Immature hematopoietic cells from mice with a large segmental deletion found in human myeloid malignancies exhibit cardinal features of myelodysplastic syndrome.

Multi-omics factor analysis reveals transposable element expression as a risk factor and inflammation as a protective factor in myelodysplastic syndromes (MDS).

SF3B1 mutation in myelodysplastic syndromes and acute myeloid leukemia lead to oncogenic long isoforms of IRAK4 that are therapeutically targetable.

Dysregulated erythroblast-specific iron trafficking and regulation of iron metabolism provides evidence of a novel potential therapeutic target to reverse ineffective erythropoiesis in MDS.

Single-cell transcriptomics reveals altered pathways, gene expression dynamics, and activation of transcriptional programs in human early hematopoiesis during healthy aging and myelodysplastic syndromes.

Reduced expression of MYBL2 contributes to malignancies of the blood by permitting uncontrolled expansion of blood cell progenitors, implying a tumor suppressor function for this gene.

Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.

compaRe can be used to optimize cytometric high-parameter immunophenotypic characterization of heterogeneous cell populations.

Thalidomide and its derivates induce degradation of many C₂H₂ zinc-finger transcription factors, including SALL4, providing insight into a long-standing mystery in modern pharmacology, and starting points for future drug development.

Real-time single-molecule visualization of transcription and splicing in living cells reveals that RNA synthesis and processing can occur through multiple pathways on the same gene.