ArticleOncogene2010
Chromosomal rearrangements after ex vivo Epstein-Barr virus (EBV) infection of human B cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
Who cites it
34 citing papers in PubMed, 77 citations in OpenAlex.
- Genome-wide mapping of EBV-induced genomic variations identifies the role of MUC19 in EBV latency.mBio · 2025Article
- Beyond Telomeres: Unveiling the Extratelomeric Functions of TERT in B-Cell Malignancies.Cancers · 2025Review
- Review
- Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.Current research in neurobiology · 2022Review
- Using telomeric chromosomal aberrations to evaluate clastogen-induced genomic instability in mammalian cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
- Long-term Culture of EBV-induced Human Lymphoblastoid Cell Lines Reveals Chromosomal Instability.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Article
- Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge.Frontiers in oncology · 2020Review
- Extra-telomeric functions of telomerase in the pathogenesis of Epstein-Barr virus-driven B-cell malignancies and potential therapeutic implications.Infectious agents and cancer · 2018Review
- Take your PIKK: tumour viruses and DNA damage response pathways.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Regulation of Telomere Homeostasis during Epstein-Barr virus Infection and Immortalization.Viruses · 2017Review
- Disruption of direct 3D telomere-TRF2 interaction through two molecularly disparate mechanisms is a hallmark of primary Hodgkin and Reed-Sternberg cells.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- LMP1 and Dynamic Progressive Telomere Dysfunction: A Major Culprit in EBV-Associated Hodgkin's Lymphoma.Viruses · 2017Review
- Limited nucleotide pools restrict Epstein-Barr virus-mediated B-cell immortalization.Oncogenesis · 2017Article
- Epstein-Barr virus particles induce centrosome amplification and chromosomal instability.Nature communications · 2017Article
- Short-term inhibition of TERT induces telomere length-independent cell cycle arrest and apoptotic response in EBV-immortalized and transformed B cells.Cell death & disease · 2016Article
- Integrity of genome-wide genotype data from low passage lymphoblastoid cell lines.Genomics data · 2016Article
- Gene dosage reductions of Trf1 and/or Tin2 induce telomere DNA damage and lymphoma formation in aging mice.Leukemia · 2016Article
- Article
- Epstein-Barr virus and Burkitt lymphoma.Chinese journal of cancer · 2014Review
- c-MYC-induced genomic instability.Cold Spring Harbor perspectives in medicine · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The Epstein-Barr virus (EBV) is carried by more than 90% of the adult world population and has been implicated in several human malignancies. Its ability to induce unlimited in vitro proliferation of B cells is frequently used to generate lymphoblastoid cell lines (LCLs). In this study, we have investigated the evolution of two LCLs up to 25 weeks after EBV infection. LCLs were karyotyped once a month by spectral karyotyping (SKY). LCLs but not mitogen-activated B cells showed evidence of DNA damage and DNA damage response within the first 2 weeks. After 4 weeks, the former, but not the latter, showed a high level of non-clonal structural aberrations, mainly deletions, fragments, dicentric chromosomes and unbalanced translocations. Genomic instability decreased thereafter over time. Nonrandom aneuploidy 12 weeks after infection showed clonal evolution in culture. After 25 weeks post-infection, most cells exhibited karyotypic stability. Chromosomal aberrations were compatible with telomere dysfunction, although in the absence of telomere shortening. The telomere capping protein TRF2 was partially displaced from telomeres in EBV-infected cells, suggesting an EBV-mediated uncapping problem. In conclusion, this study suggests that DNA damage and telomere dysfunction contribute to EBV-related chromosomal instability in early LCLs.
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Registered trials
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.