{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Hofvander J"],"funding":["NCI NIH HHS"],"pubmed_abstract":["Synovial sarcoma (SyS) is an aggressive soft-tissue malignancy characterized by a pathognomonic chromosomal translocation leading to the formation of the SS18::SSX fusion oncoprotein. SS18::SSX associates with mammalian BAF complexes suggesting deregulation of chromatin architecture as the oncogenic driver in this tumour type. To examine the epigenomic state of SyS we performed comprehensive multi-omics analysis on 52 primary pre-treatment human SyS tumours. Our analysis revealed a continuum of epigenomic states across the cohort at fusion target genes independent of rare somatic genetic lesions. We identify cell-of-origin signatures defined by enhancer states and reveal unexpected relationships between H2AK119Ub1 and active marks. The number of bivalent promoters, dually marked by the rep"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2024.05.14.594262"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11118320"],"repository":["biostudies-literature"],"pubmed_title":["Synovial Sarcoma Chromatin Dynamics Reveal a Continuum in SS18:SSX Reprograming."],"pmcid":["PMC11118320"],"funding_grant_id":["U54 CA231652"],"pubmed_authors":["Su E","Jones KB","Hill LA","Andrulis IL","Moksa M","Wunder JS","Lee K","Nielsen TO","Banito A","Hofvander J","Goytain A","Underhill TM","Singer S","Mertens F","Bilenky M","Carles A","Hirst M","Qiu A","Sotiriou A","Steif J","Cao Q"],"additional_accession":[]},"is_claimable":false,"name":"Synovial Sarcoma Chromatin Dynamics Reveal a Continuum in SS18:SSX Reprograming.","description":"Synovial sarcoma (SyS) is an aggressive soft-tissue malignancy characterized by a pathognomonic chromosomal translocation leading to the formation of the SS18::SSX fusion oncoprotein. SS18::SSX associates with mammalian BAF complexes suggesting deregulation of chromatin architecture as the oncogenic driver in this tumour type. To examine the epigenomic state of SyS we performed comprehensive multi-omics analysis on 52 primary pre-treatment human SyS tumours. Our analysis revealed a continuum of epigenomic states across the cohort at fusion target genes independent of rare somatic genetic lesions. We identify cell-of-origin signatures defined by enhancer states and reveal unexpected relationships between H2AK119Ub1 and active marks. The number of bivalent promoters, dually marked by the rep","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-07-02T03:16:55.054Z","creation":"2026-07-02T03:11:38.144Z"},"accession":"S-EPMC11118320","cross_references":{"pubmed":["38798672"],"doi":["10.1101/2024.05.14.594262"]}}