Acute Myeloid Leukemia Research

Exome-wide association study reveals 7 functional variants associated with ex-vivo drug response in acute myeloid leukaemia patients

Single cell transcriptional evolution of myeloid leukaemia of Down syndrome

The paper examines the transcriptional evolution of myeloid leukaemia in Down syndrome by analyzing single-cell RNA sequencing data from patient samples and fetal tissues.

Altered chromatin accessibility mediated by somatic cohesin mutations amplifies FLI1-Menin output to promote leukemogenesis

This study shows that cohesin mutations alter chromatin accessibility, enhancing FLI1-Menin interaction and promoting leukemogenesis through therapeutic vulnerabilities.

Pyjacker identifies enhancer hijacking events in acute myeloid leukemia including MNX1 activation via deletion 7q

Pyjacker detects enhancer hijacking in AML, identifying MNX1 activation via 7q deletion as a novel oncogenic mechanism.

TP53 Inactivation Confers Resistance to the Menin Inhibitor Revumenib in Acute Myeloid Leukemia

This study shows TP53 mutations cause resistance to revumenib in AML and suggests combining MCL-1 inhibitors with menin inhibitors could be effective.

Peripheral blood somatic mosaicism and clonal hematopoiesis across ancestry backgrounds

The paper catalogs somatic mosaicism and clonal hematopoiesis mutations across diverse ancestry groups, finding ancestry-specific mutation patterns and associations with tumor types and age.

Fetal context conveys heritable protection against MLL-rearranged leukemia that depends on MLL3

The paper shows fetal exposure to MLL::ENL creates a heritable leukemia-resistant state by altering hematopoietic progenitor behavior, which can be overcome by MLL3 inactivation or cooperating mutations.

Granulocyte Derived Resistin Inhibits Monocyte Maturation and Induces Immune Suppression in CMML

This study identifies granulocyte-derived resistin as a key factor in CMML that inhibits monocyte maturation and promotes immune suppression.

Clinical progression of clonal hematopoiesis is determined by a combination of mutation timing, fitness, and clonal structure

The paper investigates how mutation timing, fitness, and clonal structure influence the clinical progression of clonal hematopoiesis using longitudinal cohort data.

Hierarchical Lineage Tracing Reveals Diverse Pathways of AML Treatment Resistance

This study uses FLARE to track AML cell lineage evolution under AraC treatment, revealing resistance mechanisms and validating them in a clinical cohort.

Pre-existing stem cell heterogeneity dictates clonal responses to acquisition of cancer driver mutations

The paper develops STRACK to trace clonal gene expression and expansion dynamics in leukemia, showing pre-existing stem cell heterogeneity dictates clonal responses to cancer mutations.

CCRL2 promotes the interferon-γ signaling response in myeloid neoplasms with erythroid differentiation and mutated TP53

This study identifies CCRL2 as a driver of IFN-γ signaling in TP53-mutated AML with erythroid differentiation, linking it to disease progression and poor outcomes.

RUNX1::RUNX1T1 Depletion Eliminates Stemness and Induces Bidirectional Differentiation of Acute Myeloid Leukemia

This study shows that depletion of RUNX1::RUNX1T1 in AML cells reduces stemness and promotes differentiation into granulocytic and eosinophilic/mast cell-like populations.

The cellular state space of AML unveils novel NPM1 subtypes with distinct clinical outcomes and immune evasion properties

This study uses single-cell RNA sequencing to identify novel NPM1 subtypes in AML with distinct clinical outcomes and immune evasion properties.

Posttranscriptional activity of the eukaryotic translation initiation factoreIF4E contributes to HoxA9-driven leukemogenesis

This study shows that disrupting the interaction between HoxA9 and eIF4E delays AML onset and reduces disease penetrance, suggesting eIF4E as a therapeutic target in HoxA9-driven leukemia.

