Conserved features of TERT promoter duplications reveal an activation mechanism that mimics hotspot mutations in cancer

Abstract

TERT promoter mutations are the most common noncoding alterations in cancers, although some remain to be characterised. Here, the authors identify TERT promoter duplications across seven cancer types that are functionally equivalent to well-known hotspot TERT mutations and are clonal in a multifocal glioblastoma patient.