in TET2 CHIP and shows that targeting CXCR2 and ICAM1 can restore normal interactions.

This study compares clonal haematopoiesis (CH) between admixed Americans and Europeans, finding ancestry-specific genetic factors and lower CH prevalence in admixed populations.

This study identifies four transcriptionally distinct venetoclax-resistant clusters in AML, revealing phenotypic, genetic, and drug response differences and their implications for treatment resistance.

This study shows that high IL-3 concentrations prime murine 32D myeloid progenitor cells for granulocytic differentiation, while intermediate concentrations reduce this potential without affecting proliferation.

This study identifies two sphingolipidomic subtypes in AML, with one subtype associated with poor clinical outcomes and high-risk features.

The paper analyzes age-related changes in clonal haematopoiesis (CH) using whole exome data from 420,000 UK Biobank participants, finding a deceleration of clonal expansion with age.