Thomas A. Milne

This paper introduces ZEN, a normalization method for genomic data that reduces technical noise while preserving biological signals, improving alignment across different experimental platforms.

This study identifies LIN28B as essential for fetal B-lymphopoiesis and KMT2A::AFF1 infant leukemia initiation, showing its role in promoting proliferation and leukemogenesis.

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 paper identifies CD180 as a marker for chemoresistant stem-like blasts in KMT2A-rearranged paediatric AML, showing its absence on normal HSCs and its role as a therapeutic target.

This study shows FACT maintains promoter topology by preserving nucleosomes and preventing chromatin factor spreading into gene bodies.

TRANCERs convert enhancers into autonomous tissue-specific promoters, enabling precise and programmable gene expression for research and therapy.

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 iron deficiency impairs CD8+ T cell proliferation and metabolism by disrupting mitochondrial function, but exogenous aspartate can rescue this defect.

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.

The paper shows that active enhancers recruit cohesin to form cell-specific chromatin domains, using the alpha globin cluster as a model.

This paper develops bi-specific CAR-iNKT cells targeting CD19 and CD133 for KMT2A-rearranged leukemia, showing superior efficacy over CAR-T in eradicating leptomeningeal disease and inducing remission.

The paper shows HDAC inhibitors induce AML cell differentiation via two distinct mechanisms: one through G1 arrest and another through G2 arrest via Aurora A and GSK3 inhibition.

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.

This paper introduces miSFITs, synthetic microRNA response elements that allow precise control of gene expression levels in mammalian cells, showing their utility in modulating antigen expression in a mouse melanoma model.