Gene Causes Cancer to Spread

Research Could Lead to Better, Milder Cancer Treatments

From the WebMD Archives

March 5, 2003 -- A gene seems to trigger the lethal spread of cancer cells linked with breast, uterine, ovarian, and prostate cancer, new research shows. This discovery may make possible new, less toxic, more effective chemotherapies to halt this spread.

"Slowing down the disease may change cancer from a fatal disease to one that can be lived with, like diabetes," says researcher Richard G. Pestell, MD, PhD, director of the Lombardi Cancer Center at Georgetown University in Washington, in a news release.

The groundbreaking yet preliminary study appears in the May 2003 issue of the journal Molecular Biology of the Cell.

"Patients who do not survive their cancer often don't die from their primary cancer. Usually they die from the spread of the disease through the body," Pestell says.

"If we can understand what causes the metastasis [the spread of cancer cells], then we can pinpoint new targets to block the spread of disease," he says.

In studies involving mice, Pestell and his team have spent the past decade studying the cyclin D1 gene and the protein it produces. They have found that by switching off this gene, the migration of cancer cells can be halted.


Evidence of excessive cyclin D1 has been found in breast, uterine, ovarian, and prostate cancer.

Pestell says he foresees a new form of chemotherapy that targets just this cell migration. Only cancerous cells migrate, he says.

"Killing only migrating cancer cells is thus less toxic, producing fewer side effects, than current chemotherapy, which targets dividing cells of all types," Pestell explains. Many healthy dividing cells, such as in the stomach and hair, are destroyed by chemotherapy.

WebMD Health News


SOURCES: Molecular Biology of the Cell, May 2003. News release, Georgetown University Medical Center.
© 2003 WebMD, Inc. All rights reserved.