Evidence map›Paper›PMID 36270981›Full record

ArticleCell death & disease2022

Epstein Barr virus-mediated transformation of B cells from XIAP-deficient patients leads to increased expression of the tumor suppressor CADM1.

Christine Engelmann, Patrick Schuhmachers, Hana Zdimerova, Sanamjeet Virdi, Mathias Hauri-Hohl, Jana Pachlopnik Schmid, Adam Grundhoff, Rebecca A Marsh, Wendy Wei-Lynn Wong, Christian Münz

Open access · goldAbstract read
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Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

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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

10 authors at 4 institutions in 3 countries.

Christine EngelmannViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Patrick SchuhmachersViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Hana ZdimerovaViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.
Sanamjeet VirdiVirus Genomics, Heinrich Pette Institute, Hamburg, Germany.
Mathias Hauri-HohlDivision of Immunology, University Children's Hospital Zurich, Zurich, Switzerland.
Jana Pachlopnik SchmidDivision of Immunology, University Children's Hospital Zurich, Zurich, Switzerland.
Adam GrundhoffVirus Genomics, Heinrich Pette Institute, Hamburg, Germany.
Rebecca A MarshDepartment of Pediatrics, University of Cincinnati, Cincinnati, OH, USA.
Wendy Wei-Lynn WongCell Death and Regulation of Inflammation, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland.ORCID 0000-0003-3155-1211
Christian MünzViral Immunobiology, Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland. christian.muenz@uzh.ch.ORCID 0000-0001-6419-1940
University of Zurich · CHLeibniz Institute of Virology (LIV) · DEUniversity Children's Hospital Zurich · CHUniversity of Cincinnati · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

X-linked lymphoproliferative disease (XLP) is either caused by loss of the SLAM-associated protein (SAP; XLP-1) or the X-linked inhibitor of apoptosis (XIAP; XLP-2). In both instances, infection with the oncogenic human Epstein Barr virus (EBV) leads to pathology, but EBV-associated lymphomas only emerge in XLP-1 patients. Therefore, we investigated the role of XIAP during B cell transformation by EBV. Using humanized mice, IAP inhibition in EBV-infected mice led to a loss of B cells and a tendency to lower viral titers and lymphomagenesis. Loss of memory B cells was also observed in four newly described patients with XIAP deficiency. EBV was able to transform their B cells into lymphoblastoid cell lines (LCLs) with similar growth characteristics to patient mothers' LCLs in vitro and in vivo. Gene expression analysis revealed modest elevated lytic EBV gene transcription as well as the expression of the tumor suppressor cell adhesion molecule 1 (CADM1). CADM1 expression on EBV-infected B cells might therefore inhibit EBV-associated lymphomagenesis in patients and result in the absence of EBV-associated malignancies in XLP-2 patients.

Indexed as

Epstein-Barr Virus InfectionsLymphoproliferative DisordersAnimalsB-LymphocytesCell Adhesion Molecule-1Herpesvirus 4, HumanHumansMiceSignaling Lymphocytic Activation Molecule Associated ProteinX-Linked Inhibitor of Apoptosis ProteinCADM1 protein, humanCell Adhesion Molecule-1Signaling Lymphocytic Activation Molecule Associated ProteinXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID36270981
PMCPMC9587222
OpenAlexW4307140194

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.