Evidence map›Paper›PMID 23269792›Full record

ArticleJournal of virology2013

Different patterns of Epstein-Barr virus latency in endemic Burkitt lymphoma (BL) lead to distinct variants within the BL-associated gene expression signature.

Gemma L Kelly, Julianna Stylianou, Jane Rasaiyaah, Wenbin Wei, Wendy Thomas, Deborah Croom-Carter, Christian Kohler, Rainer Spang, Ciaran Woodman, Paul Kellam and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Imaging in Tumor Immunology.Nuclear medicine and molecular imaging · 2021
    Review
  10. Review
  11. Review
  12. Adoptive T-Cell Therapy for Epstein-Barr Virus-Related Lymphomas.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.Frontiers in cellular and infection microbiology · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. 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

12 authors at 3 institutions in 3 countries.

Gemma L KellySchool of Cancer Sciences, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, United Kingdom.
Julianna Stylianou
Jane Rasaiyaah
Wenbin Wei
Wendy Thomas
Deborah Croom-Carter
Christian Kohler
Rainer Spang
Ciaran Woodman
Paul Kellam
Alan B Rickinson
Andrew I Bell
University of Birmingham · GBUniversity College London · GBUniversity of Regensburg · DE

Funding

Cancer Research UK 15032Cancer Research UK C910/A8829
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) is present in all cases of endemic Burkitt lymphoma (BL) but in few European/North American sporadic BLs. Gene expression arrays of sporadic tumors have defined a consensus BL profile within which tumors are classifiable as "molecular BL" (mBL). Where endemic BLs fall relative to this profile remains unclear, since they not only carry EBV but also display one of two different forms of virus latency. Here, we use early-passage BL cell lines from different tumors, and BL subclones from a single tumor, to compare EBV-negative cells with EBV-positive cells displaying either classical latency I EBV infection (where EBNA1 is the only EBV antigen expressed from the wild-type EBV genome) or Wp-restricted latency (where an EBNA2 gene-deleted virus genome broadens antigen expression to include the EBNA3A, -3B, and -3C proteins and BHRF1). Expression arrays show that both types of endemic BL fall within the mBL classification. However, while EBV-negative and latency I BLs show overlapping profiles, Wp-restricted BLs form a distinct subgroup, characterized by a detectable downregulation of the germinal center (GC)-associated marker Bcl6 and upregulation of genes marking early plasmacytoid differentiation, notably IRF4 and BLIMP1. Importantly, these same changes can be induced in EBV-negative or latency I BL cells by infection with an EBNA2-knockout virus. Thus, we infer that the distinct gene profile of Wp-restricted BLs does not reflect differences in the identity of the tumor progenitor cell per se but differences imposed on a common progenitor by broadened EBV gene expression.

Indexed as

TranscriptomeAntigens, ViralBurkitt LymphomaCell Line, TumorDNA-Binding ProteinsDown-RegulationEpstein-Barr Virus Nuclear AntigensGene Expression ProfilingGene Expression Regulation, ViralHerpesvirus 4, HumanHumansInterferon Regulatory FactorsPositive Regulatory Domain I-Binding Factor 1Proto-Oncogene Proteins c-bcl-6Repressor ProteinsUp-RegulationAntigens, ViralBCL6 protein, humanBHRF1 protein, Human herpesvirus 4DNA-Binding ProteinsEBNA-2 protein, Human herpesvirus 4EBNA-3A antigenEBNA-3B antigenEBNA-3C, epstein-barr virusEBV-encoded nuclear antigen 1Epstein-Barr Virus Nuclear AntigensInterferon Regulatory FactorsPositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanProto-Oncogene Proteins c-bcl-6Repressor Proteinsviral interferon regulatory factorsViral Proteins

Identifiers

PMID23269792
PMCPMC3571367
OpenAlexW2011857676

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.