Olaf T Heidenreich

This paper uses spatial multi-omics to identify immunosuppressive interactions between AML, macrophages, and T cells in bone marrow, highlighting the Galectin-9 - CD44/TIM-3 axis as a therapeutic target.

This paper reviews clinical and demographic features of IGH::CEBP-rearranged BCP-ALL cases and introduces new cases to encourage further study of this rare subtype.

This study identifies an immunosuppressive bone marrow microenvironment in RAS-mutant B-ALL, enriched for regulatory T cells, and suggests CTLA-4 blockade could enhance T-cell-engager efficacy.

The paper generates a single-cell multi-omics atlas of pediatric bone marrow, revealing age-related shifts in lineage differentiation linked to stromal cell heterogeneity.

This study examines lymphocyte dynamics during chemotherapy in pediatric AML, finding preserved or increased lymphocytes alongside blast reduction, suggesting a potential window for BiTE therapy.

This study identifies distinct stromal cell populations in B-ALL bone marrow and shows their roles in supporting leukemic cell survival and chemoresistance.

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

This study evaluates CD19 expression in pediatric AML and shows that CD19-directed immunotherapies are effective against CD19+ AML, similar to their efficacy in BCP-ALL.

The paper identifies a distinct developmental state in KMT2A-rearranged infant B-cell acute lymphoblastic leukemia using single-cell transcriptome analysis.

This study identifies two genome-wide significant susceptibility loci for acute myeloid leukemia through a meta-analysis of GWAS data.

This study identifies two mechanisms by which RUNX1/RUNX1T1 regulates alternative splicing in t(8;21)-positive acute myeloid leukemia cells, affecting RNA isoform production and protein structure.