ArticleBrain pathology (Zurich, Switzerland)2003
Molecular characterization of BCL6 breakpoints in primary diffuse large B-cell lymphomas of the central nervous system identifies GAPD as novel translocation partner.
Article in Brain pathology (Zurich, Switzerland), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 36 citations in OpenAlex.
- Clinicopathological, Genomic, and Transcriptomic Feature Analysis of Primary Adrenal Large B-cell Lymphoma: Insights Into Immune-privileged Sites.The American journal of surgical pathology · 2025Article
- Establishment and molecular characterisation of patient-derived organoids for primary central nervous system lymphoma.Leukemia · 2025Article
- Extranodal lymphoma: pathogenesis, diagnosis and treatment.Molecular biomedicine · 2023Review
- Two cases of primary diffuse large B-cell lymphoma of the CNS associated with t(8;14)(q24;q32) or t(3;14)(q27;q32) identified by G-banding and fluorescence in situ hybridization applied to metaphase spreads.Journal of clinical and experimental hematopathology : JCEH · 2022Article
- Review
- Characterization of genomic alterations in primary central nervous system lymphomas.Journal of neuro-oncology · 2018Article
- Article
- A Novel Non-Immunoglobulin (non-Ig)/BCL6 Translocation in Diffuse Large B-Cell Lymphoma Involving Chromosome 10q11.21 Loci and Review on Clinical Consequences of BCL6 Rearrangements.Pathology oncology research : POR · 2016Review
- The mutational pattern of primary lymphoma of the central nervous system determined by whole-exome sequencing.Leukemia · 2015Article
- Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma.Leukemia · 2009Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary central nervous system lymphomas (PCNSL) constitute diffuse large B-cell lymphomas arising in and remaining confined to the brain. Little information is available on cytogenetic changes in PCNSL, and recurrent chromosomal translocations have not yet been identified. Fluorescence in situ hybridization (FISH) of a series of 13 PCNSL from immunocompetent patients revealed 3 cases with signal patterns of a BCL6-specific probe suggesting a breakpoint in this oncogene locus in chromosome band 3q27. Here, we describe cloning of the translocation breakpoints by long-distance inverse polymerase chain reaction (LDI-PCR) in 2 of these tumors. Both breakpoints affected the first intron of BCL6. In one PCNSL, the HSPCA (HSP90A) gene in 14q32.31 was identified as BCL6 partner. In the second lymphoma, the gene encoding glyceraldehyde-3-phosphate dehydrogenase (GAPD) on 12p13.31 was detected as a hitherto unknown partner of BCL6. Our results suggest translocation-mediated BCL6 oncogene activation as a so far unknown pathogenetically relevant mechanism in PCNSL.
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