Triple-negative breast cancer is one of the most deadly forms of the disease, does not respond to hormonal therapies such as tamoxifen, or targeted drugs like Herceptin and nearly one quarter of patients diagnosed will not survive for more than five years.
Now researchers at Cambridge University and the Wellcome Trust’s Sanger Institute have found that the BCL11A gene is overactive in eight out of ten patients.
The study opens the door for therapies which suppress the gene and for screening that would pick up the risk early when women still had time to opt for life-saving mastectomies.
“Our gene studies in human cells clearly marked BCL11A as a driver for triple-negative breast cancers,” says Dr Walid Khaled of the University of Cambridge.
“We also showed that adding an active human BCL11A gene to human or mouse breast cells in the lab drove them to behave as cancer cells.
“As important, when we reduced the activity of BCL11A in three samples of human triple-negative breast cancer cells, they lost some characteristics of cancer cells and became less tumorigenic when tested in mice.
“So by increasing BCL11A activity we increase cancer-like behaviour; by reducing it, we reduce cancer-like behaviour.”
“This exciting result identifies a novel breast cancer gene in some of the more difficult-to-treat cases,” said Professor Carlos Caldas, Director of the Cambridge Breast Cancer Research Unit at the University of Cambridge.
“It builds on our work to develop a comprehensive molecular understanding of breast cancer that will inform clinical decisions and treatment choices. Finding a novel gene that is active in cancer should also help in the search for new treatments.”
