ArticleJournal of the European Academy of Dermatology and Venereology : JEADV2022
Genetic landscape of indolent and aggressive Kaposi sarcomas.
Article in Journal of the European Academy of Dermatology and Venereology : JEADV, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Bypass of LANA-DNA crosslinks by Polη ensures KSHV genome maintenance and tumor growth.Cell reports · 2026Article
- Virus-immune signatures reveal distinct clinical phenotypes and predict prognosis in patients with Kaposi's sarcoma.Journal of translational medicine · 2026Article
- Comparative study of clinical features, pathology, and immunophenotype between HIV-related cutaneous and visceral Kaposi's sarcoma.BMC cancer · 2026Article
- Exome Sequencing Reveals a Sparse Genomic Landscape in Kaposi Sarcoma.Molecular cancer research : MCR · 2025Article
- Developing hypoxia and lactate metabolism-related molecular subtypes and prognostic signature for clear cell renal cell carcinoma through integrating machine learning.Discover oncology · 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
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundKaposi sarcoma (KS) is a rare skin tumour caused by herpesvirus 8 infection and characterized by either indolence or an aggressive course necessitating systemic therapies. The genetic basis of this difference remains unknown.
objectivesTo explore the tumour mutational burden in indolent and aggressive KS.
methodsWe performed whole-exome sequencing on a cohort of 21 KS patients. We compared genetic landscape including tumor mutational burden between the two forms of indolent and agressive KS.
resultsAggressive KS tumours had a significantly higher TMB and a larger cumulative number of deleterious mutations than indolent KS tumours. In addition, all aggressive tumours had at least three deleterious mutations, whereas most indolent tumours harboured only one or no predicted deleterious mutations. Deleterious mutations listed in the Cancer Gene Census were detected exclusively in patients with aggressive disease. An analysis of somatic copy-number alterations (SCNA) revealed a tendency towards higher number of alterations in aggressive KS.
conclusionsThese data suggest that SCNA alterations and an increase in mutational burden promote aggressive KS and that it might be more appropriate to consider indolent KS as an opportunistic skin disease rather than a cancer.
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