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With this as a clue, Polyak and her colleagues determined that the protein provides the same service to cells in invasive breast cancers. "We found that when DCD is produced in large amounts, breast tumors tend to be larger and more likely to spread beyond the breast," remarks Polyak, who is also an assistant professor of medicine at Harvard Medical School. "The protein was expressed at these high levels only in invasive tumors, not in early-stage ones."

At the same time, the investigators found that DCD apparently contributes to cachexia. A disorder in which muscle and fat cells essentially digest themselves, leading to a wasting-away of the body, cachexia is one of cancer's most notorious hallmarks. While the precise nature of DCD's involvement in cachexia isn't known, it's clear that the protein has a very different effect on muscle cells than on nerve cells.

The response to DCD, whether in nerve cells or invasive breast cancer cells, is triggered when a chemical signal docks at "receptors" on the cells' surface. Polyak and her associates are currently exploring ways of influencing those receptors. Blocking them in invasive breast cancers may slow the tumors' growth, while stimulating them in patients with stroke or Alzheimer's disease may protect nerve cells from dying.

"DCD's role in a variety of different disorders makes it an attractive target for new therapies," Polyak remarks. "Increasing or decreasing its production in certain sets of cells may offer a promising approach to treatment."

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Contact: Bill Schaller
william_schaller@dfci.harvard.edu
617-632-5357
Dana-Farber Cancer Institute
8-Sep-2003