Evidence map›Paper›PMID 42261377›Full record

ArticleHemaSphere2026

Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.

Filip Filipsky, Katarina B Chapman, Johannes Bloehdorn, Oscar Maiques, Abigail Lee, Andrew Clear, Jun Wang, John Gribben, Michael Hausmann, Christoph Cremer and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in HemaSphere, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Filip FilipskyCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.
Katarina B ChapmanKirchhoff-Institute for Physics, Heidelberg University, Heidelberg Germany.
Johannes BloehdornCentre for Cancer Immunology, Faculty of Medicine University of Southampton Southampton UK.
Oscar MaiquesCancer Biomarkers & Biotherapeutics, Barts Cancer Institute, Queen Mary University of London London UK.
Abigail LeeDepartment of Cellular Pathology Barts Health NHS Trust, Royal London Hospital London UK.
Andrew ClearCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.
Jun WangCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.
John GribbenCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.
Michael HausmannKirchhoff-Institute for Physics, Heidelberg University, Heidelberg Germany.
Christoph CremerKirchhoff-Institute for Physics, Heidelberg University, Heidelberg Germany.
Andrejs BraunCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.
Marta C SallanCentre for Haemato-Oncology, Barts Cancer Institute, Queen Mary University of London, 3rd Floor John Vane Science Centre, Charterhouse Square London UK.ORCID https://orcid.org/0000-0002-5781-3059
Tanya KlymenkoSchool of Biological and Behavioural Sciences, Queen Mary University of London London UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lamin B1 is a structural component of the nuclear lamina that participates in genome organization and transcriptional control. During adaptive immune responses, B lymphocytes in germinal centers (GCs) undergo clonal expansion and programmed DNA damage at immunoglobulin loci, while simultaneously downregulating Lamin B1. Likewise, Lamin B1 downregulation has been observed in GC-derived lymphomas and myeloid malignancies, yet the functional consequences of Lamin B1 loss during B cell development remain poorly understood. Here, we used in vivo and in vitro B cell models of conditional hypomorphic Lamin B1 expression, which showed elevated DNA damage and disrupted transcriptional profiles. Using sBLISS (in situ labeling and sequencing of double-strand breaks), we identified nonrandom double-strand break hotspots in both mouse and human GC B cells depleted of Lamin B1. These breaks are preferentially located near transcriptional start sites (TSSs) and regulatory elements that control translation and mRNA fate, suggesting Lamin B1 has a role in protecting regulatory genomic regions. Moreover, low LMNB1 expression is associated with poor clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL). Together, this study reveals a crucial role for Lamin B1 in preserving genomic stability in B cells, underscoring its impact on the pathogenesis of B cell-derived malignancies.

Identifiers

PMID42261377
PMCPMC13242629

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.