Ryan Asby

This study creates a mouse model of myeloid neoplasm with spontaneous RTK-RAS mutations, showing a premalignant phase and lineage restriction in tumors.

This study identifies CREBBP mutations as a targetable vulnerability in B-ALL, showing that CREBBP inhibition sensitizes these cells to Venetoclax-induced ferroptosis.

This study shows that DNMT3A R882H mutant HSCs resist inflammatory stress through delayed p53 activation, leading to clonal expansion and increased AML risk.

This study shows that JAK inhibition increases uSTAT5 levels, which promotes HSC maintenance and stemness, and reveals a new role for uSTAT5 in controlling HSC function.