Scientists identify novel breast cancer genePublished On: Fri, Jan 9th, 2015 | Breast Cancer | By BioNews
British researchers have identified a novel gene that is especially active in a difficult-to-treat form of breast cancerand could thereby help in the search for new treatments.
“Our understanding of genes that drive stem cell development led us to search for consequences when these genes go wrong. BCL11A activity stood out because it is so active in triple-negative cancers. It had all the hallmarks of a novel breast cancer gene,” said Pentao Liu, senior study author from the Wellcome Trust Sanger Institute.
After combing through 3,000 patients with breast cancer, the team from the Wellcome Trust Sanger Institute found that the overactive BCL11A gene drives the development and progression of “triple-negative” breast cancer.
The research that appeared in the journal Nature Communications and was conducted in mice as well as human cells provided new routes to explore targeted treatments for this aggressive tumour type.There are many types of breast cancers that respond differently to treatments and have different prognoses.
Higher activity of the BCL11A gene was found in approximately eight out of 10 patients with basal-like breast cancer and was associated with a more advanced grade of tumour.
“Our gene studies in human cells clearly marked BCL11A as a novel driver for triple-negative breast cancers,” added joint first author Walid Khaled.
Approximately one in five patients is affected by triple-negative breast cancer.
The team also showed that BCL11A is required for normal development of breast stem cells and progenitors, which are thought to be the cells that, when mutated, give rise to basal-like breast cancer.
A woman’s risk of developing breast and/or ovarian cancer is greatly increased if she inherits a deleterious mutation in the BRCA1 gene or the BRCA2 gene.
Khaled, WT, Lee SC et al. BLC11A is a triple-negative breast cancer gene with critical functions in stem and progenitor cells. Nature Communications 2015. DOI: 10.1038/ncomms6987