ArticleLeukemia2008
KSHV-transformed primary effusion lymphoma cells induce a VEGF-dependent angiogenesis and establish functional gap junctions with endothelial cells.
Article in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 27 citations in OpenAlex.
- Phase II study of bevacizumab in patients with HIV-associated Kaposi's sarcoma receiving antiretroviral therapy.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2012Trial
- Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025Review
- Review
- SUMO Modification of Histone Demethylase KDM4A in Kaposi's Sarcoma-Associated Herpesvirus-Induced Primary Effusion Lymphoma.Journal of virology · 2022Article
- Connexins in Cancer: Jekyll or Hyde?Biomolecules · 2020Review
- Lenalidomide in Combination with Arsenic Trioxide: an Effective Therapy for Primary Effusion Lymphoma.Cancers · 2020Article
- Review
- Towards Better Understanding of KSHV Life Cycle: from Transcription and Posttranscriptional Regulations to Pathogenesis.Virologica Sinica · 2019Review
- Convergent perturbation of the human domain-resolved interactome by viruses and mutations inducing similar disease phenotypes.PLoS computational biology · 2019Article
- Mind the Gaps in Tumor Immunity: Impact of Connexin-Mediated Intercellular Connections.Frontiers in immunology · 2017Review
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- Targeting of prosurvival pathways as therapeutic approaches against primary effusion lymphomas: past, present, and Future.BioMed research international · 2015Review
- Molecular biology of human herpesvirus 8: novel functions and virus-host interactions implicated in viral pathogenesis and replication.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2014Review
- Kaposi's sarcoma-associated herpesvirus glycoproteins B and K8.1 regulate virion egress and synthesis of vascular endothelial growth factor and viral interleukin-6 in BCBL-1 cells.Journal of virology · 2010Article
- Modulation of brain hemichannels and gap junction channels by pro-inflammatory agents and their possible role in neurodegeneration.Antioxidants & redox signaling · 2009Review
- Angiogenesis, Kaposi's Sarcoma and Kaposi's Sarcoma-Associated Herpesvirus.Virologica Sinica · 2008Article
- Functional role of gap junctions in cytokine-induced leukocyte adhesion to endothelium in vivo.American journal of physiology. Heart and circulatory physiology · 2008Article
- Glial connexins and gap junctions in CNS inflammation and disease.Journal of neurochemistry · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of primary effusion lymphoma (PEL) and of Kaposi's sarcoma. PEL is an aggressive proliferation of B cells with poor prognosis. We evaluated both in vitro and in vivo the potential role of angiogenic factors secreted by PEL cells, that is, their interaction with endothelial cells and their implication in the invasive behavior of tumoral cells. In vitro, PEL-induced angiogenesis is dependent on vascular endothelial growth factor (VEGF) and VEGF receptors. However, although PEL cells produce VEGF and basic fibroblast growth factor (b-FGF) transcripts, they only secrete VEGF in vitro. In vivo, very high levels of both VEGF and b-FGF were found in the ascitic fluid of NOD/SCID mice injected with PEL cells. We then show evidence of cell adhesion and gap junction-mediated heterocellular communication between PEL cells and endothelial cells. Finally, we show that PEL cells extravasate through the endothelial barrier and that the specific tyrosine kinase inhibitor of VEGF receptors, PTK-787/ZK-222584, the anti-VEGF antibody, bevacizumab or the gap junction inhibitor 18-alpha-glycyrrhetinic acid, partially attenuate PEL cell extravasation. Angiogenesis, cell adhesion and communication likely contribute to the development of PEL and represent potential therapeutic targets.
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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.