Study suggests common mechanism activating cancer driver genes
In a new paper published online by Nature Genetics, researchers from Dana-Farber Cancer Institute (DFCI) and the Broad Institute systematically investigated somatic copy number alterations of noncoding regions across cancers, integrating genomic, epigenomic, and transcriptomic data.
The team found six super-enhancer regions that are focally amplified across different cancer types, including two that are associated with overexpression of the MYC oncogene, suggesting that this type of modification may be a common mechanism activating cancer driver genes.
The team, which was led by senior author Matthew Meyerson and first authors Xiaoyang Zhang, Peter Choi, and Joshua Francis – all of Broad and DFCI – also used genome-editing technologies to validate the oncogenic function of these focally amplified super-enhancers.
More information: Xiaoyang Zhang et al. Identification of focally amplified lineage-specific super-enhancers in human epithelial cancers, Nature Genetics (2015). DOI: 10.1038/ng.3470
