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Researchers uncover gene related to acute leukemia

Vanderbilt-Ingram Cancer Center researchers have uncovered another clue in the mystery of how chromosomal translocations cause acute leukemias. The findings suggest new treatment possibilities for these cancers of the bone marrow and blood.

In the October 26th issue of the Proceedings of the National Academy of Sciences, Scott W. Hiebert, Ph.D., professor of Biochemistry and Medicine, and colleagues report the molecular outcome of the most frequent translocation in acute myeloid leukemia (AML). The inv(16) translocation results in the production of a protein that collaborates to turn genes off, even when they should be turned on.

"This work really changes the paradigm for thinking about how this molecule works. And now that we know how it works, we can start thinking about potential therapies that block its action," Hiebert said.

Acute leukemia is a rapidly progressing disease and results in the accumulation of immature, functionless cells in the blood that interfere with the body's production of healthy blood cells. According to the Leukemia Society of America, 12,500 new cases will be diagnosed and some 7,900 persons will die from acute leukemia this year. About half of all acute leukemias are caused by chromosomal translocations, Hiebert said.

A chromosomal translocation happens when chromosomes--the structures containing genes--break and rejoin in a different way, creating new genes at the breakpoints. Think about breaking up a red stick and a blue stick, mixing up the pieces, and gluing them back together to make two new sticks. If the sticks were chromosomes, new genes would be created where red meets blue. Hiebert's goal has been to figure out what these new red-blue genes do, and how they participate in causing cancer.

The current work focuses on inv(16), the most frequent of several translocations associated with AML. Inv(16) happens when the middle section of chromosome 16 breaks and flips around--an inversion translocation.


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Contact: Cynthia Manley/Matt Scanlan
matt.scanlan@mcmail.vanderbilt.edu
615-322-4747
Vanderbilt University Medical Center
25-Oct-1999


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