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Enzyme discovery sheds light on causes of rare disease, cancer

Discovery of a new enzyme, PHF9, is providing insight into the biological processes involved in development of Fanconi anemia (FA), a rare genetic disorder that primarily affects children. The detection of the enzyme enhances understanding of the common DNA repair pathways involved in FA, as well as certain cancers and aging, scientists say. Better understanding of these pathways could lead to new therapies for Fanconi anemia.

Scientists at the National Institute on Aging (NIA) found that genetic mutations in an important protein complex inactivate PHF9. This disrupts critical intracellular repair mechanisms and leads to many serious complications associated with FA including the inability to make red blood cells.

"FA is a disease that appears to be the result of breakdowns in DNA repair mechanisms, which are important for all of us," said Weidong Wang, Ph.D., an investigator in the NIA's Laboratory of Genetics. "Some scientists theorize that DNA damage, which gradually accumulates as we age, leads to malfunctioning genes and deteriorating tissues and organs as well as increased risks of cancer as years go by. So every time we learn something more about DNA repair, we can hope to use that new knowledge to find ways to prevent the excessive damage to DNA that appears to occur with aging."

The finding is scheduled for advanced online publication in the journal, Nature Genetics (http://www.nature.com/ng/), during the week of September 14, 2003. The report also will be published in journal's October 2003 print edition.

Dr. Wang and his colleagues detected PHF9 and its corresponding gene while attempting to verify the existence of the Fanconi protein complex and identify its structure. Based on earlier work, the researchers suspected that the complex incorporated proteins produced by at least five previously known FA genes. Today's findings not only confirm that the complex exists, they also for the first tim
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Contact: Doug Dollemore
dollemod@nia.nih.gov
301-496-1752
NIH/National Institute on Aging
14-Sep-2003


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