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Tags: Cancer | angelina | jolie | gene | breast | cancer

New Finding Made in 'Angelina Jolie Gene'

New Finding Made in 'Angelina Jolie Gene'
(Copyright AP)

By    |   Friday, 04 March 2016 04:50 PM

Texas scientists have uncovered new evidence of how the breast cancer gene BRCA1 — sometimes referred to as the “Angelina Jolie gene” — leads to the disease.

Researchers from the Cancer Therapy & Research Center in San Antonio have determined BRCA1 regulates a second gene — called COBRA1 — that is closely linked with breast cell growth.

BRCA1 is known to suppress cancer by repairing breaks in DNA, the molecule that contains the genetic blueprint of each cell. This DNA damage occurs with aging and environmental impacts.

The new study, published in Nature Communications, helps deepen researchers’ understanding of the genetic links to breast cancer and could translate into better diagnostic and treatment tools for breast cancer, the second leading cancer in women.

"We now have solid and compelling evidence that BRCA1 in breast tissue is doing something independent of DNA repair," said study lead researcher Rong Li, a professor of molecular medicine at the Health Science Center. "We still think DNA repair is important for BRCA1 to suppress tumor development, but we just don't think it's the whole story.

"The ultimate goal would be to slow down or even prevent breast cancer development in BRCA1 mutation carriers."

BRCA1 defects are associated with up to 10 percent of invasive breast cancers —about 25,000 new cases in the U.S. annually. Women who carry the mutation have an 80 percent increased risk of developing breast cancer. Such cancers are frequently very difficult to cure.

Jolie learned she was a carrier of the BRCA1 gene defect during genetic testing and she opted to undergo a double mastectomy to prevent it.

© 2022 NewsmaxHealth. All rights reserved.


Health-News
Texas scientists have uncovered new evidence of how the breast cancer gene BRCA1 leads to the disease.
angelina, jolie, gene, breast, cancer
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2016-50-04
Friday, 04 March 2016 04:50 PM
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