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Novel SMARCA4::VEZF1 Rearrangement in Pediatric Sarcomas.

Libing Fu1, Rongjun Mao2,3, Changliang Zhang4,5

  • 1Department of Pathology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.

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|May 5, 2026
PubMed
Summary

Pediatric soft-tissue sarcomas can harbor novel SMARCA4-VEZF1 gene fusions. These fusions may lead to altered gene regulation and tumor development by aberrantly recruiting chromatin remodelers.

Keywords:
SMARCA4::VEZF1 fusionSWI/SNF (BAF) chromatin‐remodeling complexVEZF1 rearrangementmolecular pathologypediatric sarcoma

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • SMARCA4 is crucial for the SWI/SNF (BAF) chromatin-remodeling complex, vital for gene regulation and differentiation.
  • Loss-of-function SMARCA4 alterations are frequent in cancers, but rare gain-of-function fusions have been observed.

Purpose of the Study:

  • To identify and characterize novel gene fusions in pediatric soft-tissue sarcomas.
  • To investigate the potential role of SMARCA4-VEZF1 fusions in tumorigenesis.

Main Methods:

  • Somatic fusion detection in pediatric soft-tissue sarcoma samples.
  • Analysis of predicted fusion protein domains and comparison with known oncogenic fusions.
  • Hypothesizing the mechanism of tumorigenesis driven by BAF complex component fusions.

Main Results:

  • Discovery of a recurrent, in-frame fusion between SMARCA4 and VEZF1 in two pediatric soft-tissue sarcomas.
  • The fusion protein retains SMARCA4's N-terminal interaction domain and VEZF1's DNA-binding domains.
  • Similar SS18-VEZF1 fusions have been reported in uterine sarcoma, suggesting a pattern.

Conclusions:

  • SMARCA4-VEZF1 fusions represent a potential oncogenic mechanism in pediatric sarcomas.
  • These fusions may aberrantly recruit chromatin-remodeling complexes to VEZF1 target genes.
  • This aberrant recruitment can alter chromatin structure, dysregulate transcription, and drive tumor formation.