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.

Integrated analyses of acute myeloid leukemia genetics and epigenetics demonstrate that epigenetic evolution occurs in a convergent manner in the absence of DNA mutations at relapse post-chemotherapy.

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.

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

Cellular and molecular analyses of human AML cells reveal a novel pathway activated by the bone marrow microenvironment that confers resistance to FLT3 inhibition and can be exploited to improve the efficacy of FLT3 inhibitor therapy for AML.

Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.

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

The morphology and deformability of all blood cells can be measured continuously and with high throughput directly in whole blood without prior enrichment or separation.

Age-specific transcriptional responses to Flt3-ITD and cooperating Flt3/Runx1 mutations cause hematopoietic stem cell depletion and myeloid progenitor expansion during adult, but not fetal/neonatal, stages of development.