Wellcome-Beit Prize Fellowships
The Wellcome-Beit Prize Fellowships are intended to provide additional recognition for four outstanding biomedical researchers who have been awarded other Wellcome Trust fellowship funding. The awards were inaugurated in 2009 and replaced the Beit Memorial Fellowships for Medical Research.
The Beit Memorial Fellowships were originally founded and endowed in 1909 by Sir Otto Beit as a memorial to his brother Alfred, to promote the advancement by research of medicine and allied sciences, and their relation to medicine
£25 000 is awarded to each of four selected Research Career Development Fellows, Sir Henry Dale Fellows or Intermediate Clinical Fellows in addition to the salary and research expenses already to be funded by the Wellcome Trust. The £25 000 prize money can be used flexibly in support of the fellows' ongoing research.
Wellcome-Beit Prize Fellowships are considered during the interview process for Wellcome Trust Research Career Development Fellowships, Sir Henry Dale Fellowships and Intermediate Clinical Fellowships. No separate application is required.
Details of awarded Fellows
Researchers who have been awarded a Wellcome-Beit Prize Fellowship since 2009 and information about the work they are carrying out during their Fellowship. Information about individuals awarded the Beit Memorial Fellowship for Medical Research before 2009 is available in the
Dr Bungo Akiyoshi, University of Oxford
Elucidating the mechanism of chromosome segregation in Trypanosoma brucei
From September 2013, Bungo will be working in the Department of Biochemistry, University of Oxford, studying trypanosomal kinetochores as a group leader.
Dr Francesca Barone, University of Birmingham
The role of leukocyte-stromal cell interactions in the pathogenesis of salivary gland inflammation and Sjogren's Syndrome
Dr Paul Bays, University College London
Prioritisation of sensory resources for action in the healthy and lesioned brain
Paul is interested in how we use short-term memory and visual attention to guide our actions. He conducts psychophysical, memory and motor performance experiments to investigate these topics in both healthy individuals and neurological patients. His goal is to identify computational mechanisms underlying sensory control of action, and relate them to the neural processes by which they are implemented in the nervous system.
Dr Michael Chapman, University of Cambridge
The role of aberrant RNA processing in the pathogenesis of multiple myeloma
Dr Mark Dawson, University of Cambridge
Chromatin regulation of self-renewal transcriptional programmes in leukaemia stem cells
Mark has spent his Fellowship helping to establish a novel therapeutic paradigm for the treatment of aggressive haematological malignancies. His work, published in 'Nature' in 2011, demonstrated that targeting chromatin/epigenetic readers could provide excellent efficacy in acute myeloid leukaemia. This study, with others, has provided the platform for phase I clinical trials with this new class of compounds. In addition, Mark has authored three book chapters and nine other manuscripts and has been invited to speak at several national and international conferences on cancer epigenetics. These opportunities have strengthened his long-term ambition to be a leading researcher in this field.
Dr Yi Feng, University of Edinburgh
Live imaging and genetic analysis of the inflammatory response upon oncogene-induced tissue homeostasis disruption and its contribution to tumour initiation in zebrafish larvae
Yi’s lab at the MRC Centre for Inflammation Research at the University of Edinburgh uses a combination of live imaging and genetic analysis in zebrafish to study the earliest events of tumour initiation in vivo. Her research focuses on interactions between normal host tissue with transformed cells and infiltrating innate immune cells, and she has demonstrated that the latter mount a trophic response toward emergent transformed cells. Her research aims to understand underlying cellular and molecular mechanisms regulating this trophic inflammation response during tumour initiation.
Dr Eva Frickel, National Institute for Medical Research
A new perspective on anti-Toxoplasma immunity
The long-term goal of Eva’s group is to identify novel pathways and mechanisms of host resistance to Toxoplasma gondii. This protozoan parasite infects a broad range of hosts, with a seroprevalence in man of about 30 per cent. It is unclear how Toxoplasma maintains the intricate balance between survival and host defence. Eva is studying how the parasitophorous vacuole is remodelled within host cells to limit parasite replication, as well as how antigen processing is facilitated for presentation to CD8 T cells. In addition, she is characterising the properties and phenotype of memory CD8 T cells in the Toxoplasma-infected brain.
Dr Serge Mostowy, Imperial College London
Controlling the intracellular fate of cytosolic pathogens
Serge studies how host cells control infection by cytosolic host responses, including autophagy and cytoskeleton reorganisation. Using bacterial infection, his research is currently focused on identifying and characterising host and pathogen determinants underlying the intracellular fate of cytosolic bacteria, and investigating the role of discovered molecules and mechanisms in vivo using zebrafish models of bacterial infection. Completion of these objectives may suggest the development of new therapeutic strategies aimed at bacterial infection, and possibly other disease states that also implicate cytosolic host responses.
Dr Serena Nik-Zainal, Sanger Institute
Exploring the biological processes underlying mutational signatures identified in cancers
Somatic mutations in cancer genomes have been generated by multiple DNA damage processes, the effects of which are mitigated by the cellular repertoire of DNA repair pathways. Each process leaves a characteristic imprint, or mutational signature, on the cancer genome. Current biological understanding of these mutational signatures is remarkably limited. Serena aims to explore the biological basis of mutational signatures that emerge from cancer genomes by studying mutational signatures that arise in patients with inherited genetic defects in DNA repair/replication machinery. She will also explore signatures generated through the experimental manipulation of components of the DNA repair/replicative machinery in model systems.
Dr Elspeth Payne, UCL
Identifying novel therapeutics and disease mechanisms for ribosomal protein-mediated human haematopoietic diseases
Beth is a haematologist with an interest in bone marrow failure and myelodysplastic syndromes. Her Fellowship focuses on understanding the contribution of aberrant protein translation in haematopoietic cells of patients with ribosomal protein disorders and identifying novel therapeutics through in vivo chemical screens using the zebrafish model.
Dr Markus Ralser, University of Cambridge
Genome-wide analysis of the interactions that mediate communication between central carbon metabolism and the cellular regulome
Markus is interested in the stability and regulatory role of the metabolic network during ageing and the stress response. Regulatory mechanisms that involve the metabolic network are studied by combining mass spectrometry and functional yeast genomics. His laboratory is primarily interested in dynamic metabolic rearrangements within central carbon metabolism, and their influence on growth and ageing of eukaryotic cells.
Dr Rhys Roberts, University of Cambridge
The Charcot-Marie Tooth diseases and associated defects in membrane transport
Rhys is based at the Cambridge Institute for Medical Research, investigating the inherited peripheral neuropathy Charcot-Marie-Tooth disease. He is focusing on the demyelinating forms of the disease, in which many of the patient-associated mutated genes encode proteins known to have important roles in intracellular membrane transport. Rhys's overall goal is to understand the molecular mechanisms that underlie peripheral nerve myelination by Schwann cells and the processes that become dysfunctional when disease-associated genes are mutated.
Dr George Tofaris, University of Oxford
Studies on alpha-synuclein degradation and its relevance to Lewy body disease
George is using his Fellowship to establish his laboratory at the University of Oxford. He aims to study mechanisms of lysosomal degradation and their relevance to Parkinson's disease. He is also investigating whether key enzymes in these pathways could be targets for neuroprotective therapies.