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Study suggests common mechanism activating cancer driver genes 23 December 2015 – 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 Provided by Broad Institute of MIT and Harvard This stylistic diagram shows a gene in relation to the double helix structure of DNA and to a chromosome (right). The chromosome is X-shaped because it is dividing. Introns are regions often found in eukaryote genes that are removed in the splicing process (after the DNA is transcribed into RNA): Only the exons encode the protein. The diagram labels a region of only 55 or so bases as a gene. In reality, most genes are hundreds of times longer. Credit: Thomas Splettstoesser/Wikipedia/CC BY-SA 4.0 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 1/2 APA citation: Study suggests common mechanism activating cancer driver genes (2015, December 23) retrieved 13 May 2017 from https://medicalxpress.com/news/2015-12-common-mechanism-cancerdriver-genes.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. 2/2 Powered by TCPDF (www.tcpdf.org)