ArticleBlood cancer journal2024
Large B-cell lymphomas with CCND1 rearrangement have different immunoglobulin gene breakpoints and genomic profile than mantle cell lymphoma.
Article in Blood cancer journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Genomic architecture of IRF4 rearrangements in childhood and adult large B-cell lymphomas.Blood advances · 2026Article
- Genomic heterogeneity in primary cutaneous follicular center lymphomas reveals different clinicopathological subgroups.HemaSphere · 2026Article
- Targeted panel sequencing for refining B-cell lymphoma diagnosis: a real-life, reference center experience.Virchows Archiv : an international journal of pathology · 2026Article
- Review
- Establishment and characterization of a CCND1-rearranged non-mantle cell lymphoma cell line and patient-derived xenograft model.Leukemia · 2026Article
- The B-cell-autoantibody axis in lung cancer immunity.Theranostics · 2026Review
- Article
- Article
- IGH/IGK gene rearrangement in the diagnosis of B-cell non-Hodgkin lymphoma: experience from three centers.Annals of hematology · 2025Article
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Authors and funding
34 authors.
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Abstract
Mantle cell lymphoma (MCL) is genetically characterized by the IG::CCND1 translocation mediated by an aberrant V(D)J rearrangement. CCND1 translocations and overexpression have been identified in occasional aggressive B-cell lymphomas with unusual features for MCL. The mechanism generating CCND1 rearrangements in these tumors and their genomic profile are not known. We have reconstructed the IG::CCND1 translocations and the genomic profile of 13 SOX11-negative aggressive B-cell lymphomas using whole genome/exome and target sequencing. The mechanism behind the translocation was an aberrant V(D)J rearrangement in three tumors and by an anomalous IGH class-switch recombination (CSR) or somatic hypermutation (SHM) mechanism in ten. The tumors with a V(D)J-mediated translocation were two blastoid MCL and one high-grade B-cell lymphoma. None of them had a mutational profile suggestive of DLBCL. The ten tumors with CSR/SHM-mediated IGH::CCND1 were mainly large B-cell lymphomas, with mutated genes commonly seen in DLBCL and BCL6 rearrangements in 6. Two cases, which transformed from marginal zone lymphomas, carried mutations in KLF2, TNFAIP3 and KMT2D. These findings expand the spectrum of tumors carrying CCND1 rearrangement that may occur as a secondary event in DLBCL mediated by aberrant CSR/SHM and associated with a mutational profile different from that of MCL.
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