Evidence map›Paper›PMID 28031537›Full record

ArticleOncotarget2017

Activation of ATR-Chk1 pathway facilitates EBV-mediated transformation of primary tonsillar B-cells.

Vanessa Mordasini, Seigo Ueda, Roberta Aslandogmus, Christoph Berger, Claudine Gysin, Daniela Hühn, Alessandro A Sartori, Michele Bernasconi, David Nadal

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. ATR/CHK1 inhibitors and cancer therapy.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2018
    Review
  13. Review
  14. Article
  15. Review
  16. 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

9 authors at 3 institutions in 2 countries.

Vanessa MordasiniExperimental Infectious Diseases and Cancer Research, University Children's Hospital of Zürich, Zürich, Switzerland.
Seigo UedaExperimental Infectious Diseases and Cancer Research, University Children's Hospital of Zürich, Zürich, Switzerland.
Roberta AslandogmusExperimental Infectious Diseases and Cancer Research, University Children's Hospital of Zürich, Zürich, Switzerland.
Christoph BergerDivision of Infectious Diseases and Hospital Epidemiology, University Children's Hospital of Zürich, Zürich, Switzerland.
Claudine GysinDivision of Otolaryngology, University Children's Hospital of Zürich, Zürich, Switzerland.
Daniela HühnInstitute of Molecular Cancer Research, University of Zürich, Zürich, Switzerland.
Alessandro A SartoriInstitute of Molecular Cancer Research, University of Zürich, Zürich, Switzerland.
Michele BernasconiExperimental Infectious Diseases and Cancer Research, University Children's Hospital of Zürich, Zürich, Switzerland.
David NadalExperimental Infectious Diseases and Cancer Research, University Children's Hospital of Zürich, Zürich, Switzerland.
University Children's Hospital Zurich · CHUniversity of Zurich · CHAsahikawa Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary infection of the immunocompromised host with the oncovirus Epstein-Barr virus (EBV) that targets mainly B-cells is associated with an increased risk for EBV-associated tumors. The early events subsequent to primary infection with potential for B-cell transformation are poorly studied. Here, we modeled in vitro the primary infection by using B-cells isolated from tonsils, the portal of entry of EBV, since species specificity of EBV hampers modeling in experimental animals. Increasing evidence indicates that the host DNA damage response (DDR) can influence and be influenced by EBV infection. Thus, we inoculated tonsillar B-cells (TBCs) with EBV-B95.8 and investigated cell proliferation and the DDR during the first 96 hours thereafter. We identified for the first time that EBV infection of TBCs induces a period of hyperproliferation 48-96 hours post infection characterized by the activation of ataxia telangiectasia and Rad3-releated (ATR) and checkpoint kinase-1 (Chk1). Whereas inhibition of Chk1 did not affect B-cell transformation, the specific inhibition of ATR robustly decreased the transformation efficiency of EBV. Our results suggest that activation of ATR is key for EBV-induced B-cell transformation. Thus, targeting the interaction between ATR/Chk1 and EBV could offer new options for the treatment of EBV-associated malignancies.

Indexed as

Cell Transformation, ViralAntigens, CD19Ataxia Telangiectasia Mutated ProteinsB-LymphocytesCD40 LigandCell ProliferationCells, CulturedCheckpoint Kinase 1DNA DamageDNA RepairEnzyme ActivationEpstein-Barr Virus InfectionsHerpesvirus 4, HumanHost-Pathogen InteractionsHumansPalatine TonsilAntigens, CD19Ataxia Telangiectasia Mutated ProteinsATR protein, humanCD19 molecule, humanCD40 LigandCheckpoint Kinase 1CHEK1 protein, humanProtein Kinase InhibitorsATRChk1DDREBVhyperproliferation

Identifiers

PMID28031537
PMCPMC5351645
OpenAlexW2566720391

What OpenQuestion 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 OpenQuestion graph.