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BSMS > About BSMS > Contact us > Staff > Dr Timothy Chevassut

Dr Timothy Chevassut

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Dr Timothy Chevassut (BMBCh MA, MPH, PhD)

Senior Lecturer in Haematology
E: t.chevassut@bsms.ac.uk
T: +44 (0)1273 873232
Location: Medical Research Building, BSMS, University of Sussex, BN1 9PS

Other roles: Honorary Consultant; Director of Clinical Academic Training at BSMS; Director of Cancer Translation Advisory Group (CTAG); Lead for Haematology Clinical Trial Portfolio (CIRU)
Areas of expertise: Clinical haematology; acute myeloid leukaemia; myelodysplastic syndromes; stem cells; DNA methylation; epigenetics; targeted therapies; cancer trials

Biography

Dr Timothy Chevassut is both a clinical haematologist and basic scientist. He studied medicine and molecular biology at Oxford before spending a research fellowship at Harvard where he conducted research on embryonic stem cells and DNA methylation. He subsequently completed a PhD at Edinburgh working on RNA interference before returning to medicine and completing specialist training in clinical haematology.  In 2007 he was appointed to the post of Senior Lecturer at BSMS. He also practices as an honorary Consultant Haematologist at the Royal Sussex County Hospital.

Timothy's clinical area of interest is blood cancers with a particular focus on acute myeloid leukaemia (AML) and the myelodysplastic syndromes (MDS). These are related diseases of the blood for which we now have a remarkable understanding of the molecular basis of disease, yet the treatment options remain very limited, particularly in the elderly where stem cell transplantation is often not possible.

Dr Chevassut’s recent work has focussed on one particular gene mutation that carries a particularly poor prognosis in AML, namely the DNA methyltransferase gene DNMT3A. His laboratory has shown that mutations in DNMT3A often initiate leukaemia and can be detected rapidly using PCR to improve diagnosis. More importantly, they have shown that leukaemias carrying DNMT3A mutations can be effectively targeted using novel compounds called bromodomain inhibitors that block epigenetic reader proteins in the cell.

Qualifications

  • BMBCh MA – Oxford University, 1993

  • MPH – Harvard University, 1998

  • PhD – Edinburgh University, 2006

Fellowships 

  • Royal College of Pathologists (2010)

  • Royal College of Physicians (2011)

Memberships   

  • British Society of Haematology

  • NCRI Myelodysplasia Subgroup

Research

Timothy conducts a successful translational research programme in AML and MDS that aims to better understand the biology of these conditions through basic science with a view to improving treatments for patients through clinical trials. The basic laboratory research is conducted at the BSMS Medical Research Building at the University of Sussex and focuses on the molecular mechanisms of leukaemogenesis. Dr Helen Stewart is the Senior Research Fellow overseeing the research with key collaborators in London, Oxford, Edinburgh and the United States. There are three main research themes: firstly, to understand how mutations of the DNA methyltransferase gene DNMT3A commonly lead to AML; secondly, to study how histone abnormalities lead to expansion of leukaemic stem cells; and thirdly to explore novel epigenetic therapies in AML including hypomethlyating agents and bromodomain inhibitors.

Timothy has also established the Brighton Bone Marrow Tissue Bank containing samples from patients with AML, MDS and other forms of blood cancer that serves as an invaluable research resource. In collaboration with other investigators at the University of Sussex, notably the Genome Centre and the Drug Discovery Centre, the Tissue Bank will facilitate the development of diagnostic assays for disease profiling and drug testing.

Finally, Timothy has established a highly regarded early phase clinical trial unit at CIRU (Clinical Investigation Research Unit), based at the Royal Sussex County Hospital. He is principal investigator for four studies in MDS and AML, including two for which he is the UK Chief Investigator, that aim to improve treatment options for patients using a variety of targeted therapies such as monoclonal antibodies, antisense molecules and DNA hypomethylation. The ambitious goal of the programme is to bring to the clinic a new and effective treatment in MDS/AML, discovered and developed at BSMS and the University of Sussex, over the next ten years.

