ArticleJournal of virology2007
Epstein-barr virus-induced resistance to drugs that activate the mitotic spindle assembly checkpoint in Burkitt's lymphoma cells.
Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 56 citations in OpenAlex.
- Epstein-Barr Virus Encoded BCL2, BHRF1, Downregulates Autophagy by Noncanonical Binding of BECN1.Biochemistry · 2023Article
- Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge.Frontiers in oncology · 2020Review
- Review
- Viral-Targeted Strategies Against EBV-Associated Lymphoproliferative Diseases.Frontiers in oncology · 2019Review
- Combinatorial Antitumor Activity of Oxaliplatin with Epigenetic Modifying Agents, 5-Aza-CdR and FK228, in Human Gastric Cancer Cells.Biomolecules & therapeutics · 2018Article
- Shugoshin 1 is dislocated by KSHV-encoded LANA inducing aneuploidy.PLoS pathogens · 2018Article
- Counteracting survival functions of EBNA3C in Epstein-Barr virus (EBV)-driven lymphoproliferative diseases by combination of SAHA and bortezomib.Oncotarget · 2018Article
- Therapeutic Strategies against Epstein-Barr Virus-Associated Cancers Using Proteasome Inhibitors.Viruses · 2017Review
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- EBNA3C regulates p53 through induction of Aurora kinase B.Oncotarget · 2015Article
- Epstein-Barr virus nuclear antigen 3A promotes cellular proliferation by repression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1.PLoS pathogens · 2014Article
- Article
- Genomic Instability and Cancer.Journal of carcinogenesis & mutagenesis · 2014Article
- Downregulation of integrin receptor-signaling genes by Epstein-Barr virus EBNA 3C via promoter-proximal and -distal binding elements.Journal of virology · 2012Article
- The DNA damage response in viral-induced cellular transformation.British journal of cancer · 2012Review
- Upregulation of the cell-cycle regulator RGC-32 in Epstein-Barr virus-immortalized cells.PloS one · 2011Article
- Latent Epstein-Barr virus can inhibit apoptosis in B cells by blocking the induction of NOXA expression.PloS one · 2011Article
- Epigenetic reprogramming of host genes in viral and microbial pathogenesis.Trends in microbiology · 2010Review
- Comprehensive analysis of Rhesus lymphocryptovirus microRNA expression.Journal of virology · 2010Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is associated with a number of human cancers, and latent EBV gene expression has been reported to interfere with cell cycle checkpoints and cell death pathways. Here we show that latent EBV can compromise the mitotic spindle assembly checkpoint and rescue Burkitt's lymphoma (BL)-derived cells from caspase-dependent cell death initiated in aberrant mitosis. This leads to unscheduled mitotic progression, resulting in polyploidy and multi- and/or micronucleation. The EBV latent genes responsible for this phenotype are expressed from the P3HR1 strain of virus and several viruses with similar genomic deletions that remove the EBNA2 gene. Although EBNA2 and the latent membrane proteins are not expressed, the EBNA3 proteins are present in these BL cells. Survival of the EBV-positive cells is not consistently associated with EBV lytic gene expression or with the genes that are expressed in EBV latency I BL cells (i.e., EBNA1, EBERs, and BARTs) but correlates with reduced expression of the cellular proapoptotic BH3-only protein Bim. These data suggest that a subset of latent EBV gene products may increase the likelihood of damaged DNA being inherited because of the impaired checkpoint and enhanced survival capacity. This could lead to greater genetic diversity in progeny cells and contribute to tumorigenesis. Furthermore, since it appears that this restricted latent EBV expression interferes with the responses of Burkitt's lymphoma-derived cells to cytotoxic drugs, the results of this study may have important therapeutic implications in the treatment of some BL.
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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.