Histone acetyl-transferase Kat2a preserves leukemia stem cells through frequent transcriptional firing of metabolic and regulatory gene promoters and maintenance of a largely invariant self-renewal program.

In the pancreas, reciprocal interactions between epithelial cells and myeloid cells determine the balance between tissue repair and carcinogenesis by regulating acinar cell plasticity through differential activation of EGFR/MAPK signaling.

In metastatic NSCLC patients, CHIP showed minimal impact on immunotherapy response but was more prevalent and associated with inflammatory pathways in myeloid cells, particularly in lung squamous cell carcinoma.

Deletion of Arginase 1 in myeloid cells delays tumor formation in pancreatic cancer.

The ubiquitin ligase c-Cbl preferentially targets unique-region phosphorylated LynA for rapid degradation, regulating its expression and differentially tuning signaling responsiveness in macrophages and mast cells.

A novel population of hematopoietic cells unmasked by mTORC1 inactivation reveals a new mechanism of innate immune tolerance and a new consequence of defective hematopoiesis.

Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.

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

Quantitative analysis of protein and mRNA expression across a minimally perturbed cell cycle in human myeloid cells has identified myeloid-specific and cell cycle-regulated gene expression, including examples of isoform- and phosphorylation-specific regulation, with all data made available in a searchable, online database.

Genetic engineering of murine myeloid cells reveals the challenges in ectopic expression of chemiric receptors and provides a novel framework to endow them with tumor-specific cytotoxic ability.