
Major cash boost For two leading Oxford geneticists
TWO Oxford geneticists, at the forefront of tracking down the genes responsible for an incurable rheumatic disease, have been given a major cash boost of more than half a million pounds by a leading medical research charity.
Dr Paul Wordsworth and Dr Matthew Brown, of the Wellcome Trust Centre for Human Genetics in Headington, have been awarded a five-year programme grant of £632,580 from the Arthritis Research Campaign, to help them establish the genetic basis for ankylosing spondylitis.
Dr Brown also has a £300,00 three-year Clinician Scientist Fellowship from the charity.
Around 115,000 people in the UK have AS, which leads to inflammation and severe stiffness of the spine and less frequently other joints, causing pain, tiredness and discomfort.
"AS runs in families and is largely caused by genetic factors, but otherwise we know very little about what causes the disease, and there is no treatment which slows down progress," explained Dr Wordsworth, clinical reader in rheumatology the Nuffield Department of Medicine.
"Preliminary studies by our own group have localised regions of certain chromosomes which may contain genes relevant to causing the disease. One of these, known as HLA-B27, accounts for about a quarter of the genetic risk.
"This programme aims to find the remaining genes involved by a variety of methods which have been shown to be effective in tracking down such disease genes in other complex genetic traits such as diabetes. One particular candidate is already being targeted by the Oxford team."
A better understanding of the genetic causes of the disease will enable the team to understand what causes the disease, result in better diagnostic tests, and ultimately lead to the development of preventative therapies.
- Dr Frances Hall, of Stanford University in California, has been awarded an ARC Clinician Scientist Fellowship of £422,088, to be based at the Institute for Molecular Medicine at the John Radcliffe Hospital, investigating immune responses to human cartilage antigen and their role in the perpetuation of arthritis.





