John E. Pimanda

Cell-state-specific mechanisms of 5-azacytidine response in myelodysplastic neoplasms

The paper identifies cell-state-specific mechanisms of 5-azacytidine response in myelodysplastic neoplasms, showing distinct differentiation and transcriptional changes in cycling progenitors and quiescent stem cells.

Azacitidine Response in Myelodysplastic Syndromes is Marked by NK-like CD8 T-Cell Expansion and CXCL12+ Reticular Cell Remodeling

The paper identifies NK-like CD8 T-cell expansion and CXCL12+ reticular cell remodeling as markers of azacitidine response in MDS through longitudinal bone marrow profiling.

Single cell multiomics reveal clonal and functional dynamics of MDS stem/progenitor cells during hypomethylating therapy

This study uses single-cell multiomics to show that AZA response in MDS involves hematopoietic regeneration from mutated HSPCs and that AZA-refractive sub-populations contribute to disease progression.

MECOM is a master repressor of myeloid differentiation through dose control of CEBPA in acute myeloid leukemia

This study shows MECOM represses myeloid differentiation by inhibiting CEBPA, and its overexpression in AML reduces CEBPA levels, maintaining stem cell state.

Genome-Wide CRISPR-Cas9 Screening Identifies a Synergy between Hypomethylating Agents and SUMOylation Blockade in MDS/AML

This study identifies a synergy between hypomethylating agents and SUMOylation blockade in MDS/AML using CRISPR-Cas9 screening, showing improved therapeutic outcomes in xenograft models.

Cell Type-Specific Regulation by a Heptad of Transcription Factors in Human Hematopoietic Stem and Progenitor Cells

The paper identifies cell-type-specific regulatory roles of a heptad of transcription factors in human hematopoietic stem and progenitor cells.

Mesoderm-Derived PDGFRA+ Cells Regulate the Emergence of Hematopoietic Stem Cells in the Dorsal Aorta

The paper shows that mesoderm-derived PDGFRA+ stromal cells in the AGM region support endothelial-to-hematopoietic transition and LT-HSC generation.

Induction of a SALL4-dependency for targeted cancer therapy

This study shows that SALL4 can be induced in cancer cells to make them dependent on it, enabling targeted therapy with drugs like DAC and ENT.