Area of research
Hematology · Oncology
Research interest
David Scadden is the Gerald and Darlene Jordan Professor of Medicine at Harvard University. He is a practicing hematologist/oncologist who focuses on bringing stem cell biology to patient care. Scadden is a hematologist/oncologist, and founded and directs the Center for Regenerative Medicine at the Massachusetts General Hospital. Together with Douglas Melton, he co-founded and co-directs HSCI. Scadden is a member of the Institute of Medicine of the National Academies of Science, the Board of External Experts for the National Heart, Lung and Blood Institute and a former member of the National Cancer Institute’s Board of Scientific Counselors. He has received multiple honorary degrees, awards and memberships in honorary societies.
Studying clonal heterogeneity of acute myeloid leukemia under nutrient and chemotherapy stress.
Iron overload damages mitochondria and induces metabolic rewiring of hematopoietic stem cells towards glycolysis.
Human Progenitor T-Cell Differentiation Regulated by the Mechanical Resistance of Thymus-Mimetic Extracellular Matrices.
Protein
<i>S</i>
-acylation dynamics provide metabolic plasticity to acute myeloid leukemia cells
Microbiome depletion rejuvenates the aging brain
PSTK inhibition activates cGAS-STING, precipitating ferroptotic cell death in leukemic stem cells.
Mesenchymal thymic niche cells enable regeneration of the adult thymus and T cell immunity
Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells
Mesenchymal thymic niche cells enable regeneration of the adult thymus and T cell immunity.
Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells.
Hematopoietic stem cells undergo bidirectional fate transitions
<i>in vivo</i>
Adult thymectomy is associated with increased mortality risk from cancer but not cardiovascular disease.
Author Correction: Niche-derived Semaphorin 4A safeguards functional identity of myeloid-biased hematopoietic stem cells.
Interrupting ELMSAN1 repression of nuclear acetyl-CoA production therapeutically reprograms cancer cells
Kinetics of
<i>de novo</i>
Bone and Bone Marrow Niche Formation with Hybrid Click Cryogels
Human progenitor T-cell differentiation regulated by the mechanical resistance of thymus-mimetic extracellular matrices
Single-cell analysis of immune and stroma cell remodeling in clear cell renal cell carcinoma primary tumors and bone metastatic lesions
A mitochondrial NADPH-cholesterol axis regulates extracellular vesicle biogenesis to support hematopoietic stem cell fate
Cyclophilin A supports translation of intrinsically disordered proteins and affects haematopoietic stem cell ageing
Integration of clinical outcomes and molecular features in extramedullary disease in multiple myeloma.
Cell of origin epigenetic priming determines susceptibility to Tet2 mutation.
Alloengraftment without significant toxicity or GVHD in CD45 antibody-drug conjugate-conditioned Fanconi anemia mice.
Dissecting the immune suppressive human prostate tumor microenvironment via integrated single-cell and spatial transcriptomic analyses
PPM1D modulates hematopoietic cell fitness and response to DNA damage and is a therapeutic target in myeloid malignancy
PPM1D modulates hematopoietic cell fitness and response to DNA damage and is a therapeutic target in myeloid malignancy.
Limited plasticity of monocyte fate and function associated with epigenetic scripting at the level of progenitors.
The bone marrow stroma in human myelodysplastic syndrome reveals alterations that regulate disease progression.
Clearing and replacing tissue-resident myeloid cells with an anti-CD45 antibody-drug conjugate.
Cell of origin epigenetic priming determines susceptibility to
<i>Tet2</i>
mutation
A transcriptional metastatic signature predicts survival in clear cell renal cell carcinoma