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To: scaram(o)uche who wrote (454)	3/1/1999 6:51:00 PM
From: mike head	Respond to of 4974

Sorta OT: Simply 'breaking news that I found interesting...mch y Maggie Fox, Health and Science Correspondent WASHINGTON (Reuters) - A new drug just approved for use against breast cancer might work in some cases of prostate cancer as well, researchers said Monday. They said they found some cases of prostate cancer involve a part of cells known as the estrogen receptor, which is targeted by a new drug known as Herceptin. Writing in the journal Nature Medicine, Dr. Charles Sawyers and colleagues at the University of California Los Angeles said their finding also explained why therapy aimed at blocking the male hormones involved in prostate cancer often stops working. Prostate cancer is expected to kill 37,000 American men this year and 200,000 men will be diagnosed with the disease, according to the American Cancer Society. It is known to be related to hormones, and a standard treatment is chemical or surgical castration, which removes the male hormones that stimulate cancer growth. But once treated this way, it sometimes converts and no longer responds to anti-male hormone treatment. "Until we started treating prostate cancer with hormone therapy, androgen-independent cancer didn't even exist," Sawyers said in a telephone interview. "It's the consequence of the therapy, but it's the cells that have learned to become resistant." What Sawyers found, to their surprise, was that the cells become resistant by over expressing a gene called HER-2/neu. This could mean such cases of prostate cancer can be treated with Herceptin, now approved for breast cancer. Herceptin, made by South San Francisco-based biotechnology company Genentech Inc., works by blocking the HER-2/neu (human epidermal growth factor receptor-2) gene, which seems to promote the growth of cancer cells. The drug is a monoclonal antibody, a genetically engineered version of the body's own system for flagging invaders or cancerous cells. Herceptin, also called trastuzumab, blocks HER-2's action and thus stops production of the protein, slowing down the cancer's growth. Sawyers' team said it was logical to look for HER-2 involvement with prostate cancer. "In some but not all studies, HER-2/neu is overexpressed and or/amplified ... in a subset of prostate cancer patients and has been associated with shortened survival," they wrote in their report. Working with mice, they found chemical or surgical castration caused development of androgen-resistant prostate cancer when the mice were infected with human prostate cancer cells. They found the cancer cells were producing too much HER-2, meaning the HER-2 gene was over expressing.