STANFORD, Calif. - Researchers at Stanford University Medical Center have tricked cancer cells into self- destructing by briefly disabling a cancer-causing gene. Although the gene revs back up after deactivation, the brief hiatus gives the affected cells a chance to alter their cancerous destiny. This work in mice could open new avenues for treating some human cancers, researchers believe.

Cancer usually results after a cell accumulates a handful of mutations in cancer-related genes called oncogenes or tumor-suppressor genes. Researchers had thought that cancer cells would side-step attempts to fix any single genetic change, especially after treatment ends. But in a study published in the July 5 issue of Science, researchers found that by briefly tinkering with only one mutant gene they could forever alter the course of the cancer.

"Nobody had ever seen that turning off a cancer gene for a few days caused irreversible change," said Dean Felsher, MD, PhD, assistant professor of oncology and lead researcher on the study. "Most people thought that cancer would come back once treatment that turned off an oncogene stopped."

Felsher and his colleagues worked with a gene called MYC, which normally tells a cell when to grow or divide. In many types of cancers, such as lymphoma, breast, colon, and prostate, this gene produces excess protein that allows the rapid growth characteristic of cancer cells. "Anything you learn about MYC should be applicable to a lot of tumors," Felsher said. He added that because the gene is so important, any results may carry significant weight.

Felsher created bone cancer cells containing an altered version of MYC that could be shut down by adding a molecular off switch. He then injected those cells into mice, which went on to develop bone cancer. When he fed mice the off switch, MYC production stopped and the cancer cells quickly reverted to normal bone cells. After 10 days, he stopped treatment, allowing the gene
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Contact: Amy Adams
amyadams@stanford.edu
650-723-3900
Stanford University Medical Center
4-Jul-2002

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