Its prevalence differs widely among different geographic areas.
To account for the environmental factors associated with the disease, researchers structured their investigation to ensure that cases of childhood asthma were matched to children without disease from the same geographical areas.
The team of scientists, including Liming Liang, a U-M doctoral student in Abecasis' lab and co-first author on the paper, compared the genetic makeup of 994 patients with childhood onset asthma and 1,243 non-asthmatics. They looked at mutations in the building blocks that make up DNA, called nucleotides.
There are mutations in around one in every 600 nucleotides, and scientists examined more than 317,000 of these mutations, known as single-nucleotide polymorphisms, to find those specific to childhood asthma. The researchers also looked at how genes were being expressed within human blood cells. The U-M was one of the major data analysis sites.
The team confirmed its findings by analyzing the genetic makeup of more than 2,000 children from Germany and more than 3,000 subjects from the United Kingdom born in 1958 and monitored until now for the presence of disease.
"This is a large study involving doctors and scientists from many countries, and we are confident that we have discovered something new and exciting about childhood asthma," said Dr. Miriam Moffatt of the National Heath and Lung Institute, Imperial College, London, and one of the first authors of the study.
"These novel findings do not explain completely how asthma is caused, but they do provide a further part of the gene-environment jigsaw that makes up the disease. We and our colleagues are currently preparing even bigger studies to find other genes of smaller effect and to relate these to environmental factors that increase asthma risk."
Professor William Cookson, also of the National Heart and Lung Institut
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