{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["DeMartino J"],"funding":["European Research Council"],"pagination":["3074"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10224926"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Paediatric rhabdomyosarcoma (RMS) is a soft tissue malignancy of mesenchymal origin that is thought to arise as a consequence of derailed myogenic differentiation. Despite intensive treatment regimens, the prognosis for high-risk patients remains dismal. The cellular differentiation states underlying RMS and how these relate to patient outcomes remain largely elusive. Here, we use single-cell mRNA sequencing to generate a transcriptomic atlas of RMS. Analysis of the RMS tumour niche reveals evidence of an immunosuppressive microenvironment. We also identify a putative interaction between NECTIN3 and TIGIT, specific to the more aggressive fusion-positive (FP) RMS subtype, as a potential cause of tumour-induced T-cell dysfunction. In malignant RMS cells, we define transcriptional programs re"],"journal":["Nature communications"],"pubmed_title":["Single-cell transcriptomics reveals immune suppression and cell states predictive of patient outcomes in rhabdomyosarcoma."],"pmcid":["PMC10224926"],"funding_grant_id":["850571"],"pubmed_authors":["Brok M","Visser LL","DeMartino J","Holstege FCP","Hiemcke-Jiwa LS","Wezenaar AKL","Drost J","Margaritis T","de Souza T","Rios AC","Meister MT","Groot Koerkamp MJA","Merks JHM"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell transcriptomics reveals immune suppression and cell states predictive of patient outcomes in rhabdomyosarcoma.","description":"Paediatric rhabdomyosarcoma (RMS) is a soft tissue malignancy of mesenchymal origin that is thought to arise as a consequence of derailed myogenic differentiation. Despite intensive treatment regimens, the prognosis for high-risk patients remains dismal. The cellular differentiation states underlying RMS and how these relate to patient outcomes remain largely elusive. Here, we use single-cell mRNA sequencing to generate a transcriptomic atlas of RMS. Analysis of the RMS tumour niche reveals evidence of an immunosuppressive microenvironment. We also identify a putative interaction between NECTIN3 and TIGIT, specific to the more aggressive fusion-positive (FP) RMS subtype, as a potential cause of tumour-induced T-cell dysfunction. In malignant RMS cells, we define transcriptional programs re","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2026-05-29T00:03:13.483Z","creation":"2025-04-07T05:08:25.504Z"},"accession":"S-EPMC10224926","cross_references":{"pubmed":["37244912"],"doi":["10.1038/s41467-023-38886-8"]}}