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Complications Found in Proposed Prostate Cancer Treatment

Efforts to hinder a protein called IGF-1 not entirely successful, studies find

THURSDAY, May 1, 2008 (HealthDay News) -- The idea that prostate cancer can be treated successfully just by blocking the activity of a protein called insulin-like growth factor (IGF-1) has been undermined by two new studies.

IGF-1 blockage is a goal being pursed by a number of drug companies and academic researchers, stimulated by studies showing an association between high levels of the protein and prostate cancer risk. Many efforts are aimed at blocking the receptors for IGF-1 in prostate cancer cells.

The new studies showing that blocking IGF-1 receptors isn't as simple a matter as might be wished are published back to back in the May 1 issue of Cancer Research.

One of the studies, by a group led by Norman Greenberg, a member of the clinical research division at the Fred Hutchinson Cancer Research Center in Seattle, found an unexpected interaction with a tumor suppressor gene, p53. The researchers created mice whose prostate cells lacked receptors for IGF-1 and crossed them with mice whose P53 gene function was crippled.

"When the function of p53 is abrogated, the cancers seem to accelerate," Greenberg said. "So when you interfere with the IGF-1 receptor, you might be taking the foot off the brake."

That wouldn't matter in human males whose p53 genes were working properly, Greenberg said. "What we are suggesting is that when p53 is compromised, patients might not respond as indicated," he said.

This might mean that a check of p53 function in someone with prostate cancer might be needed before IGF-1 blockage therapy is started, Greenberg said. That idea has to be checked out, he said.

"So we would get data on a patient's tumor before treatment and after treatment, and see if the status of p53 shows whether it would respond more or less to IGF-1 treatment," Greenberg said.

The other study, this one led by Dr. Pinchas Cohen, chief of pediatric endocrinology at the University of California, Los Angeles, also used mice bred to develop prostate cancer, with some also bred to lack IGF-1 receptors.

"The conventional wisdom was that without the IGF receptors, the tumors would fail to develop or be much smaller," Cohen said. "What happened was that they were not reduced in size. In fact, they were exactly the same size."

Low IGF-1 levels in the mice were accompanied by higher levels of growth hormone and insulin, which stimulated growth of the cancer cells, Cohen said.

"This doesn't argue against IGF-1 blockage as a treatment," he said. "But it shows the need for targeting multiple pathways. As the cancers find ways to overcome IGF-1 blockage, it should be used in conjunction with other therapies."

More information

Learn more about prostate cancer from the U.S. National Cancer Institute.

SOURCES: Norman Greenberg, Ph.D., Fred Hutchinson Cancer Research Center, Seattle; Pinchas Cohen, M.D., professor and chief, pediatric endocrinology, University of California, Los Angeles; May 1, 2008, Cancer Research
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