Evidence map›Paper›PMID 31681608›Full record

ReviewFrontiers in oncology2019

Epigenetic Targets in Synovial Sarcoma: A Mini-Review.

Ryland Hale, Sami Sandakly, Janet Shipley, Zoë Walters

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. bioRxiv : the preprint server for biology · 2024
    Article
  13. Article
  14. Combination of HDAC and FYN inhibitors in synovial sarcoma treatment.Frontiers in cell and developmental biology · 2024
    Article
  15. Review
  16. TargetedCell reports methods · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ryland HaleTranslational Epigenomics Team, Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Sami SandaklySarcoma Molecular Pathology Team, Divisions of Molecular Pathology and Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom.
Janet ShipleySarcoma Molecular Pathology Team, Divisions of Molecular Pathology and Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom.
Zoë WaltersTranslational Epigenomics Team, Human Development and Health, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Institute of Cancer Research · GBUniversity of Southampton · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial Sarcomas (SS) are a type of Soft Tissue Sarcoma (STS) and represent 8-10% of all STS cases. Although SS can arise at any age, it typically affects younger individuals aged 15-35 and is therefore part of both pediatric and adult clinical practices. SS occurs primarily in the limbs, often near joints, but can present anywhere. It is characterized by the recurrent pathognomonic chromosomal translocation t(X;18)(p11.2;q11.2) that most frequently fuses SSX1 or SSX2 genes with SS18. This leads to the expression of the SS18-SSX fusion protein, which causes disturbances in several interacting multiprotein complexes such as the SWItch/Sucrose Non-Fermentable (SWI/SNF) complex, also known as the BAF complex and the Polycomb Repressive Complex 1 and 2 (PRC1 and PRC2). Furthermore, this promotes widespread epigenetic rewiring, leading to aberrant gene expression that drives the pathogenesis of SS. Good prognoses are characterized predominantly by small tumor size and young patient age. Whereas, high tumor grade and an increased genomic complexity of the tumor constitute poor prognostic factors. The current therapeutic strategy relies on chemotherapy and radiotherapy, the latter of which can lead to chronic side effects for pediatric patients. We will focus on the known roles of SWI/SNF, PRC1, and PRC2 as the main effectors of the SS18-SSX-mediated genome modifications and we present existing biological rationale for potential therapeutic targets and treatment strategies.

Indexed as

chromatin remodelingepigeneticsPRC1PRC2SS18-SSXSWI/SNFsynovial sarcomatherapeutic targets

Identifiers

PMID31681608
PMCPMC6813544
OpenAlexW2981264938

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.