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Researchers ID New Gene Linked to Lung Cancer

Discovery could lead to new therapies

TUESDAY, Oct. 16 (HealthDay News) -- A new gene associated with human lung cancer has been identified. The finding about the Dmp1 gene may help improve understanding of what goes wrong at the cellular level to cause lung cancer.

The Wake Forest University School of Medicine researchers analyzed 51 samples of human non-small-cell lung cancers and found that the Dmp1 gene -- which normally works to suppress tumor formation -- was non-functional in about 35 percent of lung cancers.

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The study was published Oct. 15 in the journal Cancer Cell.

Previous studies in mice had found that Dmp1 helps activate tumor suppressors called p53 and Arf. When Dmp1 isn't functioning, these tumor suppressors aren't available to kill cancer cells.

"No one thought it was involved in human tumors. This was the first study to explore its involvement in human cancer," senior scientist Dr. Kazushi Inoue, assistant professor of pathology, said in a prepared statement.

The Dmp1 gene is located on human chromosome 7q21, a region that is often deleted in human cancers, and abnormality of the p53 gene is a common feature in human lung cancers, the researchers noted.

"This work provides evidence that Dmp1 is a physiological regulator of the Arf-p53 pathway in humans and is primarily involved in lung cancer," and offers a number of opportunities to gain more understanding about lung cancer, Inoue said.

"We hope to learn how the gene affects outcome. It's possible that knowing which patients have the gene may be a prognostic factor for how they will respond to chemotherapy. The gene may also be a target for future drug development, since high expression of Dmp1 significantly inhibited the growth of some lung cancer cells," Inoue said.

More information

The U.S. National Cancer Institute has more about lung cancer.

-- Robert Preidt

SOURCE: Wake Forest University Baptist Medical Center, news release, Oct. 15, 2007

Copyright © 2007 ScoutNews, LLC. All rights reserved.
Last updated 10/16/2007



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Nov 20, 2008
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