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. 2018 Aug 2;7:F1000 Faculty Rev-1173. [Version 1] doi: 10.12688/f1000research.14499.1

Figure 3. Overview of ERG fusion and targeted therapies.

Figure 3.

( A) The most common ETS fusion arises from a 3 Mb deletion on chromosome 21, which brings the androgen receptor (AR)-regulated TMPRSS2 promoter (light red) upstream of the ERG gene (dark blue), usually clipping the first three to five exons of ERG in the process. ( B) A schematic showing mechanisms of anti-ERG therapies. Inhibitory peptides block ERG binding to DNA and cause protein destabilization 110. Verteporfin blocks YAP1, a downstream target of ERG 93. YK-4-279 blocks ERG interaction with RNA helicase A (RHA), thereby disrupting transcription of targets 111, 112. Lastly, trabectedin binds minor grooves in ERG binding sites and disrupts its binding to target promoters 113.