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Integrative Functional Genomics Analysis of Kaposis Sarcoma Cohorts

ABSTRACT: Kaposi’s sarcoma (KS) is an AIDS-defining cancer and a significant global health challenge caused by Kaposi's sarcoma-associated herpesvirus (KSHV). KS lesions have been profiled by NGS-based approaches in a very limited number of studies compared with other neoplastic diseases. Here we present a compiled and harmonized dataset of 131 KS and non-tumor cutaneous samples in the context of their predicted pathway activities, immune infiltrate, KSHV and HIV gene expression profiles and their associated clinical data representing patient populations from Argentina, USA and Sub-Saharan Africa cohorts. First, RNA-seq data from 9 Argentinian KS lesions were generated and integrated with previously published datasets derived form USA and sub-Saharan African cohorts from Tanzania, Zambia and Uganda. Second, the compiled RNA-seq profile is shared with the research community through the UCSC Xena browser for further visualization, download and analysis (http://xena.ucsc.edu/). Third, unsupervised analysis of 131 KS related samples allowed us to identify four KS clusters based on their host and KSHV gene expression profiles, immune infiltrate and in the activity of specific signaling pathways. These resources will allow biologists without bioinformatics knowledge to explore and correlate the host and viral (KSHV and HIV) transcriptome in a curated dataset of different KS RNA-seq-based cohorts, which can lead to novel biological insights and biomarker discovery.

ORGANISM(S): Homo sapiens

PROVIDER: GSE271303 | GEO | 2025/12/01

REPOSITORIES: GEO

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Project description:In sub-Saharan Africa, endemic Kaposi’s sarcoma (EnKS) is still prevalent despite high incidence of epidemic Kaposi’s sarcoma (EpKS) resulting from the on-going HIV-1 epidemic. While KSHV is clearly the etiologic agent of KS, the mechanisms underlying KS development are not fully understood. For example, HIV-1 co-infection and concomitant immune dysfunction have been associated with EpKS development. However, the direct or indirect role(s) of HIV-1, and therefore of immune suppression, in EpKS remains unclear. How, or whether, EpKS is mechanistically distinct from EnKS is unknown. Thus, the absence of HIV-1 co-infection in EnKS provides a unique control for investigating and deciphering whether HIV-1 plays a direct or indirect role in the EpKS tumor microenvironment. We hypothesized that HIV-1 co-infection would induce transcriptome changes that differentiate EpKS from EnKS, thereby defining the direct intra-tumor role of HIV-1 in KS. Comparison of ART-treated and -naïve patients would further define the impact of ART on the KS transcriptome. We utilized RNA-seq followed by multiparameter bioinformatics analysis to compare transcriptomes from KS lesions to uninvolved control skin. We provide the first transcriptomic comparison of EpKS versus EnKS, ART-treated vs. –naïve EpKS and male vs. female EpKS to define the roles of HIV-1 co-infection, the impact of ART, and gender on KS gene expression profiles. Our findings suggest that ART-use and gender have minimal impact on transcriptome profiles of KS lesions. Gene expression profiles strongly correlated between EpKS and EnKS patients (Spearman r=0.83, p<10-10). A subset of genes involved in tumorigenesis and inflammation/immune responses showed higher magnitude, but not unique dysregulation in EnKS compared to EpKS. While gender and ART had no detectable contribution, the trend toward higher magnitude of gene dysregulation in EnKS coupled with the absence of HIV-1 transcripts in EpKS may suggest an indirect or systemic effect of HIV-1 to promote KS tumorigenesis.

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Integrative Functional Genomics Analysis of Kaposis Sarcoma Cohorts

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