Joseph C. Hamley

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.

The paper uses single-cell CRISPR activation screens in human B cells to link non-coding autoimmune risk loci to their cis-regulatory target genes, revealing shared genetic mechanisms across diseases.

This study uses CRISPR-Cas genome editing to selectively inactivate JAK2 V617F mutations in patient cells, showing that heterozygous cells are not oncogene addicted while homozygous cells are eradicated, suggesting genome editing as a potential treatment for MPNs.

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.