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Building on basics

Prostate Progress

A landmark experiment sheds light on how some prostate cancers become untreatable - and how this deadly process can be prevented.

Xu Bao Shi is checking on his mice. Housed in pairs, the rodents share shoe-box-sized plastic containers in a squeaky-clean, climate-controlled room on the UC Davis Medical Center campus.

They are nude mice, bred to be hairless. All are female. This morning they’re napping in the wood shavings carpeting their containers, grazing on food pellets or drinking from their water bottles. Shi, a cancer research biologist, takes the lid off one of the containers and scoops up a mouse. Cupping the red-eyed, pink-skinned animal in the palm of his hand, he notes a pea-sized tumor, the color of a bruise, on its hip. Shi returns the mouse to its container and picks up its housemate. It, too, has a small bluish growth on its flank.

The growths are tiny, but they represent a significant step forward in prostate cancer research. They prove that p53 mutations play a direct role in the development of androgen independence, a poorly understood process that can render prostate cancer untreatable. By identifying p53 mutations as a causative factor in this lethal process, UC Davis Cancer Center researchers have moved medicine one step closer to controlling it.

Nearly 190,000 men develop prostate cancer every year, and a substantial proportion eventually wind up on a hormone treatment known as androgen suppression therapy. The therapy works because prostate cancer cells depend on testosterone, a type of androgen, for their growth. Depriving the cells of androgen weakens or even kills them.


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Message to Editor
Supporting Cancer Center
UC Davis Cancer CenterUC Davis Health System

Through animal research, Xu Bao Shi is learning what makes prostate cancer untreatable.