ReviewViruses2017
LMP1 and Dynamic Progressive Telomere Dysfunction: A Major Culprit in EBV-Associated Hodgkin's Lymphoma.
Review in Viruses, 2017. 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, 26 citations in OpenAlex.
- Oncoviruses at the Crossroads of Ageing and Cancer: Molecular Mechanisms and Key Signalling Pathways.Reviews in medical virology · 2026Review
- Epigenetic control of telomeric RNA maintains heterochromatin in telomerase-driven cancers.Signal transduction and targeted therapy · 2026Article
- Structural patterns and transcriptional effects of integrated Epstein-Barr Virus revealed by long-read sequencing and RNA-sequencing in nasopharyngeal carcinoma.Virology journal · 2026Article
- Molecular mechanisms of Epstein-Barr Virus in the pathogenesis of lymphomas and new opportunities for precision medicine.Discover oncology · 2026Review
- Telomerase in cancer- ongoing quest and future discoveries.Molecular biology reports · 2025Review
- Review
- Epstein-Barr Viruses: Their Immune Evasion Strategies and Implications for Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Hemophagocytic Lymphohistiocytosis Secondary to Hodgkin's Lymphoma with Isolated Bone Marrow Involvement in a Newly Diagnosed HIV Patient.Medicina (Kaunas, Lithuania) · 2023Article
- TRF2 inhibition rather than telomerase disruption drives CD4T cell dysfunction during chronic viral infection.Journal of cell science · 2022Article
- Virus-Mediated Inhibition of Apoptosis in the Context of EBV-Associated Diseases: Molecular Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2022Review
- The Association of Epstein-Barr Virus With Cancer.Cureus · 2022Review
- New Look of EBV LMP1 Signaling Landscape.Cancers · 2021Review
- Non-canonical roles of canonical telomere binding proteins in cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Molecular Pathogenesis of Hodgkin Lymphoma: Past, Present, Future.International journal of molecular sciences · 2020Review
- Role for the shelterin protein TRF2 in human herpesvirus 6A/B chromosomal integration.PLoS pathogens · 2020Article
- Polyploid Giant Cancer Cells, a Hallmark of Oncoviruses and a New Therapeutic Challenge.Frontiers in oncology · 2020Review
- Review
- Contribution of Epstein⁻Barr Virus Latent Proteins to the Pathogenesis of Classical Hodgkin Lymphoma.Pathogens (Basel, Switzerland) · 2018Review
- The Transition between Telomerase and ALT Mechanisms in Hodgkin Lymphoma and Its Predictive Value in Clinical Outcomes.Cancers · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) is expressed in germinal-center-derived, mononuclear Hodgkin (H) and multinuclear, diagnostic Reed-Sternberg (RS) cells in classical EBV-positive Hodgkin's lymphoma (cHL). LMP1 expression in EBV-negative H-cell lines results in a significantly increased number of RS cells. In a conditional, germinal-center-derived B-cell in vitro system, LMP1 reversibly down-regulates the shelterin proteins, telomeric repeat binding factor (TRF)1, TRF2, and protection of telomeres (POT)1. This down-regulation is associated with progressive 3D shelterin disruption, resulting in telomere dysfunction, progression of complex chromosomal rearrangements, and multinuclearity. TRF2 appears to be the key player. Thus, we hypothesize that the 3D interaction of telomeres and TRF2 is disrupted in H cells, and directly associated with the formation of H and RS cells. Using quantitative 3D co-immuno-TRF2-telomere fluorescent in situ hybridization (3D TRF2/Telo-Q-FISH) applied to monolayers of primary H and RS cells, we demonstrate TRF2-telomere dysfunction in EBV-positive cHL. However, in EBV-negative cHL a second molecular mechanism characterized by massive up-regulation of TRF2, but attrition of telomere signals, is also identified. These facts point towards a shelterin-related pathogenesis of cHL, where two molecularly disparate mechanisms converge at the level of 3D Telomere-TRF2 interactions, leading to the formation of RS cells.
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.