ArticleNature2009
Long-range oncogenic activation of Igh-c-myc translocations by the Igh 3' regulatory region.
Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 91 citations in OpenAlex.
- Human antibody heavy chain variable region exon interacts with the 3' regulatory region to form a stable somatic hypermutation center.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies.Cell genomics · 2026Article
- DIS3 mutations enhance AID-driven translocations during B-cell activation, promoting transformation to multiple myeloma.Nature communications · 2026Article
- Selective Enhancer Dependencies in MYC-Intact and MYC-Rearranged Germinal Center B-cell Diffuse Large B-cell Lymphoma.Blood cancer discovery · 2025Article
- Inhibiting the RNA helicase DDX3X in Burkitt lymphoma induces oxydative stress and impedes tumor progression in xenografts.Frontiers in cell and developmental biology · 2025Article
- HYENA detects oncogenes activated by distal enhancers in cancer.Nucleic acids research · 2024Article
- HYENA detects oncogenes activated by distal enhancers in cancer.bioRxiv : the preprint server for biology · 2024Article
- Somatic structural variation signatures in pediatric brain tumors.Cell reports · 2023Article
- Somatic structural variation signatures in pediatric brain tumors.medRxiv : the preprint server for health sciences · 2023Article
- CTCF shapes chromatin structure and gene expression in health and disease.EMBO reports · 2022Review
- The role of B cells in the development, progression, and treatment of lymphomas and solid tumors.Advances in immunology · 2022Review
- Contribution of Immunoglobulin Enhancers to B Cell Nuclear Organization.Frontiers in immunology · 2022Review
- DNA damage-induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- Genome instability and lymphoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2021Article
- How Chaotic Is Genome Chaos?Cancers · 2021Review
- Eμ and 3'RR transcriptional enhancers of the IgH locus cooperate to promote c-myc-induced mature B-cell lymphomas.Blood advances · 2020Article
- Mouse Models ofFrontiers in immunology · 2020Review
- Ontogeny, Genetics, Molecular Biology, and Classification of B- and T-Cell Non-Hodgkin Lymphoma.Hematology/oncology clinics of North America · 2019Review
- Two modes ofProceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
B-cell malignancies, such as human Burkitt's lymphoma, often contain translocations that link c-myc or other proto-oncogenes to the immunoglobulin heavy chain locus (IgH, encoded by Igh). The nature of elements that activate oncogenes within such translocations has been a long-standing question. Translocations within Igh involve DNA double-strand breaks initiated either by the RAG1/2 endonuclease during variable, diversity and joining gene segment (V(D)J) recombination, or by activation-induced cytidine deaminase (AID, also known as AICDA) during class switch recombination (CSR). V(D)J recombination in progenitor B (pro-B) cells assembles Igh variable region exons upstream of mu constant region (Cmu) exons, which are the first of several sets of C(H) exons ('C(H) genes') within a C(H) locus that span several hundred kilobases (kb). In mature B cells, CSR deletes Cmu and replaces it with a downstream C(H) gene. An intronic enhancer (iEmu) between the variable region exons and Cmu promotes V(D)J recombination in developing B cells. Furthermore, the Igh 3' regulatory region (Igh3'RR) lies downstream of the C(H) locus and modulates CSR by long-range transcriptional enhancement of C(H) genes. Transgenic mice bearing iEmu or Igh3'RR sequences fused to c-myc are predisposed to B lymphomas, demonstrating that such elements can confer oncogenic c-myc expression. However, in many B-cell lymphomas, Igh-c-myc translocations delete iEmu and place c-myc up to 200 kb upstream of the Igh3'RR. Here we address the oncogenic role of the Igh3'RR by inactivating it in two distinct mouse models for B-cell lymphoma with Igh-c-myc translocations. We show that the Igh3'RR is dispensable for pro-B-cell lymphomas with V(D)J recombination-initiated translocations, but is required for peripheral B-cell lymphomas with CSR-associated translocations. As the Igh3'RR is not required for CSR-associated Igh breaks or Igh-c-myc translocations in peripheral B-cell lymphoma progenitors, we conclude that this regulatory region confers oncogenic activity by long-range and developmental stage-specific activation of translocated c-myc genes.
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