ArticleJournal of translational medicine2023
Transcriptional landscape of Kaposi sarcoma tumors identifies unique immunologic signatures and key determinants of angiogenesis.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Omics-Level Approaches to Studying Gammaherpesvirus Infection.Pathogens (Basel, Switzerland) · 2026Review
- KSHV-infected endothelial cells expand and up-regulate angiogenic pathways and CXCR4 in patient-derived Kaposi sarcoma models.Science translational medicine · 2026Article
- Vascular Endothelial Growth Factor Receptor 2 (VEGFR2/KDR) Promotes KSHV Lytic Replication and Drives Pro-Inflammatory Cytokine Release and Cancer Signaling.Journal of medical virology · 2026Article
- Spatial and bulk transcriptomics reveal distinct molecular signatures in Kaposi sarcoma with and without other KSHV-associated diseases.Journal of translational medicine · 2026Article
- Spatial and Bulk Transcriptomics Reveal Distinct Molecular Signatures in Kaposi Sarcoma with and Without other KSHV-Associated Diseases.medRxiv : the preprint server for health sciences · 2025Article
- Spatial Transcriptomics of Patients With Kaposi Sarcoma Identifies Mechanisms of Immune Evasion.Journal of medical virology · 2025Article
- Characteristics and outcomes of Kaposi sarcoma herpesvirus-associated inflammatory cytokine syndrome.Blood advances · 2025Article
- Integrative functional genomics analysis of Kaposi sarcoma cohorts.Scientific reports · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- Heat shock factor 2 regulates oncogenic gamma-herpesvirus gene expression by remodeling the chromatin at the ORF50 and BZLF1 promoter.PLoS pathogens · 2025Article
- The elevated expression of ORF75, a KSHV lytic gene, in Kaposi sarcoma lesions is driven by a GC-rich DNA cis element in its promoter region.PLoS pathogens · 2025Article
- Exploration of RNA-binding proteins identified RPS27 as a potential regulator associated with Kaposi's sarcoma development.BMC cancer · 2025Article
- Article
- Analysis of tumor infiltrating immune cells in Kaposi sarcoma lesions discovers shifts in macrophage populations.Global health & medicine · 2024Article
- 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
- The Elevated Expression of ORF75, a Lytic KSHV Gene, in Kaposi Sarcoma Lesions is Driven by a GC-rich DNA cis Element in its Promoter Region.bioRxiv : the preprint server for biology · 2024Article
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
Corrections and comments
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Authors and funding
20 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundKaposi sarcoma (KS) is a multicentric tumor caused by Kaposi sarcoma herpesvirus (KSHV) that leads to morbidity and mortality among people with HIV worldwide. KS commonly involves the skin but can occur in the gastrointestinal tract (GI) in severe cases.
methodsRNA sequencing was used to compare the cellular and KSHV gene expression signatures of skin and GI KS lesions in 44 paired samples from 19 participants with KS alone or with concurrent KSHV-associated diseases. Analyses of KSHV expression from KS lesions identified transcriptionally active areas of the viral genome.
resultsThe transcript of an essential viral lytic gene, ORF75, was detected in 91% of KS lesions. Analyses of host genes identified 370 differentially expressed genes (DEGs) unique to skin KS and 58 DEGs unique to GI KS lesions as compared to normal tissue. Interleukin (IL)-6 and IL-10 gene expression were higher in skin lesions as compared to normal skin but not in GI KS lesions. Twenty-six cellular genes were differentially expressed in both skin and GI KS tissues: these included Fms-related tyrosine kinase 4 (FLT4), encoding an angiogenic receptor, and Stanniocalcin 1 (STC1), a secreted glycoprotein. FLT4 and STC1 were further investigated in functional studies using primary lymphatic endothelial cells (LECs). In these models, KSHV infection of LECs led to increased tubule formation that was impaired upon knock-down of STC1 or FLT4.
conclusionsThis study of transcriptional profiling of KS tissue provides novel insights into the characteristics and pathogenesis of this unique virus-driven neoplasm.
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