Current Month 2011
Article Features
  Cancer Therapy More Potent When It Hits Two Targets
Combining Two Previously-Used Drugs That Had Stopped Working May Boost Each Otherís Efficacy
Enhancing the Effectiveness of a Breast Cancer Treatment
Fasting Weakens Cancer in Mice
First Prospective Analysis Links Breast and Pancreatic Cancer Risk with Lynch Syndrome
How Early Breast Tumors Become Deadly
Mammography-Detected Breast Cancer in 40-49-Year-Olds Has Better Prognosis
Nanotube Therapy Takes Aim at Breast Cancer Stem Cells
New Member of the Breast Cancer Gene Network Found
Promoting Instability in Cancer Cells
Protein That Functions in Normal Breast May Also Contribute to Breast Cancer Metastasis
Radiation Treatment Transforms Breast Cancer Cells into Cancer Stem Cells
Researchers Reveal Digital Transcriptome of Breast Cancer
Researchers Uncover Inflammatory Circuit That Triggers Breast Cancer
Risk of Death from Breast Cancer Higher Among Older Patients
Scientists Use an Old Theory to Discover New Targets in the Fight Against Breast Cancer
Study Finds Subtle Impairment Among Women Who Received Chemotherapy

New Member of the Breast Cancer Gene Network Found

The infamous BRCA genes do not act alone in causing cancer; there is a molecular syndicate at work preventing the way cells normally repair breaks in DNA that is at the root of breast cancer. But finding all of the BRCA molecular collaborators has been elusive.

Researchers at the Perelman School of Medicine at the University of Pennsylvania and the University of Oulu, Finland, published their discovery of a mutation in the Abraxas gene, which interacts with the well-known breast-cancer gene BRCA1, in the journal Science Translational Medicine.

The mutation affects the ability of the Abraxas protein to enter the nucleus and bind to sites adjacent to damaged DNA. Abraxas organizes a large BRCA1 protein-containing complex that is required to fix DNA-damage. A mutated Abraxas protein impairs the BRCA1 complex's ability to migrate to sites of DNA damage and repair breaks. This results in alterations to the genome that increase breast-cancer risk, notes senior author Roger Greenberg, PhD, associate professor of Cancer Biology.

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