ArticleLeukemia2017
HIV Tat induces a prolonged MYC relocalization next to IGH in circulating B-cells.
Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 66 citations in OpenAlex.
- In the South African setting, HIV-associated Burkitt lymphoma is associated with frequent leukaemic presentation, complex cytogenetic karyotypes, and adverse clinical outcomes.Annals of hematology · 2020Trial
- Interaction between HIV-1 Tat and EBV Zta favours immune escape of B cells by downregulating HLA-ABC expression.Cellular and molecular life sciences : CMLS · 2026Article
- HIV reservoirs in lymphomagenesis: hidden driver in the era of viral suppression?Microbiology and molecular biology reviews : MMBR · 2025Review
- Circulating Biomarker Panorama in HIV-Associated Lymphoma: A Bridge from Early Risk Warning to Prognostic Stratification.Biomolecules · 2025Review
- Lymphoproliferations in People Living with HIV: Oncogenic Pathways, Diagnostic Challenges, and New Therapeutic Opportunities.Cancers · 2025Review
- Pathological Mechanisms Involved in HIV-Associated Lymphomagenesis: Novel Targeted Therapeutic Approaches.Cells · 2025Review
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.Frontiers in immunology · 2025Review
- Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure.Journal of cellular physiology · 2025Article
- HIV Tat as a latency reversing agent: turning the tables on viral persistence.Frontiers in immunology · 2025Review
- Review
- Virus-driven dysregulation of the BCR pathway: a potential mechanism for the high prevalence of HIV related B-cell lymphoma.Annals of hematology · 2024Review
- Immune Characteristics and Immunotherapy of HIV-Associated Lymphoma.Current issues in molecular biology · 2024Review
- Specificity of cancer-related chromosomal translocations is linked to proximity after the DNA double-strand break and subsequent selection.NAR cancer · 2023Article
- 3D genome alterations and editing in pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Review
- Review
- Article
- Multilevel view on chromatin architecture alterations in cancer.Frontiers in genetics · 2022Review
- New insights into pathogenesis point to HIV-1 Tat as a key vaccine target.Archives of virology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With combined antiretroviral therapy (cART), the risk for HIV-infected individuals to develop a non-Hodgkin lymphoma is diminished. However, the incidence of Burkitt lymphoma (BL) remains strikingly elevated. Most BL present a t(8;14) chromosomal translocation which must take place at a time of spatial proximity between the translocation partners. The two partner genes, MYC and IGH, were found colocalized only very rarely in the nuclei of normal peripheral blood B-cells examined using 3D-FISH while circulating B-cells from HIV-infected individuals whose exhibited consistently elevated levels of MYC-IGH colocalization. In vitro, incubating normal B-cells from healthy donors with a transcriptionally active form of the HIV-encoded Tat protein rapidly activated transcription of the nuclease-encoding RAG1 gene. This created DNA damage, including in the MYC gene locus which then moved towards the center of the nucleus where it sustainably colocalized with IGH up to 10-fold more frequently than in controls. In vivo, this could be sufficient to account for the elevated risk of BL-specific chromosomal translocations which would occur following DNA double strand breaks triggered by AID in secondary lymph nodes at the final stage of immunoglobulin gene maturation. New therapeutic attitudes can be envisioned to prevent BL in this high risk group.
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.