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May 9, 2005 -- By studying
mice with skin cancer, researchers at the Huntsman Cancer Institute
at the University of Utah discovered a way to inhibit a mutant gene
found in up to 30 percent of human tumors.
Called Ras, normal copies of this gene are important in cell signaling,
or communication among cells. When mutated, however, Ras is an “oncogene”
or cancer-causing gene that has been shown to promote the growth
of cancers in the pancreas, colon and lung, as well as thyroid cancer
and leukemia.
Attempts to inhibit activated Ras have had limited success until
now, but the Huntsman Cancer Institute researchers explain that
they have discovered an enzyme that, when inhibited, appears to
reduce the incidence of Ras-induced tumors in mice.
They reported their findings in the May 9 - 13, 2005, issue of the
journal Proceedings of the National Academy of Sciences Online
Early Edition.
Matthew K. Topham, M.D., assistant professor of internal medicine
at the University of Utah School of Medicine and lead investigator
on the study, explains that the research team had originally been
testing a group of enzymes that regulate the function of the Ras
gene. These enzymes, called diacylglycerol kinases (DGKs), are implicated
in tumor growth.
“When we began our investigation using a type of DGK, called
DGK iota, we thought that its absence would cause more tumors to
develop, as has happened with other DGKs we have tested. This time,
though, when we tested mice with an activated Ras gene, but an absent
DGK iota gene, the number of tumors was significantly reduced,”
Topham says. “This result is interesting because it happened
when the Ras gene was activated. The implication is that a drug
therapy could be developed to reduce tumors caused by Ras without
significant side effects.”
The research team also included Huntsman Cancer Institute scientists
Debra Regier, Ph.D.; Jared Higbee; Katrina Lund; Fumio Sakane, Ph.D.;
and Stephen M. Prescott, M.D., professor of internal medicine at
the University of Utah and executive director of Huntsman Cancer
Institute.
The researchers used mice that were bred to have a highly “expressed”
– meaning highly active – mutant of the Ras oncogene.
Such mice were first developed years ago. Prior studies had demonstrated
that these mice were very prone to tumors. For the new study, the
Huntsman Cancer Institute team deleted the DGK iota gene in these
mice and found that they developed few tumors, while mice with an
intact DGK iota gene and an activated Ras gene exhibited significantly
more tumors.
Topham says his team will now examine more closely the mechanism
behind how DGK iota works to inhibit tumor formation.
Funding for the study was provided by the Huntsman Cancer Foundation,
the R. Harold Burton Foundation, the National Institutes of Health
and the National Cancer Institute.
Huntsman Cancer Institute is located in Salt Lake City. Its mission
is to understand cancer from its beginnings, to use that knowledge
in the creation and improvement of cancer treatments, to relieve
the suffering of cancer patients, and to provide education about
cancer risk, prevention, and care.
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| Media Contacts: |
| To reach Matthew K. Topham, please call
or e-mail Linda Aagard, public relations, Huntsman Cancer Institute,
University of Utah |
office (801) 587-7639, cellular (801)
243-4733, linda.aagard@hci.utah.edu
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