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Updated: May 31, 2026
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VDJ-Seq: Deep Sequencing Analysis of Rearranged Immunoglobulin Heavy Chain Gene to Reveal Clonal Evolution Patterns of B Cell Lymphoma
Published on: December 28, 2015
BCL3 rearrangement, amplification and expression in diffuse large B-cell lymphoma.
Hazem A H Ibrahim1, Furrat Amen, Alistair G Reid
1Department of Histopathology, Hammersmith Hospital and Imperial College, London, UK.
European Journal of Haematology
|July 15, 2011
Summary
BCL3 gene rearrangement is rare in diffuse large B-cell lymphoma (DLBCL), but BCL3 overexpression is common in the non-germinal center (GC) subtype, suggesting a role in DLBCL pathogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Diffuse large B-cell lymphoma (DLBCL) is a heterogeneous lymphoid malignancy.
- The role of the BCL3 gene in DLBCL pathogenesis requires further investigation.
Purpose of the Study:
- To investigate BCL3 gene rearrangement and protein expression in DLBCL.
- To correlate BCL3 alterations with DLBCL immunophenotypic subsets and pathogenetic implications.
Main Methods:
- Evaluated 78 DLBCL tissue samples using immunohistochemistry for BCL3 protein.
- Assessed BCL3 and IGH rearrangement via Fluorescent in situ hybridisation (FISH).
- Correlated BCL3 expression and gene status with DLBCL immunophenotypes (MUM1, GC vs. non-GC).
Main Results:
- BCL3 protein expression was observed in 36/78 DLBCL cases.
- BCL3 gene rearrangement was detected in only one case; trisomy of BCL3/chromosome 19 occurred in three cases.
- BCL3 overexpression was significantly associated with MUM1 expression and a non-germinal center (GC) phenotype (P < 0.001).
Conclusions:
- BCL3 gene rearrangement or amplification is infrequent in DLBCL.
- BCL3 overexpression, often without rearrangement, is a characteristic of the non-GC DLBCL subset.
- BCL3 alterations may contribute to the pathogenesis of a subset of de novo DLBCLs.
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