Acute Myeloid Leukemia Research

The paper identifies mutation patterns linked to drug sensitivity in AML using integrated computational and experimental analysis.

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 identifies convergent epigenetic evolution in AML relapse using ATAC-seq and mtscATAC, showing that epigenetic changes drive relapse independent of genetic mutations.

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

This study shows MDS hematopoietic stem cells reprogram their differentiation state to bypass venetoclax sensitivity through genetic mutations and transcriptional changes.

This study identifies NFATC2 as a novel target of KDM4A in AML cells, showing its role in cell cycle progression and mitochondrial function through interactions with MYC and CCND1.

This study identifies TIM-4-L as a novel target for T cell therapy in AML, showing engineered T cells effectively eliminate AML cells in vitro and in vivo.

This paper identifies effective and low-toxicity drug combinations for AML using a bipartite network model and patient-derived data, finding ruxolitinib-ulixertinib and sapanisertib-LY3009120 as the most synergistic.

This study shows FLT3-ITD mutations in AML retain in dendritic cells, altering their phenotype and increasing Th17 T cell frequency.

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

This study shows ZEB1 in AML suppresses CD8 T-cells and promotes Th17 cells, contributing to immune suppression and tumor progression.

This study shows that healthy hematopoietic stem and progenitor cells (HSPCs) adopt inflammatory gene expression programs in the AML niche, driven by AML-derived extracellular vesicles.

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

This study identifies epigenetic vulnerabilities in AML and MDS/MPN with EZH2 mutations, showing increased sensitivity to EZH2 and EED inhibitors and upregulation of cell death pathways.

The paper identifies critical transcription factor regulons in FLT3-ITD+ AML by analyzing gene regulatory networks and shows their necessity for AML growth.

The paper analyzes genomic data from patients with FPDMM to identify germline RUNX1 variants and somatic mutations linked to clonal hematopoiesis and myeloid malignancies.

This study identifies Oncostatin M (OSM) as a master regulator of an inflammatory network in Dnmt3a-mutant hematopoietic stem cells, showing its role in age-associated clonal hematopoiesis.

This paper develops a deep learning pipeline for automated AML diagnosis and molecular characterization using flow cytometry data, achieving high accuracy in classification and variant prediction.

This study develops a systems-based strategy to predict drug sensitivity in FLT3-ITD AML by integrating genomic, transcriptomic data with a prior-knowledge signaling network.

The paper identifies shared genetic architecture across different types of clonal hematopoiesis and finds that overlapping mutations increase hematological malignancy risk.

The paper identifies IL1RAP and AIM2 as key modifiers of CHIP-associated cardiovascular risk using UK Biobank data and CRISPR experiments in mice.

The paper identifies a high-risk subgroup in myelodysplastic syndromes with isolated trisomy 8 using mutational profiles.

The paper develops PACER to infer clonal expansion rates from single timepoint data and identifies TCL1A activation as a mediator of clonal hematopoiesis fitness.

The paper identifies two distinct subgroups of KMT2A-rearranged AML using phosphoproteomics and shows different drug response profiles.

FiLT3r is an alignment-free algorithm that accurately detects FLT3-ITDs in HTS data with high precision and low resource usage.

The paper identifies genes driving clonal hematopoiesis by analyzing somatic mutations in blood samples from cancer cohorts, discovering novel candidates and recovering known drivers.

The paper identifies transcription factors regulating MHC-II expression in AML and shows their role in immune evasion and relapse.

This study tracks clonal dynamics in human haematopoiesis across age, finding that clonal diversity sharply declines after 70, driven by positive selection on many genes and loss of Y chromosome in males.

The paper develops a cost-effective sequencing assay to detect clonal hematopoiesis and shows that most clonal mutations expand over time in longitudinal samples.

This study identifies secondary genetic events in KMT2A-PTD patients, showing their association with disease progression and higher RNA expression.