Breast Cancer Co-Conspirators

Breast cancer gene network expanded

(RxWiki News) BRCA genes aren't the only menacing genes in the breast cancer equation. No, there's a syndicate of criminal molecules that hijack normal DNA repair and create the havoc that is breast cancer. Researchers have nabbed another culprit gene.

An alteration in what's known as the Abraxas gene collaborates with the breast cancer bad boy - BRCA1. When the mutant genes get together and go to work, all hell can break loose - including cancer.

"Ask your doctor if genetic testing is appropriate for you and your family."

Scientists at the Perelman School of Medicine at the University of Pennsylvania and the University of Oulu, Finland made this discovery, which has been published in the March, 2012 issue of Science Translational Medicine.

The joint activities of BRCA1 and Abraxas interfere with the normal process of DNA repair. These alterations then increase the risk of breast cancer, says senior study author, Roger Greenberg, Ph.D., associate professor of Cancer Biology.

Roughly 10 percent of breast cancers are believed to be caused by genes that have been passed down from family members, accounting for more than 20,000 new cases of breast cancer a year in the United States. Establishing the hereditary trail is difficult to do, however.

For this study, researchers screened 125 women in Finland for Abraxas mutations. The team, which included Finnish breast cancer researcher Dr. Robert Winqvist, identified the altered gene in women who had breast cancer in four families with a history of the disease.

This finding suggests that Abraxas is another candidate that may increase a woman's odds of developing breast cancer. 

The authors say women with a family history of breast cancer could one day be tested for altered Abraxas genes, along with about 14 other mutations.

Funding for this research came in part from the National Cancer Institute, an American Cancer Society Research Scholar Grant and Abramson Family Cancer Research Institute.

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Review Date: 
March 2, 2012