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Related Experiment Video

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Comparative Lesions Analysis Through a Targeted Sequencing Approach
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Decoding UTROSCT heterogeneity: systematic clinicopathological evaluation combined with molecular profiling.

Jing Yang1, Jinku Zhang2,3, Jinmei Li2

  • 1Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences, Peking University, Beijing, PR China.

The Journal of Pathology. Clinical Research
|November 29, 2025
PubMed
Summary

Uterine tumors resembling ovarian sex cord tumors (UTROSCT) can be aggressive. Copy number variations (CNVs) in metastatic lesions, like SMARCB1 and ATRX loss, drive UTROSCT progression and metastasis.

Keywords:
SMARCB1SWI/SNFUTROSCTcopy number variationprognosis

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Area of Science:

  • Gynecologic pathology
  • Oncology
  • Molecular pathology

Background:

  • Uterine tumor resembling ovarian sex cord tumor (UTROSCT) is a rare uterine neoplasm.
  • While often benign, a subset exhibits aggressive behavior with recurrence and metastasis.
  • Recurrent fusion genes are key molecular drivers in UTROSCT.

Purpose of the Study:

  • To investigate the clinicopathologic and molecular features of UTROSCT.
  • To identify predictors of recurrence and metastasis in UTROSCT.
  • To explore the genetic basis of metastatic progression in UTROSCT.

Main Methods:

  • Molecular confirmation of 25 UTROSCT cases via fusion gene detection.
  • Integrated clinicopathologic, immunohistochemical, and molecular profiling.
  • Multi-omics analysis comparing primary and metastatic UTROSCT tumors.

Main Results:

  • Identified recurrent fusion genes: ESR1::NCOA3, GREB1::NCOA1, ESR1::NCOA2, GREB1::NCOA2, GREB1::SS18, GREB1::CTNNB1.
  • Tumor size >5cm, FIGO stage IB, and LVSI were independent predictors of recurrence/metastasis.
  • Metastatic UTROSCTs showed unique copy number variations (CNVs), including SMARCB1 and ATRX loss, absent in primary tumors.

Conclusions:

  • Fusion gene detection is crucial for UTROSCT diagnosis.
  • Clinical factors like tumor size and stage predict UTROSCT aggressiveness.
  • CNVs, particularly SWI/SNF complex dysregulation, are implicated in UTROSCT metastatic competence, representing a novel oncogenic mechanism.