"Until we get a better sense of what all the modifiers are and how they interact, the field is just not advanced enough," he said.
Researchers must first figure out how IFRD1 fits into the constellation of known and unknown CF gene modifiers and how it carries out its functions on a molecular level.
The study could drive new drug development, however, both at the level of IFRD1 itself and, more generally, at the level of neutrophil activity. In fact, Karp noted that the second most promising genetic location his team identified lies between two other genes also implicated in neutrophil development.
Though the data might not yet support a major drug development effort, Penland stressed that it is clear that people with CF need therapies that treat the underlying disease processes, not just provide symptom relief. "Therefore, what you would in the end have is patients who may die with CF rather than dying from CF," he said.
According to the Cystic Fibrosis Foundation, CF affects about 30,000 people in the United States and 70,000 worldwide.
More information
The Cystic Fibrosis Foundation has more on cystic fibrosis.
SOURCES: Christopher Karp, M.D., Gunnar Esiason/Cincinnati Bell chairman and director, Division of Molecular Immunology, and director, Cystic Fibrosis Research Center, Cincinnati Children's Hospital Medical Center, Cincinnati; Chris Penland, Ph.D., director, research, Cystic Fibrosis Foundation, Bethesda, Md.; Robert Giusti, M.D., chief, pediatric pulmonology, and director, Cystic Fibrosis Center, Long Island College Hospital, Brooklyn, N.Y.; Feb. 25, 2009, Nature, online
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