ArticleProceedings of the National Academy of Sciences of the United States of America1996
c-myc activation renders proliferation of Epstein-Barr virus (EBV)-transformed cells independent of EBV nuclear antigen 2 and latent membrane protein 1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 150 citations in OpenAlex.
- STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas.PLoS pathogens · 2025Article
- Latent Epstein-Barr virus infection collaborates with Myc over-expression in normal human B cells to induce Burkitt-like Lymphomas in mice.PLoS pathogens · 2024Article
- Epstein-Barr virus and host cell 3D genome organization.Journal of medical virology · 2023Review
- EBNA2-EBF1 complexes promote MYC expression and metabolic processes driving S-phase progression of Epstein-Barr virus-infected B cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CD4 + T cells are found within endemic Burkitt lymphoma and modulate Burkitt lymphoma precursor cell viability and expression of pathogenically relevant Epstein-Barr virus genes.Cancer immunology, immunotherapy : CII · 2022Article
- The Role of Epstein-Barr Virus in Modulating Key Tumor Suppressor Genes in Associated Malignancies: Epigenetics, Transcriptional, and Post-Translational Modifications.Biomolecules · 2022Review
- Review
- Article
- EBNA2-deleted Epstein-Barr virus (EBV) isolate, P3HR1, causes Hodgkin-like lymphomas and diffuse large B cell lymphomas with type II and Wp-restricted latency types in humanized mice.PLoS pathogens · 2020Article
- Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.Frontiers in cellular and infection microbiology · 2020Review
- TAF Family Proteins and MEF2C Are Essential for Epstein-Barr Virus Super-Enhancer Activity.Journal of virology · 2019Article
- c-Myc Represses Transcription of Epstein-Barr Virus Latent Membrane Protein 1 Early after Primary B Cell Infection.Journal of virology · 2018Article
- Epstein-Barr virus-associated lymphomas.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Apoptosis resistance, mitotic catastrophe, and loss of ploidy control in Burkitt lymphoma.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Elevation of c-MYC disrupts HLA class II-mediated immune recognition of human B cell tumors.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- EBV Persistence--Introducing the Virus.Current topics in microbiology and immunology · 2015Review
- Epstein-Barr virus and Burkitt lymphoma.Chinese journal of cancer · 2014Review
- Review
- Repression of the proapoptotic cellular BIK/NBK gene by Epstein-Barr virus antagonizes transforming growth factor β1-induced B-cell apoptosis.Journal of virology · 2014Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two genetic events contribute to the development of endemic Burkitt lymphoma (BL) infection of B lymphocytes with Epstein-Barr virus (EBV) and the activation of the protooncogene c-myc through chromosomal translocation. The viral genes EBV nuclear antigen 2 (EBNA2) and latent membrane protein 1 (LMP1) are essential for transformation of primary human B cells by EBV in vitro; however, these genes are not expressed in BL cells in vivo. To address the question whether c-myc activation might abrogate the requirement of the EBNA2 and LMP1 function, we have introduced an activated c-myc gene into an EBV-transformed cell line in which EBNA2 was rendered estrogen-dependent through fusion with the hormone binding domain of the estrogen receptor. The c-myc gene was placed under the control of regulatory elements of the immunoglobulin kappa locus composed a matrix attachment region, the intron enhancer, and the 3' enhancer. We show here that transfection of a c-myc expression plasmid followed by selection for high MYC expression is capable of inducing continuous proliferation of these cells in the absence of functional EBNA2 and LMP1. c-myc-induced hormone-independent proliferation was associated with a dramatic change in the growth behavior as well as cell surface marker expression of these cells. The typical lymphoblastoid morphology and phenotype of EBV-transformed cells completely changed into that of BL cells in vivo. We conclude that the phenotype of BL cells reflects the expression pattern of viral and cellular genes rather than its germinal center origin.
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