In their 2021 study published in Leukemia, Hübschmann et al. conducted a comprehensive analysis of 181 germinal center-derived B-cell lymphomas (gcBCLs) using whole-genome and transcriptome sequencing. The research aimed to elucidate the mutational mechanisms influencing both coding and noncoding regions of the genome in these lymphomas.

• The study identified distinct mutational signatures associated with somatic hypermutation (SHM) and class-switch recombination (CSR).
• Both SHM and CSR were found to contribute to off-target mutations in non-immunoglobulin (non-IG) genes, suggesting a broader impact on genomic integrity.

• Mutations were prevalent in noncoding regions, including promoters and enhancers, indicating potential regulatory disruptions.
• These noncoding mutations may influence gene expression and contribute to lymphomagenesis.

• Recurrent mutations were observed in pathways related to B-cell development and function, such as the NF-κB and JAK-STAT signaling pathways.
• These alterations underscore the role of specific signaling cascades in the pathogenesis of gcBCLs.

• The findings highlight the significance of both coding and noncoding mutations in the development of gcBCLs.
• Understanding these mutational mechanisms may inform targeted therapeutic strategies and improve diagnostic precision.

Hübschmann et al.'s study provides valuable insights into the mutational processes shaping the genomes of germinal center-derived B-cell lymphomas. By revealing the contributions of SHM and CSR to off-target mutations and emphasizing the importance of noncoding regions, this research advances our understanding of lymphoma biology and potential avenues for treatment.

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This study, New Tier 1, 4
New Tier 1, DLBCL Tier 1, 4
This study, New Tier 2, 20
New Tier 2, DLBCL Tier 2, 20
This study, New Tier 3, 3
New Tier 3, DLBCL Tier 3, 3
All other DLBCL studies, DLBCL Tier 1, 121
All other DLBCL studies, DLBCL Tier 2, 190
All other DLBCL studies, DLBCL Tier 3, 384