MGH team defines the mechanisms of action of key genetic abnormality in Ewing sarcoma
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A Massachusetts General Hospital (MGH) research team has used epigenome editing tools to investigate how the genetic abnormality that drives Ewing sarcoma – the second most common bone cancer in children and young adults – unleashes tumor growth. In their paper in the journal Genes & Development the researchers show that blocking the fusion protein EWS-FLI1 from binding and activating specific ‘enhancer’ sites in the genome prevents the expression of genes that promote tumor growth.

“We previously showed that binding of EWS-FLI1 to GGAA microsatellite repeats in the genome converts these sites into active enhancers,” says Miguel Rivera, MD, MGH Department of Pathology and Center for Cancer Research, co-senior author of the report. “Now we have used new epigenome editing tools to turn off individual microsatellites and demonstrate that they have important functions in controlling the expression of nearby genes that are critical for tumor growth.”

Ewing sarcoma is caused by a genetic alteration known as a chromosomal translocation in which the chromosome 22 gene EWS is fused to the chromosome 11 gene FLI1, leading to generation of the fusion protein EWS-FLI1. A 2014 Cancer Cell study led by Rivera and Bradley Bernstein, MD, PhD, also of MGH Pathology

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