Research groups
Websites
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MRC Molecular Haematology Unit
Research Unit
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MRC Weatherall Institute of Molecular Medicine
Research Institute
Paresh Vyas
MRCP FRCP FRCPath
Professor of Haematology
- Consultant Physician
Normal and Leukaemic stem/progenitor cell biology
Our aim is to characterise the heterogeneous populations of leukaemia propagating cells in adult and childhood Acute Myeloid Leukaemia (AML) at functional, genetic, epigenetic and molecular levels, eventually at a single cell level, to improve our basic understanding of leukaemia initiation and propagation. The ultimate aim is to translate this knowledge to improve survival rates in patients.
Biography
Paresh Vyas is Professor of Haematology at the University of Oxford. He studied medicine at Cambridge then Oxford. After completing his medical and haematology training in London, he did his PhD with Professor Doug Higgs and Professor Sir David Weatherall at the MRC Molecular Haematology Unit, Oxford. A three-year post-doctoral fellowship with Professor Stuart Orkin at Harvard University followed. He is a research-active Consultant Haematologist with a clinical practice in myeloid disorders: myelodysplastic syndrome, MDS, acute myeloid leukaemia, AML, and myeloproliferative disorders, MPD, as well as allogeneic stem cell transplant. His research in the MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, focuses on molecular and cellular biology of AML and MDS with specific interest in purification and therapeutic targeting of myeloid stem cells. He studies single cell biology in normal and leukaemic haemopoiesis. He is on the UK AML and MDS clinical trial groups. He is co-Lead of the Oxford BRC Haematology and Stem Cells Theme, is on the Board of NHSBT, vice-chair of the MRC Clinical Training Panel and Translational Lead for the UK Therapy Acceleration Program.
Key publications
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Journal article
Turkalj S. et al, (2023), Cell Stem Cell, 30, 722 - 740.e11
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Journal article
DiNardo CD. et al, (2021), Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 39, 57 - 65
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C/EBPalpha and GATA-2 mutations induce bi-lineage acute erythroid leukemia through transformation of a neomorphic neutrophil-erythroid progenitor
Journal article
NERLOV C. et al, (2020), Cancer Cell
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Journal article
Labuhn M. et al, (2019), Cancer Cell
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Clonal Heterogeneity of Acute Myeloid Leukemia Treated with the IDH2 inhibitor Enasidenib
Journal article
Vyas P. et al, (2018), Nature Medicine
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Journal article
Karamitros D. et al, (2018), Nat Immunol, 19, 85 - 97
Recent publications
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HDAC inhibitor derivatives induce differentiation of leukemic cells through two distinct and separable mechanisms
Preprint
Kumar P. et al, (2024)
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Real-world Effectiveness of Azacitidine in Treatment-Naive Patients With Higher-risk Myelodysplastic Syndromes.
Journal article
Rajakumaraswamy N. et al, (2023), Clin Lymphoma Myeloma Leuk
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Changing treatment changing prognosis of mutations
Journal article
Vyas P., (2023), Blood, 142, 1583 - 1585
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A protocol for simultaneous high-sensitivity genotyping and chromatin accessibility profiling in single cells.
Journal article
Turkalj S. et al, (2023), STAR Protoc, 4
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Selective advantage of mutant stem cells in clonal hematopoiesis occurs by attenuating the deleterious effects of inflammation and aging
Preprint
Jakobsen NA. et al, (2023)