ReviewFrontiers in cellular and infection microbiology2020
Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.
Review in Frontiers in cellular and infection microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Overview on Epstein-Barr Virus-Host Interactions With a Focus on Host Cell Transcriptome Alterations.Cell biochemistry and function · 2026Review
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- Dissecting Epstein-Barr Virus Dependence Across Diverse Infected Cell Models.bioRxiv : the preprint server for biology · 2025Article
- From Viral Infection to Malignancy: The Dual Threat of EBV and COVID-19 in Cancer Development.Viruses · 2025Review
- Article
- 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
- Article
- A promising predictive biomarker combined EBV NDA with PNI for nasopharyngeal carcinoma in nonendemic area of China.Scientific reports · 2023Article
- Worldwide Prevalence of Epstein-Barr Virus in Patients with Burkitt Lymphoma: A Systematic Review and Meta-Analysis.Diagnostics (Basel, Switzerland) · 2023Review
- Human DNA tumor viruses evade uracil-mediated antiviral immunity.PLoS pathogens · 2023Article
- Review
- Article
- EBV persistence in gastric cancer cases conventionally classified as EBER-ISH negative.Infectious agents and cancer · 2022Article
- Perfluoroalkyl substances (PFASs) decrease the expression of recombination-activating genes (RAG1 and RAG2) in human B lymphoma Namalwa cells.Archives of toxicology · 2022Article
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- Article
- EBV Infection and Its Regulated Metabolic Reprogramming in Nasopharyngeal Tumorigenesis.Frontiers in cellular and infection microbiology · 2022Review
- Review
- Reframing Burkitt lymphoma: virology not epidemiology defines clinical variants.Annals of lymphoma · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr Virus (EBV) can transform B cells and contributes to the development of Burkitt lymphoma and other cancers. Through decades of study, we now recognize that many of the viral genes required to transform cells are not expressed in EBV-positive Burkitt lymphoma (BL) tumors, likely due to the immune pressure exerted on infected cells. This recognition has led to the hypothesis that the loss of expression of these viral genes must be compensated through some mechanisms. Recent progress in genome-wide mutational analysis of tumors provides a wealth of data about the cellular mutations found in EBV-positive BLs. Here, we review common cellular mutations found in these tumors and consider how they may compensate for the viral genes that are no longer expressed. Understanding these mutations and how they may substitute for EBV's genes and contribute to lymphomagenesis can serve as a launchpad for more mechanistic studies, which will help us navigate the sea of genomic data available today, and direct the discoveries necessary to improve the treatment of EBV-positive BLs.
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.