David O’Connor

This paper identifies a metabolic vulnerability in leptomeningeal ALL cells due to thiol scarcity in CSF, making them susceptible to ferroptosis through disruption of selenocysteine biosynthesis and GPX4 activity.

This study identifies acidic patches in the MYC N-terminal disordered domain essential for oncogenesis and chromatin interaction, offering new therapeutic targets.

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

The paper examines the transcriptional evolution of myeloid leukaemia in Down syndrome by analyzing single-cell RNA sequencing data from patient samples and fetal tissues.

The paper identifies a novel mechanism where focal deletions of an intronic element in FTO lead to IRX3 activation in T-ALL through enhancer hijacking.