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January 10, 2015

Scientists identify gene behind triple-negative breast cancer

Scientists have successfully identified the gene behind one of the most aggressive types of breast cancer, a breakthrough which could lead to new targeted treatments and a comprehensive "molecular understanding" of the deadly disease.
The discovery of the BCL11A gene, which is overactive in eight out of 10 patients with triple-negative breast cancer, was a result of research by Cambridge University and the Wellcome Trust's Cambridge-based Sanger Institute.
Triple-negative cancer lacks the receptor proteins which usually respond to hormone therapies and the new discovery could lead to new treatment, 'Cambridge News' reported.
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," said Walid Khaled of the University of Cambridge.
Around 10,000 people a year are diagnosed with triple- negative breast cancer.
The disease does not respond to traditional breast cancer drugs like Herceptin and is one of the most aggressive types.
Just 77 per cent of people with triple-negative breast cancer will survive for five years, compared with 93 per cent for other types of the disease.
The researchers looked that the genetic profile of tumours from 3,000 patients, specifically searching for genes which affect how stem cells and tissues develop.
"Our understanding of genes that drive stem cell development led us to search for consequences when these genes go wrong," said Pentao Liu of the Wellcome Trust Sanger Institute who is a senior author on the study published in the journal?'Nature Communications'.
"BCL11A activity stood out because it is so active in triple-negative cancers. It had all the hallmarks of a novel breast cancer gene," Liu said.
"This exciting result identifies a novel breast cancer gene in some of the more difficult-to-treat cases," said Carlos Caldas, professor of cancer medicine and director of the Cambridge Breast Cancer Research Unit at the University of Cambridge and head of breast cancer functional genomics at Cancer Research UK Cambridge Institute.
"It builds on our work to develop a comprehensive molecular understanding of breast cancer that will inform clinical decisions and treatment choice," he added.
The breakthrough was welcomed by charities who said it could lead to new targeted treatments. 

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