• E-mail
• Print
• Comment
• Font Size
• Digg
• del.icio.us
• Discuss article

Researchers in Utah Find Way to Stop Many Tumors

Posted on: Tuesday, 10 May 2005, 15:00 CDT

Researchers at the Huntsman Cancer Institute have found a way to stop a gene mutation that is believed responsible for up to 30 percent of human tumors.

And that may have treatment implications for diverse cancers including pancreas, colon, lung and thyroid cancers, as well as leukemia.

Their findings are reported this week in the Proceedings of the National Academy of Sciences Online Early Edition.

The University of Utah scientists found a way to inhibit a gene called Ras, which in its normal form is important for communication among cells. Mutated or defective Ras is implicated in a third of all tumors and maybe more, according to Dr. Matthew K. Topham, assistant professor of internal medicine at the University of Utah School of Medicine and lead investigator in the study.

The expression of the abnormal Ras is "probably an early event in tumor formation," he said.

The finding was "serendipitous," he said. An activated, mutated Ras has proven hard to inhibit. But when they inhibited an enzyme "one step downstream" from Ras, the number of Ras-induced tumors dropped.

"We found that deleting that enzyme interfered with Ras downstream," he said.

Their finding, he said, is a good indication that inhibiting that enzyme could reduce formation of Ras-induced tumors -- without significant side effects.

"When we delete this enzyme, the mice are perfectly normal otherwise," he said. "They live long and function just fine."

The researchers had been testing a group of enzymes that regulate the function of the Ras gene. The enzymes, called diacylglycerol kinases (DGKs), are implicated in the tumor growth.

They were manipulating a type of DGK called DGK iota and thought removing it would cause more tumors to grow, which has happened before with DGKs. Instead, in mice with an activated Ras gene but no DGK iota gene, the number of tumors decreased. It is because that happened with the Ras gene activated that they believe drug therapy could be developed to reduce the number of Ras-induced tumors without significant side effects.

The mice they used were a line first bred years ago to have a highly active mutation of the Ras gene, called an oncogene because of its cancer-causing properties. Earlier studies have shown that these mice are prone to tumors.

Now they plan to study the mechanism by which curtailing DGK iota works to inhibit tumor formation.

The study was funded by the Hunstman Cancer Foundation, the R. Harold Burton Foundation, the National Institutes of Health and the National Cancer Institute.

Besides Topham, the research team included institute scientists Debra Regier, Ph.D.; Jared Higbee; Katrina Lund; Fumio Sakane, Ph.D.; and institute executive director and professor of internal medicine Dr. Stephen M. Prescott.

E-mail: lois@desnews.com

Source: Deseret News (Salt Lake City)

More News in this Category