Skip to main content


Figure 3 | Genome Biology

Figure 3

From: Heterogeneity in the inter-tumor transcriptome of high risk prostate cancer

Figure 3

The landscape of non-ETS fusion genes and complex genome rearrangements in high-risk prostate cancer. (A) Depicts the number of expressed fusion genes (`Fusion load’) and complex genome rearrangements (`Complex’) detected in each tumor sample, and indicates selected genes involved in fusion events. Only genes with putative links to cancer are shown (full list of involved genes in Additional file 1: Table S9). Genes marked with * indicates a putative gain-of-function. † highly complex chromothripsis-driven rearrangements; ‡ involvement in complex rearrangement but not expressed; § DNA sequence coverage too low to elucidate complex rearrangements. (B) Schematic of the complex genome rearrangement (also known as chromoplexy [6]) in tumor T20 which lead to the disruption of TP53. Breakpoints in the six genes involved are indicated on the left, together with the final configuration on the right. This particular rearrangement led to the expression of just one fusion transcript (i.e. MATR3-HMG3P22). (C-F) Further schematics of complex genome rearrangements (C) shows the same rearrangement as (B)]. Green nodes indicate a gene is disrupted by rearrangement while red and gray indicate potential activating or neutral effects, respectively. Full edges represent a DNA rearrangement, and dotted lines indicate a rearrangement that was also detected in the RNA sequence data (that is, a fusion transcript was expressed). (G) Schematics of selected fusion genes with putative gain-of-function. Tumor ID is provided in each box, and major protein domains are annotated.

Back to article page