Teaching

In recent years, BSMS has consistently ranked among the top medical schools in the UK for the quality of its teaching.  It has a vibrant and dynamic environment that encourages and motivates students to learn about human physiology, disease and clinical medicine. Timothy is the lead teacher on Blood Physiology course in year 1 (Heart, Lungs and Blood, Module 103), Cancer Biology course in year 3 (Scientific Basis of Medicine, Module 302) and Clinical Haematology in year 4 (Specialist Rotations, Module 402).  Timothy has twice been the runner-up best teacher on the BMBS course and recently received a University of Sussex Award for Excellence in Teaching.

Timothy is also the Director of Clinical Academic Training for BSMS, working closely with colleagues at Health Education Kent, Surrey and Sussex (HEKSS) and Brighton and Sussex University Hospitals Trust (BSUHT) to oversee the management of the highly successful Brighton Integrated Academic Training (IAT) Programme that comprises Academic Foundation Trainees and NIHR Academic Clinical Fellows and Lecturers. He has initiated the MRes research programme at BSMS and supervised numerous students undertaking BSc, Masters, and PhD degrees as well as mentoring IRP students and haematology AFP, ACF and SpR trainees.

Selected publications

Chowdhury B, McGovern A, Cui Y, Choudhury SR, Cho IH, Cooper B, Chevassut T, Lossie AC, Irudayaraj J. The hypomethylating agent Decitabine causes a paradoxical increase in 5-hydroxymethylcytosine in human leukemia cells. Sci Rep. 2015 Apr 22;5:9281.

Stewart HJ, Shalit E, Halliday L, Morey D, Chevassut TJ. Acute myeloid leukemia cells exhibit selective down-regulation of DNMT3A isoform 2. Leuk Lymphoma. 2015 Jun 19:1-4.

Robinson SD, Gabriel J, Webb A, Corbett T, Johnston R, Wright D, Chevassut TJ. Immunohistochemical prognostication in diffuse large B-cell lymphoma: a single center 6-year retrospective analysis. Leuk Lymphoma. 2015 Mar 6:1-3.

Ghurye RR, Stewart HJ, Chevassut TJ. Bromodomain inhibition by JQ1 suppresses lipopolysaccharide-stimulated interleukin-6 secretion in multiple myeloma cells. Cytokine. 2015 Feb;71(2):415-7.

O'Brien EC, Brewin J, Chevassut T. DNMT3A: the DioNysian MonsTer of acute myeloid leukaemia. Ther Adv Hematol. 2014 Dec;5(6):187-96.

Horne GA, Stewart HJ, Dickson J, Knapp S, Ramsahoye B, Chevassut T. Nanog requires BRD4 to maintain murine embryonic stem cell pluripotency and is suppressed by bromodomain inhibitor JQ1 together with Lefty1. Stem Cells Dev. 2015 Apr 1;24(7):879-91.

Stewart HJ, Horne GA, Bastow S, Chevassut TJ. BRD4 associates with p53 in DNMT3A-mutated leukemia cells and is implicated in apoptosis by the bromodomain inhibitor JQ1. Cancer Med. 2013 Dec;2(6):826-35.

Bisling KE, Brewin JN, McGovern AP, Horne GA, Rider T, Stewart HJ, Ramsahoye BH, Chevassut TJ. DNMT3A mutations at R882 hotspot are only found in major clones of acute myeloid leukemia. Leuk Lymphoma. 2014 Mar;55(3):711-4.

Brewin JN, Horne GA, Bisling KE, Stewart HJ, Chevassut TJ. Rapid detection of DNMT3A R882 codon mutations allows early identification of poor risk patients with acute myeloid leukemia. Leuk Lymphoma. 2013 Jun;54(6):1336-9.

McGovern AP, Powell BE, Chevassut TJ. A dynamic multi-compartmental model of DNA methylation with demonstrable predictive value in hematological malignancies. J Theor Biol. 2012 Oct 7;310:14-20.