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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Enhancer heterogeneity in acute lymphoblastic leukemia drives differential gene expression in patients.
Journal article
Smith A. et al, (2025), Blood
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PROM1/CD133 MARKS A PROLIFERATIVE STEM CELL LIKE POPULATION OF BLASTS IN KMT2A REARRANGED INFANT ALL.
Journal article
Cross JW. et al, (2025), Blood Adv
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Iron deficiency causes aspartate-sensitive dysfunction in CD8+ T cells.
Journal article
Teh MR. et al, (2025), Nat Commun, 16
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Engineering antisense oligonucleotides for targeted mRNA degradation through lysosomal trafficking.
Journal article
Kashyap D. et al, (2025), Chem Sci
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Inhibition of MLLT1 limits growth of MLL-AF4 leukaemias without killing healthy haematopoietic stem cells
Preprint
Rajhansa S. et al, (2025)
ORCID
0000-0002-0413-4271