Evidence map›Paper›PMID 25566237›Full record

ArticleFrontiers in microbiology2014

Molecular signature of Epstein Barr virus-positive Burkitt lymphoma and post-transplant lymphoproliferative disorder suggest different roles for Epstein Barr virus.

Mohsen Navari, Fabio Fuligni, Maria A Laginestra, Maryam Etebari, Maria R Ambrosio, Maria R Sapienza, Maura Rossi, Giulia De Falco, Davide Gibellini, Claudio Tripodo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  7. Biomarkers for PTLD diagnosis and therapies.Pediatric nephrology (Berlin, Germany) · 2020
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  10. Transcriptional analysis distinguishes breast implant-associated anaplastic large cell lymphoma from other peripheral T-cell lymphomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
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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 at 5 institutions in 3 countries.

Mohsen NavariHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy ; Department of Medical Biotechnology, University of Siena Siena, Italy ; Department of Basic sciences, Torbat Heydariyeh University of Medical Sciences Torbat Heydariyeh, Iran.
Fabio FuligniHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Maria A LaginestraHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Maryam EtebariHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Maria R AmbrosioDepartment of Medical Biotechnology, University of Siena Siena, Italy.
Maria R SapienzaHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Maura RossiHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Giulia De FalcoNanchang Joint Programme in Biomedical Sciences, School of Biological and Chemical Sciences, Queen Mary University of London London, UK.
Davide GibelliniMicrobiology and Virology Unit, Department of Pathology and Diagnostic, University of Verona Verona, Italy.
Claudio TripodoTumour Immunology Unit, Human Pathology Section, Department of Health Science, Palermo University School of Medicine Palermo, Italy.
Stefano A PileriHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Lorenzo LeonciniDepartment of Medical Biotechnology, University of Siena Siena, Italy.
Pier P PiccalugaHematopathology Section, Department of Experimental, Diagnostic, and Experimental Medicine, S. Orsola-Malpighi Hospital, Bologna University School of Medicine Bologna, Italy.
Policlinico S.Orsola-Malpighi · ITUniversity of Siena · ITQueen Mary University of London · GBUniversity of Palermo · ITUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein Barr virus (EBV) infection is commonly associated with human cancer and, in particular, with lymphoid malignancies. Although the precise role of the virus in the pathogenesis of different lymphomas is largely unknown, it is well recognized that the expression of viral latent proteins and miRNA can contribute to its pathogenetic role. In this study, we compared the gene and miRNA expression profile of two EBV-associated aggressive B non-Hodgkin lymphomas known to be characterized by differential expression of the viral latent proteins aiming to dissect the possible different contribution of such proteins and EBV-encoded miRNAs. By applying extensive bioinformatic inferring and an experimental model, we found that EBV+ Burkitt lymphoma presented with significant over-expression of EBV-encoded miRNAs that were likely to contribute to its global molecular profile. On the other hand, EBV+ post-transplant diffuse large B-cell lymphomas presented a significant enrichment in genes regulated by the viral latent proteins. Based on these different viral and cellular gene expression patterns, a clear distinction between EBV+ Burkitt lymphoma and post-transplant diffuse large B-cell lymphomas was made. In this regard, the different viral and cellular expression patterns seemed to depend on each other, at least partially, and the latency type most probably played a significant role in their regulation. In conclusion, our data indicate that EBV influence over B-cell malignant clones may act through different mechanisms of transcriptional regulation and suggest that potentially different pathogenetic mechanisms may depend upon the conditions of the interaction between EBV and the host that finally determine the latency pattern.

Indexed as

Burkitt lymphomaEpstein Barr Virusgene expression profilinglatencyMicroRNApost-transplant lymphoproliferative disorder

Identifiers

PMID25566237
PMCPMC4274971
OpenAlexW2051048295

What OpenQuestion holds

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LicenceCC BY
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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.