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Cancer gene is normally a 'carpenter' in the cell

DURHAM, N.C. -- A gene whose malfunction causes several leukemias normally functions as a "molecular carpenter," Duke pharmacologists have discovered. The gene, called c-Abl, triggers other molecules that construct the internal framework of cells.

According to the scientists, this discovery of c-Abl's normal function could reveal new targets for cancer drugs, and it also hints at a role for c-Abl in the brain, in building nerve cells and aiding their movement.

In an article in the September issue of Genes & Development, the researchers reported that c-Abl is mainly switched on by another protein called Src, which is also known to cause cancer when it malfunctions. Src, in turn, is activated by external growth factors such as PDGF and EGF. Growth factors are substances outside the cell that trigger them to proliferate. Once activated, c-Abl itself acts as a trigger for the cell to reorganize the internal framework, called the cytoskeleton, that gives cells their shape and allows them to move.

"We have long understood many of the things that the oncogenic, or cancer-causing, forms, of c-Abl do," said Ann Marie Pendergast, associate professor of pharmacology and cancer biology, who led the research. "But because we did not know the normal function of c-Abl, we have been missing a critical part of the picture of how the cancer-causing forms take over the cell's machinery. "If we knew how c-Abl functioned normally, we would know more precisely how the oncogenic forms alter cell function."

Lead author on the Genes & Development paper is postdoctoral fellow Rina Pattner, and other authors besides Pendergast are Lisa Kadlec, Kris DeMali and Andrius Kazlauskas. Their work was supported by the National Cancer Institute and by the Glaxo Wellcome Collaborative Program in Cancer Research.

According to Pendergast, studies over the last decade had revealed c-Abl's key role in producing two forms of leukemia-
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Contact: Dennis Meredith
Dennis.meredith@duke.edu
919-681-8054
Duke University
28-Sep-1999


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