Evidence map›Paper›PMID 38169736›Full record

ArticleFrontiers in immunology2023

LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells.

Jingwei Zhang, Thomas Sommermann, Xun Li, Lutz Gieselmann, Kathrin de la Rosa, Maria Stecklum, Florian Klein, Christine Kocks, Klaus Rajewsky

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.5field-weighted citation impact, top 4% of its field
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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  11. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  12. Review
  13. The interplay of EBV virus and cell metabolism in lung cancer.Journal of cellular and molecular medicine · 2024
    Review
  14. Review
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

9 authors at 3 institutions in 1 country.

Jingwei ZhangMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Regulation and Cancer, Berlin, Germany.
Thomas SommermannMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Regulation and Cancer, Berlin, Germany.
Xun LiMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Regulation and Cancer, Berlin, Germany.
Lutz GieselmannLaboratory of Experimental Immunology, Institute of Virology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Kathrin de la RosaMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Mechanisms and Human Antibodies, Berlin, Germany.
Maria StecklumExperimental Pharmacology and Oncology (EPO) Berlin-Buch GmbH, Berlin, Germany.
Florian KleinLaboratory of Experimental Immunology, Institute of Virology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Christine KocksMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Regulation and Cancer, Berlin, Germany.
Klaus RajewskyMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Immune Regulation and Cancer, Berlin, Germany.
Max Delbrück Center · DEUniversity of Cologne · DEHelios Hospital Berlin-Buch · DE

Funding

European Research Council 268921
6 · The paper itself

Abstract

Introduction: Epstein-Barr virus (EBV) infection in humans is associated with a wide range of diseases including malignancies of different origins, most prominently B cells. Several EBV latent genes are thought to act together in B cell immortalization, but a minimal set of EBV genes sufficient for transformation remains to be identified. Methods: Here, we addressed this question by transducing human peripheral B cells from EBV-negative donors with retrovirus expressing the latent EBV genes encoding Latent Membrane Protein (LMP) 1 and 2A and Epstein-Barr Nuclear Antigen (EBNA) 2. Results: LMP1 together with EBNA2, but not LMP1 alone or in combination with LMP2A was able to transform human primary B cells. LMP1/EBNA2-immortalized cell lines shared surface markers with EBV-transformed lymphoblastoid cell lines (LCLs). They showed sustained growth for more than 60 days, albeit at a lower growth rate than EBV-transformed LCLs. LMP1/EBNA2-immortalized cell lines generated tumors when transplanted subcutaneously into severely immunodeficient NOG mice. Conclusion: Our results identify a minimal set of EBV proteins sufficient for B cell transformation.

Indexed as

Epstein-Barr Virus InfectionsAnimalsB-LymphocytesCell Transformation, NeoplasticEpstein-Barr Virus Nuclear AntigensHerpesvirus 4, HumanHumansMiceViral ProteinsEpstein-Barr Virus Nuclear AntigensViral ProteinsB cell lymphomaEBV latent genesEpstein-Barr nuclear antigen 2 (EBNA2)Epstein-Barr virus (EBV)latent membrane protein 1 (LMP1)lymphoblastoid cell line (LCL)lymphomagenesistransduction of human primary B cells

Identifiers

PMID38169736
PMCPMC10758421
OpenAlexW4389952984

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.