Breast cancer breakthrough as Cambridge University finds gene behind killer disease

Posted: January 11, 2015 at 1:45 am

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.

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.

For the new study, researchers looked that the genetic profile of tumours from 3,000 patients, specifically searching for genes which affect how stem cells and tissues develop.

Higher activity of the BCL11A gene was found in approximately eight out of ten patients and was associated with a more advanced grade of tumour.

To test the theory that the gene was promoting tumour growth, scientists genetically engineered mice to have inactive copies. None of the animals went on to develop tumours in the mammary gland, whereas all untreated animals developed tumours.

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.

Breast cancer breakthrough as Cambridge University finds gene behind killer disease

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