Acute Myeloid Leukemia Research

Riboflavin drives nucleotide biosynthesis and iron-sulfur metabolism to promote acute myeloid leukemia

This study identifies riboflavin as a critical metabolic dependency in acute myeloid leukemia, showing its role in nucleotide biosynthesis and iron-sulfur cluster metabolism beyond energy production.

MYD88 mutations in clonal hematopoiesis promote inflammation and hematopoietic stem cell expansion

This study shows MYD88 mutations in clonal hematopoiesis drive inflammation and HSPC expansion by activating NF-κB pathways and promoting myeloid bias.

The STAT3-VDAC1 Axis Modulates Mitochondrial Function and Plays a Critical Role in the Survival of Acute Myeloid Leukemia Cells

Catalytic inhibition of KAT6/KAT7 enhances the efficacy and overcomes primary and acquired resistance to Menin inhibitors in MLL leukaemia

The paper shows that inhibiting KAT6/KAT7 enhances Menin inhibitor efficacy and overcomes resistance in MLL-FP leukemia.

MOZ and HBO1 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in NUP98-Rearranged Acute Myeloid Leukemia

This study identifies MOZ and HBO1 as molecular dependencies in NUP98-rearranged AML, showing their inhibition reduces leukemic burden and synergizes with Menin inhibitors.

AML patient blasts exhibit polarization defect upon interaction with bone marrow stromal cells.

This study shows AML blasts fail to polarize when interacting with healthy stromal cells, and AML-derived stromal cells impair polarization of healthy HSPCs and AML blasts.

Multi-selective RAS(ON) Inhibition Targets Oncogenic RAS Mutations and Overcomes RAS/MAPK-Mediated Resistance to FLT3 and BCL2 Inhibitors in Acute Myeloid Leukemia

This study evaluates RMC-7977, a RAS(ON) inhibitor, showing efficacy against RAS-driven resistance in AML and potential for combination therapies.

Acid ceramidase inhibition enhances BCL-2 targeting in venetoclax-resistant acute myeloid leukemia via a cytotoxic integrated stress response

This study shows that inhibiting acid ceramidase (AC) enhances venetoclax's effectiveness in venetoclax-resistant AML by inducing a cytotoxic integrated stress response.

Loss of Y chromosome in Alzheimer disease patients co-occurs with clonal hematopoiesis defined by post-zygotic point mutations outside canonical CHIP driver genes

The paper investigates the relationship between loss of Y chromosome (LOY) and clonal hematopoiesis in Alzheimer's disease patients, finding that LOY drives myeloid clones which may accumulate additional mutations.

ASXL1 truncating mutations drive leukemic resistance to T cell attack

This study identifies ASXL1 truncating mutations as a driver of leukemic resistance to T cell attack and proposes EZH2 inhibition as a therapeutic strategy to overcome this resistance.

Primary CD34+ cells of patients with VEXAS syndrome are highly sensitive to targeted treatment with TAK-243 and pevonedistat

This study shows that VEXAS patient-derived CD34+ cells are more sensitive to TAK-243 and pevonedistat than MDS and healthy controls, suggesting potential targeted therapy.

Therapy resistance in AML is mediated by cytoplasmic sequestration of the transcriptional repressor IRF2BP2

This study identifies IRF2BP2 cytoplasmic sequestration by MCL1 as a mechanism driving venetoclax and azacitidine resistance in AML through ACSL1 derepression.

Overcoming treatment resistance mediated by the bone marrow vascular niche in acute myeloid leukemia

This study develops a computational model of the AML bone marrow microenvironment and shows that combining TKIs with miR-126 inhibition can overcome treatment resistance by disrupting the protective vascular niche.

Identification of non-charged 7.44 analogs interacting with the NHR2 domain of RUNX1-ETO and exhibiting an improved, selective antiproliferative effect in RUNX-ETO positive cells

The paper identifies non-charged analogs of the inhibitor 7.44 that show improved antiproliferative effects against RUNX1-ETO positive cells.

