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Reports Mesh To Clarify Proteins' Importance For Cancer

MADISON, Wis. -- In back-to-back reports in Science and Cell, researchers at the University of Wisconsin Medical School describe important new data on proteins that detect and repair gene damage.

The findings provide direct evidence for the cause of a genetic disorder that greatly increases the risk of cancer, called Nijmegen Breakage Syndrome (NBS), as well as broader insights into a fundamental system that can lead to malignancy when it fails to function properly.

The Wisconsin research is featured on the cover of the current (May 1) issue of Cell, and appeared in the April 24 Science.

NBS is a rare genetic disorder, similar and probably related to the more common ataxia talangiectasia (AT). Patients with both diseases are extremely susceptible to cancer and can become severely ill if they undergo radiation therapy.

In everyday life, cells experience a moderate degree of chromosome damage through exposure to environmental chemicals, radiation and the natural byproducts of normal cellular processes. Cells constantly monitor the chromosomes, activating DNA repair systems to fix the damage once it's detected.

DNA repair systems are also responsible for regulating DNA recombination, a process during which genetic information is remodeled and diversified. A defective DNA repair system can throw the cell into serious disarray, and the result can be devastating mutations that may ultimately lead to cancer.

"Cells from NBS and AT patients exhibit fragile chromosomes and it appears they may fail to recognize DNA damage," said UW Medical School assistant professor of medical genetics John Petrini. "This can lead to high mutation rates and cancer because the cell is simply unable to warn the repair system that damage has occurred."

Petrini and his team concentrate on MR95, a four-protein complex that controls DNA repair and recombination. The Wisconsin researchers have s
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Contact: Dian Land
dianland@macc.wisc.edu
608-263-9893
University of Wisconsin-Madison
6-May-1998


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