ReviewViruses2016
KSHV-Mediated Angiogenesis in Tumor Progression.
Review in Viruses, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 52 citations in OpenAlex.
- KSHV-infected endothelial cells expand and up-regulate angiogenic pathways and CXCR4 in patient-derived Kaposi sarcoma models.Science translational medicine · 2026Article
- Review
- Endostemonine I as a Multi-Target Inhibitor of Kaposi's Sarcoma-Associated Herpesvirus Oncogenic Pathways: An Integrative Computational Study.Medical sciences (Basel, Switzerland) · 2026Article
- Classic Kaposi Sarcoma: Current Treatment Strategies and Emerging Therapeutic Approaches.Cancers · 2026Review
- KSHV and cancer: understanding the oncogenic machinery for next-generation diagnostic tools and therapies.Archives of microbiology · 2026Review
- Article
- Spatial Single-Cell Atlas Reveals KSHV-Driven Broad Cellular Reprogramming, Progenitor Expansion, Immune and Vascular Remodeling in Kaposi's Sarcoma.bioRxiv : the preprint server for biology · 2025Article
- Model Systems of Gammaherpesvirus Infection, Immunity, and Disease.Journal of medical virology · 2025Review
- Review
- Review
- Mapping herpesvirus-driven impacts on the cellular milieu and transcriptional profile of Kaposi sarcoma in patient-derived mouse models.bioRxiv : the preprint server for biology · 2024Article
- Linear ubiquitination regulates the KSHV replication and transcription activator protein to control infection.Nature communications · 2024Article
- Folate-Targeted Nanocarriers Co-Deliver Ganciclovir and miR-34a-5p for Combined Anti-KSHV Therapy.International journal of molecular sciences · 2024Article
- Small extracellular vesicles as key players in cancer development caused by human oncogenic viruses.Infectious agents and cancer · 2022Review
- Human Gammaherpesvirus 8 Oncogenes Associated with Kaposi's Sarcoma.International journal of molecular sciences · 2022Review
- Correlation of SARS‑CoV‑2 to cancer: Carcinogenic or anticancer? (Review).International journal of oncology · 2022Article
- The Chemokine System in Oncogenic Pathways Driven by Viruses: Perspectives for Cancer Immunotherapy.Cancers · 2022Review
- Overview of virus and cancer relationships. Position paper.Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia · 2021Article
- Nanotechnology Frontiers in γ-Herpesviruses Treatments.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human herpesvirus 8 (HHV-8), also known as Kaposi's sarcoma-associated herpesvirus (KSHV), is a malignant human oncovirus belonging to the gamma herpesvirus family. HHV-8 is closely linked to the pathogenesis of Kaposi's sarcoma (KS) and two other B-cell lymphoproliferative diseases: primary effusion lymphoma (PEL) and a plasmablastic variant of multicentric Castleman's disease (MCD). KS is an invasive tumor of endothelial cells most commonly found in untreated HIV-AIDS or immuno-compromised individuals. KS tumors are highly vascularized and have abnormal, excessive neo-angiogenesis, inflammation, and proliferation of infected endothelial cells. KSHV directly induces angiogenesis in an autocrine and paracrine fashion through a complex interplay of various viral and cellular pro-angiogenic and inflammatory factors. KS is believed to originate due to a combination of KSHV's efficient strategies for evading host immune systems and several pro-angiogenic and pro-inflammatory stimuli. In addition, KSHV infection of endothelial cells produces a wide array of viral oncoproteins with transforming capabilities that regulate multiple host-signaling pathways involved in the activation of angiogenesis. It is likely that the cellular-signaling pathways of angiogenesis and lymph-angiogenesis modulate the rate of tumorigenesis induction by KSHV. This review summarizes the current knowledge on regulating KSHV-mediated angiogenesis by integrating the findings reported thus far on the roles of host and viral genes in oncogenesis, recent developments in cell-culture/animal-model systems, and various anti-angiogenic therapies for treating KSHV-related lymphoproliferative disorders.
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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.