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British researchers today at Cambridge University and the Wellcome Trust’s Sanger Institute announced the results of a gene study in triple-negative breast cancer patients. The researchers found that 8 out of 10 triple-negative tumors were driven largely by overexpression from the BCL11A gene.

Between 15-25% of breast cancers are triple-negative, meaning the tumors do not express the genes for estrogen receptor, progesterone receptor, and HER2/neu. Patients with this type of tumor do not usually respond well to drugs targeting these genes, and generally have a poorer outcome than patients with other types of breast cancer. Triple-negative breast cancer strikes all ages, and if found at a late stage, can be more aggressive and more likely to recur than other types.

The researchers thus far have tested BCL11A in mice, using 3 different human xenografts: HMLER, SUM159, and MSA231. When BCL11A was inhibited, tumor size was greatly reduced compared to controls. In an experimental BCL11A knockout mouse model in which BCL11A expression was removed, none of the mice developed tumors yet there was “no significant impact on cell viability, cell cycle kinetics, or cell death.” BCL11A overexpression also correlated with higher tumor grades in these samples. Furthermore, the team found that BCL11A is required for the normal development of breast stem cells.

BCL11A has also been implicated in leukemia and hemoglobin dysregulation.

The discovery of this oncogene results from testing tumor genetic profiles in 3,000 patients, and provides a novel target for new treatments in triple-negative patients. More information about triple-negative breast cancer can be found at the Triple Negative Breast Cancer Foundation website.

The research was published today in the journal Nature Communications, an open access journal from the family of Nature journals.

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