RAS pathway activation drives clonal selection and monocytic differentiation in FLT3 and BCL2 inhibitor resistance

Delayed Trp53 activation protects Dnmt3a-mutant hematopoietic stem cells from inflammatory attrition.

This study shows that DNMT3A R882H mutant HSCs resist inflammatory stress through delayed p53 activation, leading to clonal expansion and increased AML risk.

FLT3 is genetically essential for ITD-mutated leukemic stem cells but dispensable for human hematopoietic stem cells

This study shows FLT3 is essential for ITD-mutated leukemic stem cells but not for normal hematopoietic stem cells, supporting targeted therapies for AML.

Fenretinide targets GATA1 to induce cytotoxicity in GATA1 positive Acute Erythroid and Acute Megakaryoblastic Leukemic cells.

This paper identifies Fenretinide as a GATA1-targeting agent that induces cytotoxicity in M6 and M7 AML cells by causing GATA1 loss and overcomes chemotherapeutic resistance.

Stress Granules Underlie Acute Myeloid Leukemia Stem Cell Survival and Stress Adaptation

This study identifies stress granules as critical for AML stem cell survival and stress adaptation, revealing their role in gene regulation and potential as therapeutic targets.

A novel in-vitro model of the bone marrow microenvironment in AML identifies CD44 and Focal Adhesion Kinase as therapeutic targets to reverse cell adhesion-mediated drug resistance

This study identifies CD44 and FAK as therapeutic targets to reverse adhesion-mediated drug resistance in AML by developing an in-vitro BMME model and testing their synergistic effects.

Whole Exome Sequencing and Single-Cell DNA Sequencing for Assessment of Clonal Heterogeneity and Evolution in Acute Myeloid Leukemia

The paper compares whole exome sequencing and single-cell DNA sequencing in AML to assess clonal heterogeneity and evolution, finding both methods have strengths and limitations in variant detection and clonal analysis.

Translation Initiation Represents an Acute Myeloid Leukemia Cell Vulnerability That Can Be Co-Targeted With BCL-2 Inhibition

The paper identifies EIF4A1 as a vulnerability in AML cells and shows that combining Zotatifin with Venetoclax enhances apoptosis and survival in AML models.

DNMT/G9a Complex Inhibition Uncovers Epigenetic Vulnerabilities and Induces IFN-Response in Acute Myeloid Leukemia

This study shows that inhibiting the DNMT/G9a complex targets specific epigenetic vulnerabilities in AML, inducing an IFN response and improving therapeutic outcomes.

Effects of Hypomethylating Agents on Gene Modulation in the Leukemic Microenvironment and Disease Trajectory in a Mouse Model of AML

This study examines how hypomethylating agents affect gene expression in non-leukemic cells in a mouse model of AML, identifying novel gene targets and pathways involved in treatment response and relapse.

Leukemia-mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness

This study identifies PHF6 and PHIP as a chromatin complex that represses AML stemness, showing their functional relationship and the impact of their mutations.

Developmental hematopoietic stem cell variation explains clonal hematopoiesis later in life

The paper shows that clonal hematopoiesis later in life is driven by stem cell variation established before birth, using CpG methylation patterns in twins.

Mitochondrial heteroplasmy improves risk prediction for myeloid neoplasms

This study shows that mitochondrial heteroplasmy improves risk prediction for myeloid neoplasms when added to existing CHIP-based models.

Increased inflammatory signature in myeloid cells of non-small cell lung cancer patients with high clonal hematopoiesis burden

The paper examines the relationship between clonal hematopoiesis burden and immune response in NSCLC patients, finding higher CHIP prevalence in cancer patients and inflammatory pathway enrichment in myeloid cells with severe CHIP.

Comparing machine learning models for predicting mutation status in Acute Myeloid Leukemia patients using RNA-seq data

The paper compares machine learning models to predict mutation status in AML patients using RNA-seq data, finding complex models achieve high accuracy for NPM1, IDH1/IDH2, and FLT3-ITD mutations.