ArticleOncogene2012
Reprogramming of mesenchymal stem cells by the synovial sarcoma-associated oncogene SYT-SSX2.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Primary Renal Synovial Sarcoma and Clinical and Pathological Findings: a Systematic Review.Current urology reports · 2021Pooled it
- Circulating Tumor Cells in Soft Tissue Sarcoma: Current Evidence and Clinical Implications.Cancers · 2026Review
- Biological and clinical implications of FGFR aberrations in paediatric and young adult cancers.Oncogene · 2023Review
- Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Biphasic synovial sarcoma with a striking morphological divergence from the main mass to lymph node metastasis: A case report.Medicine · 2022Article
- The Biology of Synovial Sarcoma: State-of-the-Art and Future Perspectives.Current treatment options in oncology · 2021Review
- Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells.International journal of molecular sciences · 2021Review
- ETV4 and ETV5 drive synovial sarcoma through cell cycle and DUX4 embryonic pathway control.The Journal of clinical investigation · 2021Article
- The chromatin landscape of primary synovial sarcoma organoids is linked to specific epigenetic mechanisms and dependencies.Life science alliance · 2021Article
- Mesenchymal stem/stromal cells: Developmental origin, tumorigenesis and translational cancer therapeutics.Translational oncology · 2021Review
- TRPA1 Expression in Synovial Sarcoma May Support Neural Origin.Biomolecules · 2020Article
- Synovial Sarcoma: A Complex Disease with Multifaceted Signaling and Epigenetic Landscapes.Current oncology reports · 2020Review
- Are Leukaemic Stem Cells Restricted to a Single Cell Lineage?International journal of molecular sciences · 2019Review
- TP53 in bone and soft tissue sarcomas.Pharmacology & therapeutics · 2019Review
- Proteomic signatures corresponding to the SS18/SSX fusion gene in synovial sarcoma.Oncotarget · 2018Article
- Ectomesenchymal Chondromyxoid Tumor: A Neoplasm Characterized by Recurrent RREB1-MKL2 Fusions.The American journal of surgical pathology · 2018Article
- The Making of Leukemia.International journal of molecular sciences · 2018Review
- Soft Tissue Sarcoma Cancer Stem Cells: An Overview.Frontiers in oncology · 2018Review
- Adult Neural Stem Cells: Basic Research and Production Strategies for Neurorestorative Therapy.Stem cells international · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Cell identity is determined by its gene expression programs. The ability of a cell to change its identity and produce cell types outside its lineage is achieved by the activity of transcription controllers capable of reprogramming differentiation gene networks. The synovial sarcoma (SS)-associated protein, SYT-SSX2, reprograms myogenic progenitors and human bone marrow-derived mesenchymal stem cells (BMMSCs) by dictating their commitment to a pro-neural lineage. It fulfills this function by directly targeting an extensive array of neural-specific genes as well as genes of developmental pathway mediators. Concomitantly, the ability of both myoblasts and BMMSCs to differentiate into their normal myogenic and adipogenic lineages was compromised. SS is believed to arise in mesenchymal stem cells where formation of the t(X/18) translocation product, SYT-SSX, constitutes the primary event in the cancer. SYT-SSX is therefore believed to initiate tumorigenesis in its target stem cell. The data presented here allow a glimpse at the initial events that likely occur when SYT-SSX2 is first expressed, and its dominant function in subverting the nuclear program of the stem cell, leading to its aberrant differentiation, as a first step toward transformation. In addition, we identified the fibroblast growth factor receptor gene, Fgfr2, as one occupied and upregulated by SYT-SSX2. Knockdown of FGFR2 in both BMMSCs and SS cells abrogated their growth and attenuated their neural phenotype. These results support the notion that the SYT-SSX2 nuclear function and differentiation effects are conserved throughout sarcoma development and are required for its maintenance beyond the initial phase. They also provide the stem cell regulator, FGFR2, as a promising candidate target for future SS therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.