Marc R. Mansour

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 identifies the TARZN complex, which binds de novo enhancer mutations and promotes TAL1 overexpression in T-ALL through RNA methylation.

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.

Genesis is a modular protein language model that improves immunogenicity prediction for CD8+ epitopes by integrating pMHC and TCR context, outperforming existing models in precision.