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Professor George Vassiliou is Professor of Haematological Medicine at the University of Cambridge, affiliated with the Department of Haematology and the Wellcome-MRC Cambridge Stem Cell Institute, where he serves as a Principal Investigator. He is also a Consultant Haematologist at Cambridge University Hospitals. Vassiliou studied Medicine at the Royal London Hospital, trained as a Haematologist in London and Cambridge, and obtained his PhD from the University of Cambridge in 2005. He holds qualifications including MRCP(UK) and FRCPath. His career includes establishing a research team at the Wellcome Sanger Institute in 2011 as a faculty member, followed by recruitment to his current position at the University of Cambridge in 2019, with his laboratory now based at the Cambridge Stem Cell Institute. He has held prestigious fellowships such as the Cancer Research UK Senior Fellowship, Wellcome Trust Senior Fellowship in Clinical Science, and Cancer Research UK Clinician Scientist Fellowship.
Vassiliou's research specializes in the pathogenesis of acute myeloid leukaemia (AML) and related myeloid malignancies, focusing on cell-autonomous and non-cell-autonomous processes transforming normal haemopoietic stem cells into leukaemic stem cells. He investigates genetic vulnerabilities through CRISPR screens, develops bespoke mouse models of somatic mutations, and studies clonal haematopoiesis in healthy individuals to predict leukaemic progression, enabling early detection and prevention strategies. Key contributions include leading the Specialized Center of Research into Myeloid Cancer Prevention and spearheading a £4m project for a clinical platform in blood cancer prevention. Notable publications encompass 'Prediction of acute myeloid leukaemia risk in healthy individuals' (Nature, 2018), 'Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis' (Nature, 2025), 'Telomere attrition becomes an instrument for clonal selection in aging hematopoiesis and leukemogenesis' (Nature Genetics, 2025), 'Posttranscriptional depletion of ribosome biogenesis factors engenders therapeutic vulnerabilities in NPM1-mutant AML' (Blood, 2025), 'Genome-wide analyses of 200,453 individuals yield new insights into the causes and consequences of clonal hematopoiesis' (Nature Genetics, 2022), and 'Mutant nucleophosmin and cooperating pathways drive leukemia initiation and progression in mice' (Nature Genetics, 2011). His work advances therapeutic approaches for AML, myelodysplastic syndromes, and related conditions, with applications in genetic screens and epidemiological studies.