This prestigious 3-year Fellowship aims to stimulate new scientific discovery and translation and to facilitate skills and people transfer between researchers in academia and industry.
Celgene is a global biopharmaceutical company that uses cutting-edge technology and innovative science to discover new medicines for patients. In partnership with the Oxford Medical Sciences Division, Celgene has co-developed and provided support for a Translational Research Fellowship Programme.
The goals of this scheme are to stimulate new scientific discovery and translation and to facilitate skills and people transfer between researchers in academia and industry.
This programme offers fellows an opportunity to gain exposure to the field of commercial drug discovery and development. Fellows will have an assigned company mentor and where appropriate be encouraged to spend some time based in Celgene's laboratories.
Funding will be awarded to Oxford Principal Investigators to support 3 year fellowship projects for early career researchers that demonstrate a clear translational value to the advancement of therapeutics. Three to four awards are made annually.
Currently there are 16 fellows working with Celgene and you can read about their projects here.
Fellowship funding may be used to support clinical (Grade E64) or basic research scientists (Grade 7/8) committed to translational science and interested in obtaining experience with drug development in an industrial setting.
Fellowship applications may include a named fellow, but this is not necessary as the project selection criteria are driven by scientific fit with company science and expertise.
It is expected that a suitable fellowship candidate will be identified by the Principle Investigator within 6 months of notification of successful project selection.
Prospective Principle Investigator applicants should submit their project online via the Internal Research Award Management System (IRAMS) using the standard application form (this form is also available through IRAMS).
If a proposed fellow is known at the application stage, please include their CV at the end of the form. Applicants can only upload a single PDF to IRAMS so multiple PDFs will need to be combined.
Applicants should notify their departmental administrators of their intention to submit a proposal (information on the fellowship terms for Department administrators and HoDs can be found here).
Applications must be signed off by Department Heads and Departmental Administrators before final submission on IRAMS.
Proposals should be targeted to research areas of interest for Celgene which can be found here.
If you would like to book a 1:1 to discuss you potential application with Celgene Scientists on Tuesday 19th March 2019, please complete the Pre-application questions and email to firstname.lastname@example.org before 12 noon on Monday 25th February.
Full proposals will be reviewed by a Joint Steering Committee in mid-June.
Following notification of an award, successful applicants are required to liaise with Celgene to ensure the workplan and timelines are acceptable to both parties, prior to the project agreement (contract) being signed.
Successful applications with a named fellow could expect to begin from 1st Oct 2019 (subject to contracting)
Projects needing to recruit a fellow could expect to begin from 1st Jan 2020 (subject to contracting and ease of recruitment)
The 2019 call for Fellowship Applications has now closed.
For all enquiries please contact Charlotte Bell, Industry Partnerships Manager, Medical Sciences Division Business Development and Partnering Team
If you would like to book a 1:1 to discuss you potential application with Celgene Scientists on Tuesday 19th March 2019, please complete the pre-application questions and email to email@example.com before 12 noon on Monday 25th February.
