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Scientists Find Clue for the Prevalence of Bladder Cancer More in Men

t the story of the androgen receptor and male hormones like testosterone is much more complex than was once thought. For years it's been widely thought by doctors and scientists that all male hormones, and only male hormones, work through the androgen receptor.

But he felt there was more to the story. If anyone would know, it would be Chang, who in 1988 was the first person to clone the androgen receptor, and was the first to discover that the protein needs molecular allies called co-factors to accomplish many of its tasks. Now more than 80 co-factors are known, offering many new targets to stop conditions like male-pattern baldness and diseases like prostate cancer.

Nearly a decade ago, Chang showed that molecules other than male hormones like testosterone are able to activate the androgen receptor. That finding isn't simply gathering dust in textbooks; it likely explains why hormone therapy for men in the advanced stages of prostate cancer ultimately fails. His work explained a long-baffling phenomenon in these patients, where drugs that work well for a few years suddenly make the cancer grow again late in the course of the disease.

In the recent paper, Chang continued this line of work, only in bladder cancer instead of prostate cancer. He took a closer look at the nearly disease-free male mice that didn't get bladder cancer despite exposure to a carcinogen. Some of those mice then received a drug known as DHT, a male hormone. In theory, such a drug only works if the androgen receptor is present, so the drug should not have had an effect. But 25 percent of these mice then got bladder cancer, clear evidence that the hormone is able to somehow side-step the traditional, receptor-mediated, pathway and still have an effect.

The work shows starkly that simply cutting off the supply of hormones like testosterone will have only a limited effect. The androgen receptor can still play a crucial role in the development of canc
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