irectly influence disease susceptibility, and the actual causative variant may lie nearby. This means researchers often need to take additional steps, such as sequencing every DNA base pair in that particular region of the genome, to identify the exact genetic variant that affects disease risk.
In the latest work, researchers began by scanning the genomes of more than 2,300 Finnish people who took part in the Finland-United States Investigation Of NIDDM Genetics (FUSION) and Finrisk 2002 studies. About half of the participants had type 2 diabetes and the other half had normal blood glucose levels.
"We thank all the Finnish citizens who participated in this study. Their generosity has created a lasting legacy that will help to reduce the terrible toll that diabetes is taking on the world's health," said Dr. Tuomilehto of the Diabetes Unit in Finland's National Public Health Institute.
To validate their findings, the researchers compared their initial results with results from genome scans of 3,000 Swedish and Finnish participants in the Diabetes Genetics Initiative and 5,000 British participants in the Wellcome Trust Case Control Consortium, led by Peter Donnelly, D.Phil., Oxford University. After identifying promising leads through this approach, the three research teams jointly replicated their findings using smaller, more focused sets of genetic markers in additional groups totaling more than 22,000 people from Finland, Poland, Sweden, the United Kingdom and the United States. All told, the genomes of 32,554 people were tested for the study, making it one of the largest genome-wide association efforts conducted to date.
"This is a phenomenal accomplishment, in terms of both the breadth and depth of the research. By pulling together and sharing their data, these three groups were able to achieve far more than any one of them could have done alone," said Eric D. Green, M.D., Ph.D., director of NHGRI's Division of Intra
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