'Definition of new drug targets for fibrosis in Crohns'
PI: Alison Simmons
'Protein kinase C-θ and PD-1 as a therapeutic target in inflammatory arthritis'
PI: Graham Ogg, Peter Taylor, Mike Dustin
'Single cell analysis of the fibrotic landscape in Dupuytren's Disease'
PI: Jagdeep Nanchahal
'Unravelling the role of E2F-1 citrullination in inflammatory disease'
PI: Nick La Thangue
'Defining an early signature of neutrophil extracellular trap formative predictive of responses to PAD4/2 inhibitors in rheumatic patients'
PI: Irina Udalova, Raashid Luqman
'Determining changes in clonal/sub clonal architecture and relation to immune marrow environment enabling tumour persistence/relapse in myeloma'
PI: Paresh Vyas, Udo Oppermann, Karthik Ramasamy
'Inhibition of alpha-synuclein
PI: Richard Wade-Martins
'Ultra low-dose IL-2 therapy in autoimmune diabetes'
PI: John Todd, Claudia Monaco
'Checkpoint blockade-mediated autoimmune colitis as a model for gut immune homeostasis'
PI: Paul Klenerman, Oliver Brain
'Clonal and Functional heterogeneity in AG221-treated IDH2 mutant Acute Myeloid Leukaemia'
PI: Paresh Vyas
Inhibition of alpha-synuclein aggregation and glial activation as a therapeutic strategy for Parkinson’s disease
Supervisors: Richard Wade-Martins (Oxford) and Irit Rapley (Celgene)
Fellow: Nora Bengoa-Vergniory
Several lines of research have shown that a-syn aggregation is the underlying cause of PD, and astrocytes and microglia have also been reported to play an important role in a-syn clearance and neuro-inflammation. Therefore, the aim of this project is to determine the role of glia in a-syn clearance, development of neuro-inflammation and neuronal cell death in the central nervous system using in vitro and in vivo models, in order to find novel therapeutic strategies for PD. With in situ detection methods for a-syn aggregation, patient derived iPSCs, protocols to differentiate them into neurons, microglia or astrocytes, and a highly relevant mouse model, we will be able to determine the roles glial cells play in the “oligomeric progression” of the disease. This will not only allow us to paint a global picture of the disease, but also to take advantage of these insights in order to translate findings into therapeutic approaches, which will ultimately result in an important advance for PD.
PKC-Θ AND PD-1 AS A THERAPEUTIC TARGET IN INFLAMMATORY ARTHRITIS
Fellow: Liliana Cifuentes
This project will apply advanced imaging and use of small molecule inhibitors to understand the role of PKC-θ in the pathobiology of inflammatory arthritis. In conventional T cells PKC-θ co-localises with the TCR and is necessary for downstream signals, whereas in regulatory T cells PKC-θ adopts a distal position and negatively regulates suppressive function. This study will examine the localisation and function of PKC-θ in conventional and regulatory T cells from patients with inflammatory arthritis or healthy controls. Insight provided by these studies will guide development of PKC-θ small molecule inhibitors as therapeutic agents. The co-inhibitory molecule PD-1 is upregulated on chronically stimulated T cells and delivers signals that inhibit T cell function. These studies will also evaluate the combination of PD-1 agonists and PKC-θ inhibitors as an approach to inhibit T cell responses.
UNRAVELLING PRO-FIBROTIC TNF SIGNALLING PATHWAYS IN DUPUYTREN'S DISEASE
Fellow: Thomas Layton
Dupuytren's disease is a fibrotic disorder of the hand in which the fingers progressively curl irreversibility into the palm. Recent studies showed TNF converts palmar fibroblasts from Dupuytren's patients into myofibroblasts that are responsible for matrix deposition and contraction in fibrotic disorders. The goal of this project is to identify pro-fibrotic TNF signalling pathways for development of highly specific therapeutics in Dupuytren's and other fibrotic disorders. Planned studies will investigate the molecular pathway through which TNF cooperates with canonical Wnt signalling to promote palmer fibroblast cell differentiation as well as the upstream regulators of TNF secretion. These studies will apply ex vivo models using samples from disease tissues. Data generated by these studies will complement a clinical trial of TNF inhibition for early Dupuytren's disease.
DEFINITION OF NEW DRUG TARGETS FOR FIBROSIS IN CROHN'S
Supervisors: Professor Alison Simmons (Oxford) and Kamal Puri (Celgene)
Fellow: Hannah Chen
Fibrosis is a common complication of inflammatory bowel disease that is neither prevented nor reversed by current anti-inflammatory therapies. This project will apply new methodologies for isolation and molecular phenotyping of stromal cells from colonic or small bowel biopsies. This analysis will allow reclassification of intestinal stromal subsets and will provide insight into subset composition in IBD or IBD fibrotic tissues compared with healthy controls. In addition, stromal cells subsets isolated during different stages of disease will be examined for responses to innate stimuli to uncover molecules or pathways that contribute to the pro-fibrotic state. This project will advance mechanistic understanding of intestinal fibrosis in human disease and may reveal targets for development of biomarkers or new therapies.