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The £8.6 million study, funded by the Wellcome Trust, is expected to provide critical clues that will bring new approaches to the treatment of conditions such as diabetes, heart disease and arthritis.
The Case Control Consortium, which includes 25 British research groups, will study the genetic peculiarities of more than 20,000 people to reveal variations in DNA that make them more or less likely to develop particular medical disorders.
The study will cover eight diseases that account for much of the ill health in Britain: coronary heart disease, hypertension, types 1 and 2 diabetes, bipolar disorder, Crohn’s disease, rheumatoid arthritis and tuberculosis.
A subsidiary project will look at a smaller number of genetic variations that play a part in multiple sclerosis, auto-immune thyroid disease, breast cancer and the spinal disorder ankylosing spondylitis.
For each of the main eight diseases, scientists will read the genetic codes of 2,000 sufferers and analyse variations that may play a part in causing or preventing its development.
These variations, which are known as single nucleotide polymorphisms, or SNPs (pronounced “snips”), will then be compared with DNA taken from a control group of 3,000 healthy people.
The scientists believe that they will find patterns not present in healthy individuals.
“The aim is to identify DNA variants which play a role in susceptibility or resistance to these diseases,” said Peter Donnelly, professor of statistical science at Oxford University, who is one of the study leaders. “There may be variants that make it more likely that you will get type 2 diabetes, and other variants that have a protective effect against the same disease. With most of these diseases, we understand little about the causes. If we can learn that this gene makes you more or less susceptible, we get important clues as to how the disease works.”
He added: “Once we understand these diseases better, through the foothold that the genetics provide, the hope would then be that we would see obvious or plausible candidates for drug therapies.”
The work may help to match treatments to patients whose genes may make them more responsive to certain drugs.
Professor Donnelly said: “Many of the things that we think of as one disease may be, when we understand them better, collections of similar symptoms caused by different biological processes. When a car overheats, you would not always try to repair it the same way — you want to find out the reason why it overheated and fix that. At the moment we often have only one or two sets of drugs for these diseases.”
Not all the effects will necessarily come from genes; variations in the so-called “junk DNA” that makes up most of the human genome will also be studied, as it is thought this plays an important role in switching genes on and off.
For seven of the diseases, all the case volunteers are from Britain and their DNA has already been collected. The same group of 3,000 controls will be used for all these studies.
For tuberculosis, the study group comes from the Gambia in West Africa.
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