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Cancer Therapies HOL-emblem1-web.GIF (3556 bytes)

Molecular understanding of prostate cancer could reveal a cure (March 1999)

Prostate cancer kills more than 41,000 men each year in the US and accounts for nearly one-quarter of all newly diagnosed cancer cases annually. Two papers in the March 1999 issue of Nature Medicine presented new findings about the mechanisms underlying the development of prostate cancer. Each may contribute to finding a cure for the disease, and one in particular could exploit a new drug approved for breast cancer last year-Herceptin.

A standard treatment for prostate cancer is chemical or surgical castration, which removes circulating androgens that stimulate cancer growth. But if men live through this stage of the disease, their tumor may convert from being androgen-sensitive to being androgen-independent. Until now, the mechanism of this conversion was unclear; however, Charles Sawyers and colleagues at the University of California, Los Angeles, have identified a pathway implicated in this progression.

The researchers showed that androgen-independent tumors can be generated in a mouse model through HER-2/neu receptor stimulation of the androgen receptor pathway. If this mechanism is validated in humans, Herceptin, a monoclonal antibody that blocks the HER-2/neu receptor, may also prove effective against prostate cancer.

In a separate paper, Gary Pasternack and colleagues at Johns Hopkins School of Medicine present data to resolve the paradox that, despite its tumor suppressor properties, the pp32 gene is over-expressed in 90% of malignant prostate tissue. By comparing benign prostate tissue and adjacent malignant tissue from human patients, the team found that malignant tissue expresses variants of pp32 (pp32r1 and pp32r2) which are cancer-causing, rather than pp32 itself. Benign tissue expresses pp32.

Their discovery raises new questions as to whether these variants are causative in prostate cancer, and whether their expression pattern could be manipulated therapeutically to either stop or reverse the progression from the benign to the malignant state.

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