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Growth factor gene shown to be a key to cleft palate
Date:2/2/2010

developed cleft palate.

In palate cells grown in the lab, the researchers looked at the FGF cell-signaling network, in which FGFR2 participates. They compared the effect of increased activity of FGF signaling with decreased activity of the same network, and interestingly, both led to cleft palate.

"We found that overactivation of an important signaling pathway resulted in loss of function," Snyder-Warwick says. "Our results suggest a different way of thinking about mutations in the FGF signaling network. This study clearly showed that this FGF signaling pathway is a critical regulator of palate development."

These findings strengthen the evidence that the developmental processes in which FGFR2 is involved could be targeted with drugs in order to ensure normal palate growth.

"It's possible that someday doctors might be able to administer drugs that would either slightly activate or slightly inhibit FGFR2 function," Ornitz says. "That might be enough to tip the balance from a cleft palate to a normal palate during embryonic development."


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Contact: Gwen Ericson
ericsong@wustl.edu
314-286-0141
Washington University in St. Louis
Source:Eurekalert

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