ArticlemedRxiv : the preprint server for health sciences2025
Spatial and Bulk Transcriptomics Reveal Distinct Molecular Signatures in Kaposi Sarcoma with and Without other KSHV-Associated Diseases.
Article in medRxiv : the preprint server for health sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Kaposi sarcoma (KS), caused by Kaposi sarcoma herpesvirus (KSHV), is an angioproliferative tumor that presents as skin lesions in people with HIV. Other KSHV-associated diseases (KAD) including multicentric Castleman disease (MCD), primary effusion lymphoma (PEL), and KSHV-associated inflammatory cytokine syndrome (KICS) may occur concurrently with KS and influence clinical outcomes. New sequencing technologies enabling analysis of archival KS tissues provide mechanisms to define cellular and viral characteristics that contribute to disease heterogeneity. Methods: We profiled gene expression in 42 confirmed KS formalin-fixed paraffin-embedded (FFPE) skin biopsies using the Nanostring nCounter PanCancer ImmunoOncology panel supplemented with KSHV-specific probes. Spatial RNA profiling was performed on four tissues from participants with KS and concurrent KAD (KS+KAD) using GeoMx digital spatial profiling (DSP) platform. Regions of interest were selected using LANA-1, CD45 and CD31 staining to characterize tumor (LANA-1 Results: KS samples were obtained from 42 men with HIV (median age 40 years). Median HIV viral load of 27 copies/mL and median CD4 Conclusions: Bulk and spatial transcriptomic profiling of archival HIV-associated KS lesions revealed disease-specific molecular programs associated with concurrent KAD that altered tumor and microenvironment features. These findings demonstrate the heterogeneity of KS lesions that may guide future studies on KS pathogenesis and potential therapeutic targets.
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