ArticlePLoS pathogens2007
Viral oncogene-induced DNA damage response is activated in Kaposi sarcoma tumorigenesis.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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.
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
74 citing papers in PubMed, 109 citations in OpenAlex.
- Article
- Efficacy of Immune Checkpoint Inhibitors and Oncoviruses in Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Review
- Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.Journal of medical virology · 2025Review
- Review
- [Mechanism and significance of cell senescence induced by viral infection].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.Nature communications · 2025Article
- Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome.Nucleic acids research · 2024Article
- DNA damage response(DDR): a link between cellular senescence and human cytomegalovirus.Virology journal · 2023Review
- Senotherapeutics: An emerging approach to the treatment of viral infectious diseases in the elderly.Frontiers in cellular and infection microbiology · 2023Review
- Marek's disease virus prolongs survival of primary chicken B-cells by inducing a senescence-like phenotype.PLoS pathogens · 2021Article
- Bats and viruses: a death-defying friendship.Virusdisease · 2021Review
- HIV-Associated Cancer Biomarkers: A Requirement for Early Diagnosis.International journal of molecular sciences · 2021Review
- 3D culture conditions support Kaposi's sarcoma herpesvirus (KSHV) maintenance and viral spread in endothelial cells.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Tampering of Viruses and Bacteria with Host DNA Repair: Implications for Cellular Transformation.Cancers · 2021Review
- Review
- KSHV requires vCyclin to overcome replicative senescence in primary human lymphatic endothelial cells.PLoS pathogens · 2020Article
- Interplay Between KSHV and the Host DNA Damage Response.Frontiers in cellular and infection microbiology · 2020Review
- PDGFRA defines the mesenchymal stem cell Kaposi's sarcoma progenitors by enabling KSHV oncogenesis in an angiogenic environment.PLoS pathogens · 2019Article
- Review
- K1 gene transformation activities in AIDS-related and classic type Kaposi's sarcoma: Correlation with clinical presentation.Scientific reports · 2019Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi sarcoma is a tumor consisting of Kaposi sarcoma herpesvirus (KSHV)-infected tumor cells that express endothelial cell (EC) markers and viral genes like v-cyclin, vFLIP, and LANA. Despite a strong link between KSHV infection and certain neoplasms, de novo virus infection of human primary cells does not readily lead to cellular transformation. We have studied the consequences of expression of v-cyclin in primary and immortalized human dermal microvascular ECs. We show that v-cyclin, which is a homolog of cellular D-type cyclins, induces replicative stress in ECs, which leads to senescence and activation of the DNA damage response. We find that antiproliferative checkpoints are activated upon KSHV infection of ECs, and in early-stage but not late-stage lesions of clinical Kaposi sarcoma specimens. These are some of the first results suggesting that DNA damage checkpoint response also functions as an anticancer barrier in virally induced cancers.
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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.