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. Author manuscript; available in PMC: 2016 Aug 1.
Published in final edited form as: Nat Genet. 2016 Feb 1;48(3):273–282. doi: 10.1038/ng.3500

Figure 5. Human Angiocentric Gliomas exhibit H3K27ac enhancer translocation with an aberrant enhancer associated with the MYB promoter.

Figure 5

a. H3K27ac enhancer peaks in proximity to MYB and QKI in a BRAF-duplicated Pilocytic Astrocytoma (top) and MYB-QKI Angiocentric Glioma (lower). Q3E1 is an enhancer associated with the 3’UTR of QKI. Two super-enhancer clusters (Q3SE1 and Q3SE2) are located within 500kb of QKI. Angiocentric Gliomas are associated with aberrant enhancer formation at the MYB promoter (M5E1), which is not detected in the BRAF driven pilocytic astrocytoma. The breakpoints for the MYB-QKI rearrangement are between exons 1–9 MYB and 5–8 QKI. Expression as determined by RNA-sequencing is depicted for the MYB-QKI Angiocentric Glioma.

b. 3’ QKI associated super-enhancers (Q3SE1/2) presented in two Angiocentric Gliomas.

c. MYB promoter activation following transfection of the MYB-luc construct in U87 cells and U87 cells over-expressing MYB-QKI with and without Q3E1 enhancer cloned into MYB-luc construct. Changes in luciferase activity of the MYB-luc reporter is shown as mean (± SEM) of three individual replicate experiments with n=5.