Tom Milne
Websites
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MRC Molecular Haematology Unit
Research Unit
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MRC Weatherall Institute of Molecular Medicine
Research Institute
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Twitter
@milnetom68
Thomas Milne
PhD
Professor of Haematology
Epigenetic Control of Gene Expression in Leukaemia and Haematopoiesis
Brief biography and current research interests
Tom Milne received a PhD in 2005 that was co-supervised by Dr. Hugh Brock (University of British Columbia, Vancouver, Canada) and Dr. Jay Hess (University of Pennsylvania, Philadelphia, USA) working on the wild type function of the Mixed Lineage Leukaemia (MLL) protein. Tom went on to do postdoctoral studies at The Rockefeller University (NY, USA) in the lab of Dr. C. David Allis where he worked on additional roles for the MLL protein complex in the regulation of gene targets in normal cells as well as in leukaemia. He became a Group Leader in 2010 at the MRC Molecular Haematology Unit (MRC Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford) and then an Associate Professor of Haematology in 2014.
Chromatin proteins have become key therapeutic targets in cancer treatment but it is still not fully understood exactly how these proteins function. The Milne lab aims to better understand how chromatin proteins contribute to gene regulation in normal haematopoietic cells and in disease, and in particular how these proteins influence gene expression through differential enhancer activity. We have a specific focus on high risk paediatric leukaemias, particularly those caused by rearrangements of the Mixed Lineage Leukaemia (MLL) gene. The overall goal is to use key mechanistic insights from this work to design novel combination therapies in pre-clinical models of disease, or to better understand the function of drugs that are already undergoing clinical trials.
Key publications
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MLL-AF4 Spreading Identifies Binding Sites that Are Distinct from Super-Enhancers and that Govern Sensitivity to DOT1L Inhibition in Leukemia.
Journal article
Kerry J. et al, (2017), Cell Rep, 18, 482 - 495
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DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation.
Journal article
Godfrey L. et al, (2019), Nat Commun, 10
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BET inhibition disrupts transcription but retains enhancer-promoter contact.
Journal article
Crump NT. et al, (2021), Nat Commun, 12
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A human fetal liver-derived infant MLL-AF4 acute lymphoblastic leukemia model reveals a distinct fetal gene expression program.
Journal article
Rice S. et al, (2021), Nat Commun, 12
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MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia.
Journal article
Crump NT. et al, (2023), Nat Commun, 14
Recent publications
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Correction to "DNA-Programmable Protein Degradation: Dynamic Control of Proteolysis-Targeting Chimera Activity via DNA Hybridization and Strand Displacement".
Journal article
Kashyap D. et al, (2026), JACS Au, 6, 653 - 655
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Menin maintains enhancer-promoter interactions in a leukemia-specific manner
Preprint
Sharlandjieva V. et al, (2026)
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Off-the-shelf dual CAR-iNKT cell immunotherapy eradicates medullary and leptomeningeal high-risk KMT2A-rearranged leukemia.
Journal article
Ren H. et al, (2026), Blood, 147, 180 - 196
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A genome-wide screen identifies Runx2 as a novel regulator of hematopoietic stem cell expansion and T-cell commitment.
Journal article
Meaker GA. et al, (2025), Blood, 146, 3188 - 3200
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Zone Equalisation Normalisation For Improved Alignment of Epigenetic Signal
Preprint
Wilson T. et al, (2025)
ORCID
0000-0002-0413-4271