Sophie G. Kellaway

This study identifies SPATS2L as a mediator of growth and survival in RUNX1-mutant blast-phase CML through stress granule formation, suggesting it as a therapeutic target.

The study shows that RUNX1-ETO levels determine endothelial reprogramming and hematopoietic cell growth in AML by altering the balance between these processes.

This study shows that depletion of RUNX1::RUNX1T1 in AML cells reduces stemness and promotes differentiation into granulocytic and eosinophilic/mast cell-like populations.

The paper identifies thousands of cell stage-specific enhancers that drive hematopoietic specification by responding to cytokine signals and transcription factors.

The paper shows that different RUNX1 mutations alter gene regulatory networks and chromatin programming, leading to distinct hematopoietic differentiation trajectories and disease phenotypes.