Chromosomal translocations are important drivers of haematological malignancies whereby proto-oncogenes are activated by juxtaposition with enhancers, often calledenhancer hijacking. We analyzed the epigenomic consequences of rearrangements between the super-enhancers of the immunoglobulin heavy locus (IGH) and proto-oncogeneCCND1that are common in B cell malignancies. By integrating BLUEPRINT epigenomic data with DNA breakpoint detection, we characterized the normal chromatin landscape of the humanIGHlocus and its dynamics after pathological genomic rearrangement. We detected an H3K4me3 broad domain (BD) within theIGHlocus of healthy B cells that was absent in samples withIGH-CCND1translocations. The appearance of H3K4me3-BD overCCND1in the latter was associated with overexpression and extensive chromatin accessibility of its gene body. We observed similar cancer-specific H3K4me3-BDs associated with hijacking of super-enhancers of other common oncogenes in B cell (MAF,MYC, andFGFR3/NSD2) and T cell malignancies (LMO2,TLX3, andTAL1). Our analysis suggests that H3K4me3-BDs can be created by super-enhancers and supports the new concept ofepigenomic translocation, in which the relocation of H3K4me3-BDs from cell identity genes to oncogenes accompanies the translocation of super-enhancers.