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A new animal model for prostate cancer
  
By
Charles W. Schmidt


Scientists recently engineered mice to develop cancerous tumors similar to those in humans with prostate cancer, creating a new animal model for studying the disease. Andrew Koff, of Memorial Sloan-Kettering Cancer Center, where the mice were developed, says the discovery may improve pre-clinical drug studies and enable researchers to better test hypotheses on how to treat prostate cancer in human patients.

To create the mice, the researchers inactivated a gene called PTEN, as well as a protein called p27; the combination of these two events resulted in all the mice developing prostate cancer 100 percent of the time. In human prostate tumors, p27 is diminished and low levels of the protein correlate with a poor prognosis.

Scientists have long suspected that abnormally low levels of PTEN might contribute to cancer—especially in the prostate and the breast. But knocking out PTEN in animals never produced high tumor rates in the laboratory. It was not until PTEN and p27 were knocked out simultaneously that the dramatic results were obtained.

The reason these events together can have such a dramatic effect is unclear. According to Koff, one hypothesis is that loss of PTEN, which is known to inhibit cell proliferation, may speed up the rate at which tumor cells grow and divide. And the inactivation of p27 may make the cells more sensitive to toxic exposures, both to naturally occurring compounds within the body, as well as to environmental chemicals.

Current animal models for prostate cancer express high levels of a cancer-causing gene called SV40T-antigen. Like all animal models, the mice are useful but imperfect models of human disease.

See related GNN article
»Scientists identify susceptibility gene for prostate cancer on chromosome 17

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Di Cristofano, A. et al. Pten and p27 cooperate in prostate cancer tumor suppression in the mouse. Nat Genet 27, 1-3 (February 2001).
 

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