Evidence map›Paper›PMID 41741191›Full record

ArticleCancer medicine2026

Core Epithelial-to-Mesenchymal Transition Gene Signature Predicts Metastasis and Poor Survival in Synovial Sarcoma.

Megan Jagosky, Colin Anderson, Nury Steuerwald, Jenny Chen, Anderson O' Brien Cox, HsihTe Yang, Guangxu Jin, Alicia Hamilton, Mathew Smith, Sharvil Desai and 2 more

Abstract read
In one paragraph

Article in Cancer medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

12 authors.

Megan JagoskyDepartment of Solid Tumor Oncology, Atrium Health Levine Cancer Institute, Charlotte, NC, USA.ORCID https://orcid.org/0000-0001-7277-365X
Colin AndersonAllina Health Orthopedics and Allina Health Cancer Institute, Allina Health, Minneapolis, MN, USA.
Nury SteuerwaldThe Molecular Biology and Genomics Laboratory, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Jenny ChenDepartment of Biostatistics and Data Sciences, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Anderson O' Brien CoxBioinformatics Shared Resource, Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC, USA.ORCID https://orcid.org/0000-0001-5491-1019
HsihTe YangDepartment of Biostatistics and Data Sciences, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Guangxu JinDepartment of Cancer Biology, Wake Forest University, Winston Salem, NC, USA.
Alicia HamiltonThe Molecular Biology and Genomics Laboratory, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Mathew SmithThe Molecular Biology and Genomics Laboratory, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Sharvil DesaiDepartment of Biostatistics and Data Sciences, Levine Cancer Institute, Atrium Health, Charlotte, NC, USA.
Johann HsuDepartment of Solid Tumor Oncology, Atrium Health Levine Cancer Institute, Charlotte, NC, USA.
Wei ZhangDepartment of Cancer Biology, Wake Forest University, Winston Salem, NC, USA.ORCID https://orcid.org/0000-0002-2235-1851

Funding

Paula Takacs FoundationSwim Across America
6 · The paper itself

Abstract

backgroundSynovial sarcoma (SS) is a rare soft tissue malignancy comprising 5%-10% of all sarcomas, typically affecting young adults. It is characterized by a pathognomonic SS18-SSX gene fusion, with variable histologic subtypes demonstrating epithelial and mesenchymal features. This study investigates the association between epithelial-to-mesenchymal transition (EMT) gene expression and metastatic potential in SS.

methodsA retrospective, single-institution analysis was conducted using primary tumor specimens from 21 treatment-naïve SS patients. RNA sequencing was performed on formalin-fixed paraffin-embedded (FFPE) tissue to assess gene expression profiles. EMT scores were calculated using three independent methods: Hallmark EMT gene set from GSEA, the 76-gene EMT signature (76GS), and Kolmogorov-Smirnov (KS) testing. Patients were categorized into metastatic and nonmetastatic cohorts, and phenotype-specific survival analyses were conducted.

resultsTumors from patients who developed metastases showed significant enrichment of EMT-related genes (GSEA NES 1.71, P = 0.025), oxidative phosphorylation, and immune-related pathways. EMT scores were consistently higher (more mesenchymal) in metastatic tumors across all scoring methods. Mesenchymal phenotype was associated with significantly worse overall survival (GSEA log-rank P = 0.0009).

conclusionsThis study demonstrates a correlation between mesenchymal gene expression signatures and increased metastatic risk in SS. EMT status, derived from primary tumor profiling at diagnosis, may serve as a potential prognostic biomarker. These findings support further investigation into EMT as a stratification tool for tailoring treatment intensity and surveillance strategies in SS.

Indexed as

Biomarkers, TumorEpithelial-Mesenchymal TransitionSarcoma, SynovialTranscriptomeAdultAgedFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm MetastasisPrognosisRetrospective StudiesBiomarkers, TumorEMTgene expressionmesenchymalmetastasisprognostic biomarkerssynovial sarcoma

Identifiers

PMID41741191
PMCPMC12935515

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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.