David T. Scadden

This study shows intermittent parathyroid hormone drives osteogenesis from Ebf3-expressing progenitors via both intrinsic and extrinsic mechanisms in mice and humans.

The paper develops a flow cytometry protocol to measure single-cell protein synthesis and apoptosis in human CD34+ cells, revealing distinct functional profiles of small molecules in hematopoietic expansion.

This study identifies a unique metabolic plasticity mechanism in AML cells through protein S-acylation, which is inhibited by TOFA and a glutaminase inhibitor combination.

This study investigates the kinetics of de novo bone and bone marrow niche formation using a hybrid click cryogel system, showing that BMP-2 dose, immune status, and sex influence development rates and hematopoietic cell populations.

The paper shows that depleting the gut microbiome in aged mice rejuvenates the brain by improving vascular density, myelination, neurogenesis, and reducing inflammation.

This study shows that mechanical properties of thymus-mimetic matrices regulate human T-cell differentiation by modulating Notch1 and integrin signaling pathways.

The paper shows that IRES/Cap translation increases during hematopoietic and epithelial differentiation under normal conditions, correlating with lower stemness.

This study uses spatial transcriptomics and TCR sequencing in mice to analyze thymus changes across lifespan, revealing structural and transcriptional alterations linked to immune decline.

The paper identifies ELMSAN1 as a repressor of nuclear acetyl-CoA production and shows that inhibiting this interaction reprograms cancer cells to a postmitotic state, improving survival in multiple cancer models.

The paper shows that bone marrow stromal cells in HFpEF respond to IFNγ, driving monocyte expansion and fibrosis, which can be mitigated by IFNγ receptor deletion.

This study reveals bidirectional fate transitions between myeloid-biased and lineage-balanced hematopoietic stem cells using clonal phylogenetic tracing.

This study identifies Sema4A as an extrinsic factor that protects myeloid-biased HSCs from inflammatory stress, preserving functional diversity in the hematopoietic stem cell pool.

The paper uses multiomic analysis of leukemic clones in a mouse model to identify growth regulators and validate their roles in AML.

The paper identifies six HSC states and shows niche perturbations induce rapid transitions between them, revealing HSC-specific molecular signatures and chromatin features related to regenerative potential.

The paper identifies a point of irreversible commitment in granulocytic differentiation and shows how chromatin state dynamics and transcription factor feedback loops influence this decision.

The paper introduces a pipeline for processing droplet-based single-cell RNA-seq data to improve molecular count estimation by correcting barcode biases and sequencing errors.