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Understanding IGF-1: Jefferson researcher sees drug potential in targeting enzyme

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He doesn't think that IRS-1 is the exclusive activator, but rather, one of several. "It makes sense," he says. "When you knock out the IRS-1 gene, you get flies that are 50 percent in size, so there are other ways to make cells proliferate. Cells without the IGF-1 receptor can grow."

Several years ago, Dr. Baserga, who pioneered much of the understanding of the basic behavior of the IGF-1 receptor, and his co-workers used knockouts specially bred mice lacking a particular gene to develop a cell line without IGF-1 receptors. Normal cells grew, but would not turn cancerous when placed in rodent cells with added cancer-causing genes.

The finding suggested that if cells that lacked IGF-1 receptor could not be turned cancerous, perhaps cancerous cells with IGF-1 could be reversed.

"If this is true in humans, then this is a rational target," he says. Studies by companies in the last few years have found that antibodies and various small molecules made to the IGF-1 receptor kill cancer cells without toxicity, he notes.

"The general idea is that if you find something that knocks out the IGF-1 receptor, you will kill the cancer cells and have only a modest effect on normal cells at least using cells in culture and in mice," he says. Several years ago, for example, Dr. Baserga and his group used antisense therapy to target the IGF-1 receptor, which killed cancer cells in mice but didn't work as well in people. However, clinical trials are just beginning, he says, and he is still hopeful that other approaches will work in humans.

In the meantime, pharmaceutical companies continue to pursue potential drugs and small molecules that target the IGF-1 receptor, and still seek Dr. Baserga's help.


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20-Sep-2005


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