Acute Myeloid Leukemia Research

This study shows that the Ezh2Y641F mutation causes different outcomes in hematopoiesis depending on developmental stage and cell type, leading to either bone marrow failure or lymphoma.

This study identifies GGPP, a mevalonate pathway byproduct, as critical for chemoresistance in TP53mut AML through ROS regulation and mitochondria stress response, suggesting statin-based therapies could be effective.

The paper analyzes RNA expression data to show that ALDH2 is more prognostically significant than ALDH1A1 in NPM1 mutant AML, suggesting ALDH2 inhibition as a potential therapeutic strategy.

This study shows a heterozygous CEBPA mutation in the bZIP domain causes MDS progression by altering chromatin structure and clonal composition, using patient-derived iPSCs.

This study examines how chemotherapy affects clonal diversity and mutation patterns in hematopoietic stem cells, finding that melphalan increases mutational burden and promotes clonal aging, potentially leading to therapy-related myeloid neoplasms.

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

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.

This study investigates drug-drug interactions in AML cell lines, finding widespread but non-conserved synergistic and antagonistic effects across different cell lines.

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

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

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

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

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

The paper identifies novel subgroups in myeloid malignancies using a network-based clustering approach that integrates genomic and clinical features, improving prognostic accuracy.

The paper constructs a reference atlas of human hematopoiesis and maps AML differentiation patterns, revealing genetic and non-genetic factors driving aberrant differentiation in leukemia.

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

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.

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

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.

The paper analyzes single-cell data from bone marrow samples to identify immune cell interactions that predict response to adoptive cellular therapy in myeloid leukemia.

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

This study uses single-cell DNA sequencing to analyze preleukemic hematopoietic stem cells and finds pervasive positive selection throughout preleukemic evolution, with selective advantages ranging from 9%-24% per year.

This study shows hypoxia reduces the effectiveness of hypomethylating agents in AML cells by altering DNA methylation and antigen presentation pathways.

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.

This study shows that mutant ASXL1 proteins disrupt heterochromatin integrity in clonal hematopoiesis and CMML by reducing H3K9me2/3 and H2AK119Ub, leading to increased transposable element expression.

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.

The paper identifies HMX3 as a critical vulnerability in MECOM-negative KMT2A::MLLT3 AML, showing it promotes proliferation and blocks differentiation.