ArticleCancer gene therapy2022
Aberrant somatic hypermutation of CCND1 generates non-coding drivers of mantle cell lymphomagenesis.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- BCL2 promoter region mutations are an independent marker of BCL2 level in lymphoid malignancies.NPJ genomic medicine · 2026Article
- The Experimental Procedure of Somatic Hypermutation Analysis in Splenic B Cells During Primary Response.Methods in molecular biology (Clifton, N.J.) · 2026Article
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8 authors at 1 institution in 1 country.
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Abstract
Aberrant somatic hypermutation (aSHM) can target proto-oncogenes and drive oncogenesis. In mantle cell lymphoma (MCL), CCND1 is targeted by aSHM in the non-nodal subtype (nnMCL), giving rise to exon1 encoded mutant proteins like E36K, Y44D, and C47S that contribute to lymphomagenesis by virtue of their increased protein stability and nuclear localization. However, the vast majority of somatic variants generated by aSHM are found in the first intron of CCND1 but their significance for mantle cell lymphomagenesis is unknown. We performed whole-genome and whole-transcriptome sequencing in 84 MCL patients to explore the contribution of non-coding somatic variants created by aSHM to lymphomagenesis. We show that non-coding variants are enriched in a MCL specific manner in transcription factor-binding sites, that non-coding variants are associated with increased CCND1 mRNA expression, and that coding variants in the first exon of CCND1 are more often synonymous or cause benign amino acid changes than in other types of lymphomas carrying a t(11;14) translocation. Therefore, the increased frequency of somatic variants due to aSHM might be a consequence of selection pressure manifested at the transcriptional level rather than being a mere mechanistic consequence of misguided activation-induced cytidine deaminase (AID) activity.
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