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Christopher Buckley joins the Kennedy Institute as a new Director of Clinical Research from May 2017.

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Chris joins the Kennedy Institute from the University of Birmingham, where he was previously Arthritis Research UK Professor of Rheumatology. In this new post as Kennedy Professor of Translational Rheumatology he takes up a joint appointment between the two universities; as director of Clinical Research at the Kennedy Institute in Oxford and Director of the NIHR Wellcome Trust Clinical Research Facility in Birmingham.

In his new position Chris will oversee the Arthritis Therapy Acceleration Programme (A-TAP), a translational research initiative aimed at speeding up the development and testing of new therapies for joint and related inflammatory diseases. He will also lead a research group at the Kennedy Institute focused on stromal cell biology and inflammatory disease. The A-TAP brings together basic science at the Kennedy Institute with clinical research capabilities at the Botnar Research Centre (Oxford) and the Institute of Translational Medicine (Birmingham).

Chris will facilitate the development of a partnership of clinical colleagues at five different NHS organizations along the M40 corridor. These include the Nuffield Orthopaedic Hospital, John Radcliffe Hospital, University Hospitals Coventry and Warwickshire, University Hospitals Birmingham, Sandwell and West Birmingham Hospitals incorporating the Modality Primary Care Vanguard service.  This “M40 alliance” will establish a network of clinical centres, covering over 6 million people along the M40 corridor allowing  enhanced access to patient cohorts and tissue samples to enable translational research to dissect molecular drivers of disease.  It will allow the design and delivery of experimental medicine studies to test new drugs in carefully selected patient populations at pace, at scale and on time. As Chris says “cohorts are kings; biomarkers are beggars; data is dynamite”

Professor Fiona Powrie, Director of the Kennedy Institute, said: “The partnership between the Universities of Oxford and Birmingham will harness the existing research strengths of both universities in order to accelerate the development and testing of new therapies for patients. The Arthritis Therapy Acceleration Programme (A-TAP) will develop and test therapies based on the underlying causes of inflammatory disease, rather than simply treating their clinical symptoms”

Speaking of his new position, Chris explains: 'The current rate limiting step in experimental medicine is not how to design new and safe drugs but how to improve their efficacy beyond the current best treatments. We also don’t know how to best match the right drug to the right disease. Our A-TAP will use strategies that have worked in the cancer field to both repurpose drugs to new indications, as well as use innovative concepts in trial design such as “cluster trials” where one drug is tried out in a range of different inflammatory diseases at an early stage. This process-driven-pathway- focused approach to the four immune mediated inflammatory diseases to be studied in the A-TAP (rheumatoid arthritis, sjogrens syndrome, spondyloarthropathy and inflammatory bowel disease)  will help us work out which drug is most likely to work for which disease at a much earlier stage than is currently possible.'

So what can you expect to see develop in the next 12 months? “We need more clinical fellows working with basic scientists in the Kennedy Institute to encourage a culture of translation” explains Chris. “Breaking down the silos between bedside and bedside is just as important as between the bench and the bedside. Removing these silos will encourage a more process drive approach to inflammation, fibrosis and repair; three key pillars of research at the Kennedy Institute. We have much to learn across clinical disciplines; that’s what the therapeutic use of biologics has taught us. Shared processes across different organs mean that we need clinical fellows from different disciplines working on the common process that underpin inflammation, fibrosis and repair. This might even lead to a new taxonomic approach to disease, based on underlying pathogenic drivers, rather than just the clinical symptoms in the organs in which disease first presents. Only then can we expect to see the molecular marker match the pathogenic mechanism”.

The ATAP is funded by a £7m strategic award from the Kennedy Trust for Rheumatology Research.