Nicholas T. Crump

The paper investigates Menin's role in enhancer-promoter interactions in MLL-rearranged and NPM1c leukemia models, finding context-dependent effects on transcriptional regulation and enhancer function.

This study identifies enhancer heterogeneity as a driver of transcriptional differences in KMT2A::AFF1 ALL patients, revealing patient-specific enhancer activity at oncogenes.

This study shows that inhibiting MLLT1 selectively limits MLL-AF4-driven leukemia growth without harming healthy hematopoietic stem cells.

This study shows that MYB activity sustains enhancer-promoter interactions and transcription by maintaining enhancer function in leukemia.

This study identifies PAF1 and FACT as essential for enhancer activity in MLL-AF4-driven leukemia by maintaining histone acetylation and enhancer-promoter interactions.

The paper constructs a gene regulatory network for MLL-AF4 to reveal an indirect repression of CASP9 via RUNX1 as a mechanism of apoptosis resistance.

The paper shows BET inhibition reduces transcription but not enhancer-promoter contacts, suggesting these processes are separable.

The paper identifies a distinct class of enhancers in leukemia cells that depend on H3K79 methylation and shows that DOT1L inhibition disrupts their function.