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.

Definition of leukemia gene expression mechanisms reveals general principles of cancer gene control and offers a pharmacologic strategy for its therapeutic reprogramming.

The HOXA9 reporter and genetic screens facilitated the functional interrogation of the HOXA9 regulome and advanced our understanding of the molecular regulation network in HOXA9-driven leukemia.

TRIM33 performs an essential function in B cell acute lymphoblastic leukemia through an association with a single cis element.

Convergent transcription and stalling of transcription are enriched at DNA breakpoints found in acute lymphoblastic leukemia and associate with DNA structures and sequences that mediate genetic instability.

A key molecule that connects leukemogenic proteins to aberrant HOX gene regulation turned out to be a nuclear export factor, CRM1.

Across a physiological span of ATP-free energy, leukemic mitochondria primarily consume, rather than produce, ATP.

A comprehensive analysis of long noncoding RNAs in the hematopoietic system reveals their dynamic regulation and a loss-of-function screen identifies some required for leukemia progression and involved in normal myeloid differentiation.

Interaction of the MLL and HBO1 complexes is a key nexus for leukemic transformation that can serve as a therapeutic target.

HOXA9 is a transcriptional maintenance factor for anti-apoptotic genes that accelerate MYC-driven leukemia.