Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112845 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE12592: Gene expression analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions GSE12593: DNA copy number analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions Refer to individual Series
2009-01-25 | E-GEOD-12595 | biostudies-arrayexpress
Project description:Gene expression analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions
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Project description:DNA copy number analysis of myxoinflammatory fibroblastic sarcoma, and morphologically similar lesions
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Project description:we establish a 272 Chinese STS patients cohort containing 12 sarcoma subtypes, well-differentiated liposarcoma (WDLPS), myxoid liposarcoma (MLPS), dedifferentiated liposarcoma (DDLPS), angiosarcoma (AS), undifferentiated sarcoma (UPS), myxofibrosarcoma (MFS), other fibroblastic/myofibroblastic tumors (otherFS), leiomyosarcoma (LMS), rhabdomyosarcoma (RMS), malignant peripheral nerve sheath tumor (MPNST), synovial sarcoma (SS), and epithelioid sarcoma (ES).
2024-01-03 | PXD047297 |
Project description:Genetic lesions characteristic for RCC subtypes can be identified by virtual karyotyping with SNP microarrays. In this study, we examined whether virtual karyotypes could be used to better classify a cohort of morphologically challenging/unclassified RCC.
2009-03-13 | GSE14670 | GEO
Project description:Synovial sarcoma (SyS) is an aggressive soft-tissue malignancy that is characterized by a pathognomonic t(X;18)(p11.2;q11.2) translocation, which produces the fusion oncogene named SS18::SSX. Despite recent advancements in our understanding of synovial sarcoma biology, the cell-of-origin remains undefined. Here we employ a mesenchymal stromal cell (MSC) specific CreERT2 line to express SS18::SSX in fibroblasts and related cell types, resulting in 100% penetrant synovial sarcoma development in mice, with a median latency period of 16.2 ± 2.8 weeks. Murine tumours exhibit high concordance with human synovial sarcoma subtypes at the histological and molecular levels1. Genetic refinement of the cell-of-origin reveal that synovial sarcomas derive from a rare Hic1+ Pdgfra+ Lgr5+ fibroblastic population. Furthermore, comparative transcriptomic analysis reveals the acquisition of a transformed phenotype initiated by the loss of a mature fibroblastic profile and subsequent unmasking of an epigenetically embedded embryonic MSC program. Adult and embryonic MSCs exhibite overlapping H2AK119ub and H3K4me3/H3K27me3 (bivalent) histone marks, while SS18::SSX-mediated transformation culminates in the widespread loss of H3K27me3 at these genes and their consequent transcription. Collectively, these studies define a rare MSC context, conducive for SS18::SSX-mediated transformation, and demonstrate that SyS tumorigenesis involves the induction and maintenance of an embryonic-like MSC phenotype.
2025-09-11 | GSE213265 | GEO
Project description:Synovial sarcoma is an aggressive soft-tissue malignancy that is characterized by a pathognomonic t(X;18)(p11.2;q11.2) translocation, which produces the fusion oncogene namedSS18::SSX. Despite recent advancements in our understanding of synovial sarcoma biology, the cell-of-origin remains undefined. A mesenchymal stromal cell (MSC) specific CreERT2 line was employed to expressSS18::SSXin fibroblasts and related cell types, resulting in 100% penetrant synovial sarcoma development in mice, with a median latency period of 16.2 ± 2.5 weeks. Murine tumours exhibited high concordance with human synovial sarcoma sub-types at the histological and molecular levels1. Genetic refinement of the cell-of-origin revealed that synovial sarcomas derive from a rareHic1+Pdgfra+Lgr5+fibroblastic population. Furthermore, longitudinal multi-omic profiling along the transformation continuum revealed the step-wise acquisition of a transformed phenotype initiated by the loss of a mature fibroblastic profile and subsequently, the gradual unmasking of an epigenetically embedded embryonic MSC program. Adult and embryonic MSCs exhibited overlapping H2AK119ub and H3K4me3/H3K27me3 (bivalent) histone marks, while SS18::SSX-mediated transformation culminated in the widespread loss of H3K27me3 at these genes and their consequent transcription. Collectively, these studies define a rare MSC context, conducive for SS18::SSX-mediated transformation, and demonstrate that SS tumorigenesis involves the induction and maintenance of an embryonic-like MSC phenotype.