AttentionAML: An Attention-based Deep Learning Framework for Accurate Molecular Categorization of Acute Myeloid Leukemia

AttentionAML is a deep learning framework for AML subtype classification using transcriptomic data, achieving high accuracy and outperforming existing methods.

Multimodal Spatial Proteomic Profiling in Acute Myeloid Leukemia

This study uses high-plex spatial proteomics to identify tertiary lymphoid-like structures in AML bone marrow and links them to patient outcomes.

BIRC5 dependency defines a targetable vulnerability in TP53 mutant acute myeloid leukemia

This study identifies BIRC5 as a targetable vulnerability in TP53 mutant AML, showing that survivin/IAP inhibitors can overcome therapy resistance.

Temporal Single Cell Analysis of Leukemia Microenvironment Identifies Taurine-Taurine Transporter Axis as a Key Regulator of Myeloid Leukemia

This study identifies the taurine-taurine transporter axis as a critical regulator of myeloid leukemia using temporal single-cell RNA-sequencing and functional experiments.

Targeted Irradiation and STAT3 Inhibition Reprogram the AML Microenvironment and Extend Survival: Toward Translational Immunoradiotherapy

This study combines targeted marrow irradiation with a STAT3 inhibitor to improve leukemia clearance and immune memory in AML models.

Dual Specificity Phosphatase 3 knockdown drives myeloid leukemia cells to differentiate into macrophages and polarize

This study shows that DUSP3 knockdown promotes differentiation of myeloid leukemia cells into macrophages and alters their polarization markers.

Clonal hematopoiesis driven by Dnmt3a mutations promotes metabolic disease development

This study shows that Dnmt3a mutations in clonal hematopoiesis drive metabolic diseases like obesity and diabetes in mice, especially under high-fat diet.

Transcriptomic alterations including p53 pathway dysregulation prime DNMT3A mutant cells for transformation

This study shows DNMT3A mutations reduce DNA methylation and disrupt p53 pathway, increasing self-renewal and cancer risk in hematopoietic cells.

Inhibition of MLLT1 limits growth of MLL-AF4 leukaemias without killing healthy haematopoietic stem cells

This study shows that inhibiting MLLT1 selectively limits MLL-AF4-driven leukemia growth without harming healthy hematopoietic stem cells.

A structure-based modelling approach identifies effective drug combinations for RAS-mutant acute myeloid leukemia

This paper uses a structure-based model to identify synergistic RAF inhibitor combinations effective against RAS-mutant AML in vitro and in vivo.

Unique epigenomic signatures identify biologically significant subtypes of MDS and predict response to azacitidine

This study identifies epigenetic subtypes of MDS using DNA methylation patterns and develops a predictive signature for azacitidine response.

Nucleophosmin mutations lead to abnormal, but reversible, nucleoli architecture and aggregate formation - implications for NPM1-targeting therapies in AML

This study shows that NPM1 mutations cause abnormal nucleoli structure and reversible aggregates in AML, suggesting new therapeutic targets.

Loss of transcriptional factor Zbtb33 fails to induce clonal hematopoiesis in mice but plays a role in tumor immunity

This study shows that Zbtb33 knockout in mice does not induce clonal hematopoiesis but influences tumor immunity and the tumor microenvironment.

DEK::NUP214 acts as an XPO1-dependent transcriptional activator of essential leukemia genes

This study identifies DEK::NUP214 as an XPO1-dependent transcriptional activator of leukemia genes, showing selective response to XPO1 inhibitors in t(6;9) AML cases.

Novel Strategy against AML by Rescuing Loss of Phase Separation of Pathogenic NPM1c

This study identifies a small molecule that rescues NPM1c phase separation loss, restoring nucleolar localization and showing anti-leukemia activity in AML models.

TTLL4 glutamyltransferase is a therapeutic target for NPM1-mutated acute myeloid leukemia

This study identifies TTLL4 as a therapeutic target in NPM1-mutated AML by showing its role in stabilizing NPM1c and promoting differentiation block, with a small molecule inhibitor demonstrating efficacy.