DURHAM, N.C. -- A breast cancer gene's newly discovered role in repairing damaged DNA may help explain why women who inherit a mutated copy of the gene are at increased risk for developing both breast and ovarian cancer.
The discovery also could lead to more effective therapies for women with and without mutated copies of the BRCA1 gene, according to a study led by Duke University Medical Center researchers.
Since it was discovered in 1994, BRCA1 and its role in preventing and causing cancer has been intensely studied, and our research represents an important piece of the puzzle, said Craig Bennett, Ph.D., a researcher in Dukes Department of Surgery and lead investigator on this study. This study has identified an important mechanism by which BRCA1 comes into play when DNA -- the basis for all cell function -- is damaged. We have shown that this theory holds up not just in scientific models but in human breast cancer cells as well.
The findings appear in the January 16, 2008 online edition of the journal PLoS ONE. The study was funded by the United States Department of Defense, the National Institutes of Health and the Italian Association for Research on Cancer.
The researchers first looked at yeast to demonstrate that a molecular pathway that is particularly susceptible to BRCA1 influence is also crucial to normal cell function.
The BRCA1 pathway we discovered is directly involved with the critical process of transcription, in which RNA acts as a messenger between DNA and the making of proteins," Bennett said.
DNA damage is a normal result of exposure to environmental agents, such as carcinogens, and the response to this damage can be influenced by other normal human processes such as aging and hormonal changes, Bennett said. It's what happens to RNA transcription after damage occurs in DNA that is BRCA1-dependent.
We found that BRCA1 acts together with transcription to detect DNA damage and to
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| Contact: Lauren Shaftel Williams lauren.shaftel@duke.edu 919-684-4966 Duke University Medical Center Source:Eurekalert |