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$5.9 million grant adds androgen receptor as a new driver and target in breast cancer
Date:10/1/2013

ting androgen receptors in these androgen receptor-positive (AR+) tumors can stop their growth in almost exactly the same way that doctors have used anti-estrogen therapies with ER+ tumors.

"Our preclinical work is extremely promising and we're just now starting to get results from studies in models of breast cancers resistant to current therapies. If this promising work leads to good clinical results, we could offer a new treatments for breast cancer patients who have previously been without further options," Richer says.

Dr. Elias's patient, Linda Griffin, puts it another way: "If this works, it'll make history," she says.

Androgen is not a new target in cancer. Androgens including testosterone have long been implicated as a driver of prostate cancer and so many drugs targeting both the body's production of androgens and cancer cells' ability to use the hormone are already approved, with even more treatments in the drug development pipeline. The current clinical trial uses the especially promising anti-androgen drug, Enzalutamide, which was FDA-approved in August 2012 for use in castration-resistant prostate cancer.

"Normally, the way these hormones work is by attaching to receptors in the cell cytoplasm, at which point the receptor draws itself and the hormone molecule inside the nucleus where it regulates many genes," Richer says. The genes turned on and off by ER, PR, HER2 or, now, androgen tell breast cancer cells to survive and reproduce beyond control. Enzalutamide makes androgen receptors unable to go into a cell's nucleus and so the message of growth never gets delivered.

"Interestingly, it seems that estrogen-positive breast cancers are susceptible to the same drug," Richer says, explaining that something about the way the signal of estrogen is transmitted inside a cell's nucleus requires the presence of androgen receptors in the nucleus, as well. Without androgen receptors in the nucleus, estrogen receptors may n
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Contact: Erika Matich
erika.matich@ucdenver.edu
303-724-1528
University of Colorado Denver
Source:Eurekalert

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