ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Molecular Profiling Defines Three Subtypes of Synovial Sarcoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Preliminary study on the mechanism of OPN up-regulating PD-L1 to induce CD8 + T cell exhaustion in synovial sarcoma.BMC cancer · 2026Article
- MiT fusions, TSC1-TSC2 divergence, and stem-like programs reveal distinct origins and vulnerabilities in PEComa.Nature communications · 2026Article
- Revealing novel subtypes of synovial sarcoma through single cell transcriptomics.NPJ systems biology and applications · 2026Article
- Focal adhesion kinase promotes biphasic differentiation and induces infiltration and metastasis of synovial sarcoma.Journal of translational medicine · 2026Article
- Editorial: Artificial intelligence in multi-omics: advancing tumor metastasis prediction and mechanism analysis.Frontiers in cell and developmental biology · 2026Article
- Primary Cardiac Synovial Sarcoma (PCSS): Clinicopathologic Features of 6 Cases and Literature Comparison.Cardiology research and practice · 2026Article
- Article
- Molecular and epigenetic oncogenesis in synovial sarcoma: implications for cancer biology, diagnosis and treatment.Oncogene · 2025Review
- Advancing Precision Medicine: The Role of Genetic Testing and Sequencing Technologies in Identifying Biological Markers for Rare Cancers.Cancer medicine · 2025Review
- EZH2 inhibition sensitizes retinoic acid-driven senescence in synovial sarcoma.Cell death & disease · 2024Article
- Molecular Profiling Defines Three Subtypes of Synovial Sarcoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
21 authors.
Funding
Abstract
Synovial Sarcomas (SS) are characterized by the presence of the SS18::SSX fusion gene, which protein product induce chromatin changes through remodeling of the BAF complex. To elucidate the genomic events that drive phenotypic diversity in SS, we performed RNA and targeted DNA sequencing on 91 tumors from 55 patients. Our results were verified by proteomic analysis, public gene expression cohorts and single-cell RNA sequencing. Transcriptome profiling identified three distinct SS subtypes resembling the known histological subtypes: SS subtype I and was characterized by hyperproliferation, evasion of immune detection and a poor prognosis. SS subtype II and was dominated by a vascular-stromal component and had a significantly better outcome. SS Subtype III was characterized by biphasic differentiation, increased genomic complexity and immune suppression mediated by checkpoint inhibition, and poor prognosis despite good responses to neoadjuvant therapy. Chromosomal abnormalities were an independent significant risk factor for metastasis. KRT8 was identified as a key component for epithelial differentiation in biphasic tumors, potentially controlled by OVOL1 regulation. Our findings explain the histological grounds for SS classification and indicate that a significantly larger proportion of patients have high risk tumors (corresponding to SS subtype I) than previously believed.
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