ReviewSeminars in cancer biology2009
How does Epstein-Barr virus (EBV) complement the activation of Myc in the pathogenesis of Burkitt's lymphoma?
Review in Seminars in cancer biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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.
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
53 citing papers in PubMed, 105 citations in OpenAlex.
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- Immunotherapy of Oncovirus-Induced Cancers: A Review on the Development and Efficacy of Targeted Vaccines.Vaccines · 2025Review
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- MYC directly transactivates CR2/CD21, the receptor of the Epstein-Barr virus, enhancing the viral infection of Burkitt lymphoma cells.Oncogene · 2023Article
- Review
- Cryo-EM Structure and Functional Studies of EBNA1 Binding to the Family of Repeats and Dyad Symmetry Elements of Epstein-Barr VirusJournal of virology · 2022Article
- The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms.Leukemia · 2022Review
- The Association of Epstein-Barr Virus With Cancer.Cureus · 2022Review
- EBV-associated diseases: Current therapeutics and emerging technologies.Frontiers in immunology · 2022Review
- Review
- Review
- Review
- Reframing Burkitt lymphoma: virology not epidemiology defines clinical variants.Annals of lymphoma · 2021Article
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Epstein Barr Virus: Development of Vaccines and Immune Cell Therapy for EBV-Associated Diseases.Frontiers in immunology · 2021Review
- Epstein-Barr Virus Episome Physically Interacts with Active Regions of the Host Genome in Lymphoblastoid Cells.Journal of virology · 2020Article
- Transnasal endoscopic resection of Epstein-Barr virus-associated cavernous sinus tumour.BMJ case reports · 2020Article
- IL-21 Stimulates the expression and activation of cell cycle regulators and promotes cell proliferation in EBV-positive diffuse large B cell lymphoma.Scientific reports · 2020Article
- Review
- High-throughput sequencing analysis of a "hit and run" cell and animal model of KSHV tumorigenesis.PLoS pathogens · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A defining characteristic of the aggressive B cell tumour Burkitt's lymphoma (BL) is a reciprocal chromosomal translocation that activates the Myc oncogene by juxtaposing it to one of the immunoglobulin gene loci. The consequences of activating Myc include cell growth and proliferation that can lead to lymphomagenesis; however, as part of a fail-safe mechanism that has evolved in metazoans to reduce the likelihood of neoplastic disease, activated oncogenes such as Myc may also induce cell death by apoptosis and/or an irreversible block to proliferation called senescence. For lymphoma to develop it is necessary that these latter processes are repressed. More than 95% of a subset of BL - known as endemic (e)BL because they are largely restricted to regions of equatorial Africa and similar geographical regions - carry latent Epstein-Barr virus (EBV) in the form of nuclear extra-chromosomal episomes. Although EBV is not generally regarded as a driving force of BL cell proliferation, it plays an important role in the pathogenesis of eBL. Latency-associated EBV gene products can inhibit a variety of pathways that lead to apoptosis and senescence; therefore EBV probably counteracts the proliferation-restricting activities of deregulated Myc and so facilitates the development of BL.
Indexed as
Identifiers
What OpenQuestion holds
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.