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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Super-enhancers: critical roles and therapeutic targets in hematologic malignancies

Fig. 2

Different modes of super-enhancer-mediated MYC amplification. a In CML and T-ALL, super-enhancer interacts with a common and conserved CTCF binding site in MYC promoter [62, 76]. b In ATLL, HBZ (HTLV-I encoded transcription factor) binds to BATF3 super-enhancer and regulates the expression of BATF3 and its downstream target gene MYC (upper panel) [94]. ESEs cause upregulation of MYC (middle). eRNAs at ESEs − 428 and − 525 kb upstream of the MYC oncogene transcription start site affects MYC expression and cell growth (lower panel) [93]. c In DLBCL, a t(3;8)(q27;q24) chromosomal rearrangement directly links the MYC and BCL6 loci, resulting in MYC recruitment of BCL6 super-enhancers and subsequent activation of MYC expression (left panel) [64]. In T-ALL, NOTCH1 activates MYC expression via interaction of a long-range distal enhancer named N-Me (for NOTCH MYC enhancer) (right panel) [42]. HTLV-1, human lymphotropic virus type. EBV, Epstein-Barr virus. LCLs, lymphoblastoid cell lines; EBNA, Epstein-Barr virus nuclear antigen; ESEs, Epstein–Barr virus super-enhancers; eRNAs, enhancer RNAs; DLBCL, diffuse large B cell lymphoma; T-ALL, T cell acute lymphoblastic leukemia

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