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Biological Link Between BRCA1 and Breast Cancer Detailed
Date:1/17/2008

Finding suggests the gene, when not mutated, helps repair damaged DNA

THURSDAY, Jan. 17 (HealthDay News) -- A newly discovered role played by the breast cancer gene BRCA1 in repairing damaged DNA may help explain why women who inherit a mutated version of the gene are more likely to develop breast and ovarian cancer.

The finding, reported by Duke University Medical Center researchers, could also lead to more effective treatments for women with and without mutated versions of the gene, according the report in the Jan. 16 online edition of PLoS One.

"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," lead investigator Craig Bennett, a researcher in Duke's Department of Surgery, said in a prepared statement.

"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," Bennett said.

The BRCA1 pathway identified by the researchers "is directly involved with the critical process of transcription, in which RNA acts as a messenger between DNA and the making of proteins."

"We found that BRCA1 acts together with transcription to detect DNA damage and to signal the cell to repair itself. When BRCA1 does not function correctly, as when it is mutated, DNA damage remains un-repaired and cancer can occur," Bennett said.

The finding was first made in yeast and then duplicated in human breast cancer cells.

Women with a BRCA1 mutation are up to 80 percent more likely to develop breast cancer than other women, and are also more likely to develop the disease at a much younger age.

More information

The U.S. National Cancer Institute has more about breast cancer risk.



-- Robert Preidt



SOURCE: Duke University, news release, Jan. 15, 2008


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