2025-09-11 | GSE270369 | GEO
Project description:The fibroblast growth factor receptor (FGFR) and canonical Wnt signaling pathways are important regulators of carcinogenesis; however, the interaction between these two pathways in the context of prostate cancer (PCa) has not been fully elucidated. Using novel transgenic mouse models, we describe Wnt-induced synergistic acceleration of FGFR1-driven adenocarcinoma; largely due to pronounced fibroblastic reactive stroma (RS) activation surrounding prostatic intraepithelial neoplasia (PIN) lesions in endogenous and reconstitution assays. Finally, both mouse and human RS are characterized by increases in TGF-β signaling heterogeneity immediately adjacent to PIN lesions; however, heterogeneity is lost during later stages of progression, likely contributing to tissue invasion. These studies confirm the importance of the FGFR1-Wnt-TGF-β signaling axes as driving forces behind reactive stroma and aggressive adenocarcinoma.
2014-01-07 | GSE41344 | GEO
Project description:Synovial sarcoma (SyS) is an aggressive soft-tissue malignancy that is characterized by a pathognomonic t(X;18)(p11.2;q11.2) translocation, which produces the fusion oncogene named SS18::SSX. Despite recent advancements in our understanding of synovial sarcoma biology, the cell-of-origin remains undefined. Here we employ a mesenchymal stromal cell (MSC) specific CreERT2 line to express SS18::SSX in fibroblasts and related cell types, resulting in 100% penetrant synovial sarcoma development in mice, with a median latency period of 16.2 ± 2.8 weeks. Murine tumours exhibit high concordance with human synovial sarcoma subtypes at the histological and molecular levels1. Genetic refinement of the cell-of-origin reveal that synovial sarcomas derive from a rare Hic1+ Pdgfra+ Lgr5+ fibroblastic population. Furthermore, comparative transcriptomic analysis reveals the acquisition of a transformed phenotype initiated by the loss of a mature fibroblastic profile and subsequent unmasking of an epigenetically embedded embryonic MSC program. Adult and embryonic MSCs exhibite overlapping H2AK119ub and H3K4me3/H3K27me3 (bivalent) histone marks, while SS18::SSX-mediated transformation culminates in the widespread loss of H3K27me3 at these genes and their consequent transcription. Collectively, these studies define a rare MSC context, conducive for SS18::SSX-mediated transformation, and demonstrate that SyS tumorigenesis involves the induction and maintenance of an embryonic-like MSC phenotype.
2025-09-11 | GSE216769 | GEO
Project description:Clear cell sarcoma (CCS) of tendons and aponeuroses is a deadly soft-tissue malignancy resembling melanoma, with a predilection for young adults. EWS-ATF1, the fusion product of a balanced chromosomal translocation between chromosomes 22 and 12, is considered the definitional feature of the tumor. Conditional expression of the EWS-ATF1 human cDNA in the mouse generates CCS-like tumors with 100 percent penetrance. Tumors, developed through varied means of initiating expression of the fusion oncogene, model human CCS morphologically, immunohistochemically, and by genome-wide expression profiling. We also demonstrate that while fusion oncogene expression in later stages of differentiation can transform mesenchymal progenitor cells and generate tumors resembling CCS generally, expression in cells retaining stem cell markers permits the full melanoma-related phenotype. Nielsen et al. ("Molecular characterisation of soft tissue tumours: a gene expression study"; PMID 11965276) used microarray to compare a variety of soft-tissue neoplasms morphologically similar to clear cell sarcoma. In our study, we use their expression data (not previously submitted) in the profiling of our mouse mutant that models clear cell sarcoma.
2012-12-20 | GSE43045 | GEO