Deletion of the immunoglobulin heavy chain 3′ regulatory region super-enhancer affects somatic hypermutation in B1 B cells

Issaoui, Hussein; Ghazzaui, Nour; Boyer, François; Denizot, Yves; Saintamand, Alexis

doi:10.1038/s41423-018-0091-2

Cited by 5 publications

(2 citation statements)

References 25 publications

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“…6 In contrast, deletion of the 3′RR enhancer affects B2 B-cell fate, 17 SHM, 18 and conventional CSR. [7][8][9]19 If the 3′RR deletion also affects B1 B-cell fate 16 and SHM, 20 then it has no evident effect on B1 B-cell IgA CSR. 21 If the roles of these two IgH enhancers have been observed during B-cell fate and maturation, then few data were available concerning their synergy, cooperation, and transcriptional cross talk.…”

mentioning

confidence: 99%

RETRACTED ARTICLE: 3′RR and 5′Eμ immunoglobulin heavy chain enhancers are independent engines of locus remodeling

et al. 2018

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mentioning

confidence: 99%

RETRACTED ARTICLE: 3′RR and 5′Eμ immunoglobulin heavy chain enhancers are independent engines of locus remodeling

et al. 2018

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“…3 RR is indispensable for SHM and CSR. In B cells from mice lacking 3 RR, heavy chain cannot undergo SHM, while SHM in light chain is not affected [68][69][70]. 3 RR is controlling IGH accessibility for AID to enable SHM [58,70].…”

Section: The 3 Regulatory Regionmentioning

confidence: 97%

Enhancing B-Cell Malignancies—On Repurposing Enhancer Activity towards Cancer

Kasprzyk

Sura

Dzikiewicz‐Krawczyk

2021

Cancers

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B-cell lymphomas and leukemias derive from B cells at various stages of maturation and are the 6th most common cancer-related cause of death. While the role of several oncogenes and tumor suppressors in the pathogenesis of B-cell neoplasms was established, recent research indicated the involvement of non-coding, regulatory sequences. Enhancers are DNA elements controlling gene expression in a cell type- and developmental stage-specific manner. They ensure proper differentiation and maturation of B cells, resulting in production of high affinity antibodies. However, the activity of enhancers can be redirected, setting B cells on the path towards cancer. In this review we discuss different mechanisms through which enhancers are exploited in malignant B cells, from the well-studied translocations juxtaposing oncogenes to immunoglobulin loci, through enhancer dysregulation by sequence variants and mutations, to enhancer hijacking by viruses. We also highlight the potential of therapeutic targeting of enhancers as a direction for future investigation.

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