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Gene linked to aggressive breast cancers

19 January 2015
Appeared in BioNews 786

UK researchers have identified a gene that is active in a difficult-to-treat form of breast cancer, raising the possibility of developing targeted treatments.

The researchers found that one gene - BCL11A - was particularly active in around eight out of ten patients with triple-negative breast cancer (TNBC) and was associated with a more advanced grade of tumour.

'BCL11A stood out because it is so active in many triple-negative cancers: it has all the hallmarks of a novel breast cancer gene,' said study author Dr Pentao Liu, from the Wellcome Trust Sanger Institute in Cambridge.

In triple-negative breast cancer (TNBC), cells lack three receptors that respond to hormone therapies, including herceptin and tamoxifen. Consequently, prognosis is significantly worse than for other forms of the disease.

Using data from around 3,000 breast cancer patients, the team looked specifically at genes involved in haematopoiesis - the process by which blood components develop from stem cells. This is because such genes have previously been found to have key roles in both breast tissue development and breast cancer.

The team, reporting in Nature Communications, showed that adding an active human BCL11A gene to human or mouse breast cells drove the development of tumours. Conversely, when they inhibited BCL11A activity in three samples of human TNBC, the cells lost some of their cancerous characteristics and formed smaller tumours when transplanted into mice.

Additionally, using mouse models, the researchers also found that BCL11A has important roles in tumour formation and progression and essential roles in the normal development of the breast tissue.

Dr Emma Smith, senior science information officer at Cancer Research UK, said: 'Figuring out the genes that play a role in triple negative breast cancer could lead to new ways to tackle the disease - so this study is a promising step forward.'

'The next steps will be finding out if the gene plays the same role in causing breast cancer in women, and whether drugs can be developed to target the faulty molecules.'

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