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Loss Of Tumor Suppressor Gene Triggers Colon Cancer

September 3,1998—Researchers have found the first connection between the loss of a tumor suppressor gene and activation of a cancer-promoting oncogene, a scenario thought to be prevalent in the initiation of many cancers but which has never been proven.

The newfound link also helps to explain the genesis of most cases of colon cancer, the second leading cause of cancer deaths in the United States.

The scientists found that mutated APC genes, regarded as one of the body's master brakes on cell growth, switch on c-MYC, a gene long associated with cancers of various sorts in both animals and humans.

"This connection is fascinating and we hope it leads to further understanding of this pathway," says Bert Vogelstein, an HHMI investigator at The Johns Hopkins Oncology Center. The report by Vogelstein and Johns Hopkins colleagues, Kenneth Kinzler and HHMI associate Tong-Chuan He, appears in the September 4, 1998, issue of the journal Science.

For Vogelstein, who has studied the genetic basis of colon cancer for nearly 20 years, "this ends one chapter of the APC story," but begins many more. "Master genes such as p53, another tumor suppressor, or APC usually don't work on just one pathway. So c-MYC is probably not the only gene whose expression is controlled by APC. We are working to find the others," he said.

The discovery also offers hope of finding new ways to treat colon cancer. Knowing that the c-MYC oncogene is one final link in the colon cancer chain "brings up an obvious and potentially powerful way to disrupt that interaction," Vogelstein says. Vogelstein's team plans to begin screening compounds that can block expression of the c-MYC oncogene through interference with the transcription factors regulated by APC.

In 1991, investigators including the Vogelstein-Kinzler team first identified
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Contact: Jim Keeley
keeleyj@hhmi.org
(301) 215-8858
Howard Hughes Medical Institute
4-Sep-1998


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