SALT LAKE CITY A genomewide scan of millions of genetic mutations has revealed four new DNA "hotspots" that affect the risk for psoriasis, a national group of researchers led by the University of Michigan and including several from the University of Utah School of Medicine has shown in a just-published study.
Appearing Jan. 25 in Nature Genetics online, the study also confirmed that two other previously identified DNA sites, discovered by researchers at the University of Utah and Celera Group, have a high association with psoriasis, an automimmune disease that can affect the joints and cause sore, itchy patches of skin in an estimated 7.5 million people in the United States.
The study was led by James T. Elder, M.D., Ph.D., a dermatologist who heads a group at the University of Michigan with long-standing interest in and an international reputation for its work in the genetics of psoriasis, and Goncalo Abecasis, Ph.D., a biostatistician at the University of Michigan. They elected to make the study a collaboration with researchers at Washington University in St. Louis and the University of Utah. Gerald G. Krueger, M.D., professor of dermatology and Benning Presidential Endowed Chair holder at the U of U, and his colleague Kristina Callis Duffin, M.D., assistant professor of dermatology, led the Utah portion of the study.
Krueger and Duffin said the study is important for several reasons.
"First, it shows the efficacy of using this (genomewide) approach to further understand this disease," Krueger said. "Second, it confirmed findings we reported in 2007 of polymorphisms (mutations) in the IL-12/23 pathways. Third, we now find a third polymorphism in this same cluster, IL-23A. Fourth, a treatment that knocks down IL-12 and IL-23 recently has been shown to be a very effective treatment for psoriasis."
This, plus the clustering of polymorphisms the IL-12/23 pathways, makes it apparent that this pathway is
|Contact: Phil Sahm|
University of Utah Health Sciences