ArticleBlood2011
A shared gene expression signature in mouse models of EBV-associated and non-EBV-associated Burkitt lymphoma.
Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Selective effects of cyclin dependent kinase inhibitors in gammaherpesvirus reactivation from latency.bioRxiv : the preprint server for biology · 2026Article
- Glutathione overproduction mediates lymphoma initiating cells survival and has a sex-dependent effect on lymphomagenesis.Cell death & disease · 2024Article
- Calcineurin-independent NFATc1 signaling is essential for survival of Burkitt lymphoma cells.Frontiers in oncology · 2023Article
- Latent membrane proteins from EBV differentially target cellular pathways to accelerate MYC-induced lymphomagenesis.Blood advances · 2022Article
- Two Pathways of p27mBio · 2019Article
- EBV latent membrane protein 2A orchestrates p27Blood · 2017Article
- Article
- Post-transplant lymphoproliferative disease (PTLD): risk factors, diagnosis, and current treatment strategies.Current hematologic malignancy reports · 2013Review
- Epstein-barr virus infected gastric adenocarcinoma expresses latent and lytic viral transcripts and has a distinct human gene expression profile.Infectious agents and cancer · 2012Article
- Epstein-Barr virus LMP2A reduces hyperactivation induced by LMP1 to restore normal B cell phenotype in transgenic mice.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The link between EBV infection and Burkitt lymphoma (BL) is strong, but the mechanism underlying that link has been elusive. We have developed a mouse model for EBV-associated BL in which LMP2A, an EBV latency protein, and MYC are expressed in B cells. Our model has demonstrated the ability of LMP2A to accelerate tumor onset, increase spleen size, and bypass p53 inactivation. Here we describe the results of total gene expression analysis of tumor and pretumor B cells from our transgenic mouse model. Although we see many phenotypic differences and changes in gene expression in pretumor B cells, the transcriptional profiles of tumor cells from LMP2A/λ-MYC and λ-MYC mice are strikingly similar, with fewer than 20 genes differentially expressed. We evaluated the functional significance of one of the most interesting differentially expressed genes, Egr1, and found that it was not required for acceleration of tumor onset by LMP2A. Our studies demonstrate the remarkable ability of LMP2A to affect the pretumor B-cell phenotype and tumorigenesis without substantially altering gene expression in tumor cells.
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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.