Turning tables on prostate cancer's drug resistance

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Turning tables on prostate cancer's drug resistance
10 March 2010
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DRUGS that keep prostate cancer at bay often stop working after a few years. That now appears to be because they prompt the growth of the very tumour cells they are meant to kill. It's not all bad news, though: blocking this growth pathway could buy time for men with drug-resistant tumours.

Most early prostate cancers require male sex hormones, known as androgens, to grow. Anti-androgen drugs can cause these tumours to regress, but eventually they become resistant to them and start to grow again. Yet unlike other drug-resistant cancers, these tumours have no telltale mutations.

To learn how prostate tumours become drug resistant, researchers led by Michael Karin at the University of California, San Diego, implanted prostate tumours into mice and gave them anti-androgens. They found that the resulting death of the tumour cells led to an inflammatory response in which white blood cells converged on the tumour and secreted a signalling molecule called lymphotoxin. This in turn triggered an androgen-independent cell-growth pathway in the remaining tumour cells (Nature, DOI: 10.1038/nature08782).

The researchers have yet to show the same pathway is active in human prostate cancers. If it is, it offers a promising way to delay tumour resistance. Blocking the lymphotoxin pathway in mice caused tumours to remain dormant for three to four additional weeks, equivalent to two to three years of remission in humans, Karin says.