Acute Myeloid Leukemia Research

This study identifies molecular changes in relapsed AML using transcriptomic analysis, highlighting pathways involved in chemoresistance and suggesting therapeutic targets.

This study examines laminin receptors in AML, finding that integrin α7β1 marks non-leukemic stem cells with migratory potential and correlates with poor survival.

The study shows that RUNX1-ETO levels determine endothelial reprogramming and hematopoietic cell growth in AML by altering the balance between these processes.

This paper introduces a functionalist oncology framework using edge-weighted digraphs to model AML treatment dynamics and evaluate drug combinations, including SAMHD1 inhibitors.

This study identifies IL-1/IRAK1/4 signaling as a therapeutic target in AML stem cells, showing that UR241-2 inhibits LSC clonogenicity and engraftment in both diagnosis and relapse.

This paper identifies AB8939, a novel drug that targets microtubules and ALDH enzymes, showing efficacy against drug-resistant AML cells and models.

This study shows that the developmental stage of hematopoietic stem cells influences leukemic transformation, lineage hierarchy, and therapy response in pediatric leukemia.

This study characterizes myeloid sarcoma through multi-omic profiling, identifies RAS pathway activation as a hallmark, and shows RAS inhibition reduces tumor burden in mouse models.

This study uses spatial transcriptomics to analyze AML in both medullary and extramedullary tissues, revealing inflammation and trans-differentiation states.

The paper identifies plasma proteins associated with clonal hematopoiesis and links them to cardiovascular disease through proteomic and genetic analyses.

This study identifies proteostasis stress as a driver of stem cell aging, clonal hematopoiesis, and leukemia by showing Hsf1's role in both physiological adaptation and pathological clonal expansion.

The paper identifies gene and miRNA biomarkers for AML risk stratification using PCA and SVM, validated across cohorts with high AUCs and regulatory insights.

This study uses ReSisTrace to identify pre-sensitizing agents for FLT3 inhibitors in FLT3-ITD-positive AML by analyzing transcriptional signatures and validating compounds that enhance treatment efficacy.

This study shows DNMT3AR882H mutations are not required for maintaining AML but are linked to higher leukemia stem cell frequency.

This study identifies heme biosynthesis as a selective dependency in AML, showing that its inhibition triggers cuproptosis via copper accumulation and reveals synthetic lethal pathways for therapeutic strategies.

The paper develops COMET, a method to infer clonal hematopoiesis from bulk DNA methylation data, showing it accurately detects clonal expansion and replicates known genetic associations.

This study shows that AML relapse after BET inhibitor or chemotherapy involves Myc-Ras transcriptional changes, highlighting transcriptional plasticity in relapsed leukemias.

The paper identifies recipient stem-cell persistence and T-cell dysregulation as predictors of relapse after HSCT in AML/MDS by analyzing single-cell RNA and TCR sequencing data.

This study identifies IRF2BP2 as a critical regulator of transposable element silencing in AML, showing its loss leads to TE activation and leukemia cell death.

The paper identifies PTBP1 as a RUNX1 interacting partner required for leukemia cell survival through metabolic gene regulation.

The paper uses deep learning to link TP53 genotype with expression-defined transcriptional programs in AML, finding a strong correlation between p53-low expression and TP53-inactive genotypes.

This paper identifies dual inhibition of LSD1 and Menin as a promising therapeutic strategy for non-APL AML by inducing terminal differentiation through distinct molecular mechanisms.

This study shows that resistant clones are rapidly selected in hematopoietic cell compartments with leukemic stem cell potential before relapse in patients treated with ivosidenib combination therapy.

This study analyzes genetic changes in pediatric AML relapse using whole-genome sequencing and finds that relapse is driven by the selection of pre-existing clones rather than new mutations.

This study shows that mutant NPM1 forms nuclear condensates called C-bodies, which are essential for leukemic gene expression and cell survival, and identifies them as potential therapeutic targets.

This study shows pitavastatin overcomes venetoclax resistance in AML by depleting GGPP, inducing apoptosis through PUMA upregulation and MCL-1 reduction, and suppressing mitochondrial metabolism.

This study finds that clonal hematopoiesis (CHIP) increases stroke risk across multiple cohorts, with specific gene mutations and inflammatory markers like IL-1RAP modifying this risk.

This study shows that proteasome inhibitors are ineffective in AML due to activation of HSF1 and autophagy, and that combining autophagy and proteasome inhibition effectively kills AML cells.

This study identifies molecular features of MRD progression in MDS using single-cell multi-omic profiling, revealing dynamic evolutionary processes and immunoevasive mechanisms.