Research groups
Websites
-
MRC Molecular Haematology Unit
Research Unit
-
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.
Key publications
-
Hematopoietic stem cell heterogeneity and age-associated platelet bias are evolutionarily conserved.
Aksöz M. et al, (2024), Sci Immunol, 9
-
Selective advantage of mutant stem cells in human clonal hematopoiesis is associated with attenuated response to inflammation and aging.
Jakobsen NA. et al, (2024), Cell Stem Cell, 31, 1127 - 1144.e17
-
GTAC enables parallel genotyping of multiple genomic loci with chromatin accessibility profiling in single cells.
Turkalj S. et al, (2023), Cell Stem Cell, 30, 722 - 740.e11
-
Mutant Isocitrate Dehydrogenase 1 Inhibitor Ivosidenib in Combination With Azacitidine for Newly Diagnosed Acute Myeloid Leukemia.
DiNardo CD. et al, (2021), J Clin Oncol, 39, 57 - 65
-
C/EBPα and GATA-2 Mutations Induce Bilineage Acute Erythroid Leukemia through Transformation of a Neomorphic Neutrophil-Erythroid Progenitor.
Di Genua C. et al, (2020), Cancer Cell, 37, 690 - 704.e8
-
Mechanisms of Progression of Myeloid Preleukemia to Transformed Myeloid Leukemia in Children with Down Syndrome.
Labuhn M. et al, (2019), Cancer Cell, 36, 123 - 138.e10
-
Clonal heterogeneity of acute myeloid leukemia treated with the IDH2 inhibitor enasidenib.
Quek L. et al, (2018), Nat Med, 24, 1167 - 1177
-
Single-cell analysis reveals the continuum of human lympho-myeloid progenitor cells.
Karamitros D. et al, (2018), Nat Immunol, 19, 85 - 97