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Building on basics Profiling the Enemy

Sweeney, who came to UC Davis in 2000 after four years as a postdoctoral research fellow at Harvard Medical School, has already made important headway.

She decided to investigate a molecule known as PI-3 kinase, whose function is to help cells move from one location to another when needed during early development or in wound healing. When PI-3K is not needed, it is kept in check by a regulator gene known as PTEN.

While normal bladder and most superficial bladder cancers have a functioning PTEN gene, a significant proportion of invasive bladder cancers have lost PTEN function — suggesting PTEN may be a key to invasion.

Sweeney’s work further indicts PTEN. In a series of experiments using cultured bladder cancer cells, she has discovered that when
PI-3K activity is blocked, or normal PTEN is restored to invasive bladder cancer cells, the cells lose their invasiveness.

“Tumors take advantage of PI-3K by deleting the PTEN regulator,” she says. “Tumors have recognized this is a pretty good pathway to target. By destroying PTEN, they get the opportunity to metastasize.”

Sweeney’s discovery reveals a potential target for a future anti-cancer drug — one capable of suppressing PI-3K, or substituting for PTEN.


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