Tom Milne
Websites
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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
MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia
Journal article
Crump NT. et al, (2023), Nature Communications, 14
BET inhibition disrupts transcription but retains enhancer-promoter contact
Journal article
Crump NT. et al, (2021), Nature Communications, 12
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), Nature Communications, 12
DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation
Journal article
Godfrey L. et al, (2019), Nature Communications, 10
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 Reports, 18, 482 - 495
Recent publications
Zone Equalisation Normalisation for Improved Alignment of Epigenetic Signal.
Journal article
Wilson T. et al, (2026), Bioinformatics
Inhibition of MLLT1 Limits Growth of KMT2A::AFF1 Leukemias Without Killing Healthy Hematopoietic Stem Cells
Journal article
Rajhansa S. et al, (2026), Experimental Hematology, 160
The fetal specific gene LIN28B is essential for human fetal B-lymphopoiesis and initiation of KMT2A::AFF1 infant leukemia.
Journal article
Ling RE. et al, (2026), Blood
Menin inhibitor DS-1594b drives differentiation and induces synergistic lethality in combination with venetoclax in acute myeloid leukemia cells with rearranged mixed-lineage leukemia and mutated nucleophosmin-1
Journal article
Ciaurro V. et al, (2026), Haematologica, 111, 1610 - 1624
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
ORCID
0000-0002-0413-4271
