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While most cases have benign clinical behavior, a subset of UTROSCTs exhibits clinically aggressive behavior characterized by recurrence and metastasis. Here, we present a cohort of 25 UTROSCT cases molecularly confirmed by recurrent fusion gene detection, including\n                    <jats:italic>ESR1::NCOA3<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200912),\n                    <jats:italic>GREB1::NCOA1<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20096),\n                    <jats:italic>ESR1::NCOA2<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093),\n                    <jats:italic>GREB1::NCOA2<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092),\n                    <jats:italic>GREB1::SS18<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20091), and\n                    <jats:italic>GREB1::CTNNB1<\/jats:italic>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20091). Notably, six cases (6\/25, 24%) demonstrated recurrence\/metastasis: two cases showed intrauterine recurrence (harboring\n                    <jats:italic>ESR1::NCOA3<\/jats:italic>\n                    and\n                    <jats:italic>GREB1::NCOA1<\/jats:italic>\n                    fusions), while four developed extrauterine metastases (carrying\n                    <jats:italic>ESR1::NCOA3<\/jats:italic>\n                    ,\n                    <jats:italic>ESR1::NCOA2, GREB1::NCOA1,<\/jats:italic>\n                    and\n                    <jats:italic>GREB1::NCOA2<\/jats:italic>\n                    fusions), with one fatality. To dissect the biological basis of UTROSCT aggressiveness, we performed integrated clinicopathologic, immunohistochemical, and molecular profiling. Multivariate analysis identified tumor size &gt;5\u2009cm, FIGO stage IB, and lymphovascular space invasion (LVSI) as independent predictors of recurrence\/metastasis, whereas histologic features, proliferation index, and fusion gene subtypes lacked prognostic significance. Multi\u2010omics analysis of primary versus metastatic tumors revealed striking copy number variations (CNVs) exclusively in metastatic lesions. Specifically, heterozygous losses of\n                    <jats:italic>SMARCB1<\/jats:italic>\n                    (2\/4 metastatic cases) and\n                    <jats:italic>ATRX<\/jats:italic>\n                    (1\/4 metastatic cases) were identified; both play critical roles in chromatin remodeling. These genetic alterations were conspicuously absent in primary tumors, suggesting their potential role in metastatic progression. Our findings represent the first demonstration of CNV\u2010driven oncogenic evolution in UTROSCTs, particularly implicating SWI\/SNF complex dysregulation in metastatic competence.\n                  <\/jats:p>","DOI":"10.1002\/2056-4538.70055","type":"journal-article","created":{"date-parts":[[2025,11,29]],"date-time":"2025-11-29T17:32:46Z","timestamp":1764437566000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Decoding\n                    <scp>UTROSCT<\/scp>\n                    heterogeneity: systematic clinicopathological evaluation combined with molecular profiling"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-1574-4428","authenticated-orcid":false,"given":"Jing","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences Peking University  Beijing PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinku","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Pathology First Central Hospital of Baoding  Baoding PR China"},{"name":"Key Laboratory of Molecular Pathology and Early Diagnosis of Tumor in Hebei Province First Central Hospital of Baoding  Baoding PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jinmei","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Pathology First Central Hospital of Baoding  Baoding PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4000-1273","authenticated-orcid":false,"given":"Yan","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences Peking University  Beijing PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuxiang","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences Peking University  Beijing PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ajin","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences Peking University  Beijing PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Congrong","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Pathology, Peking University Third Hospital, School of Basic Medical Sciences Peking University  Beijing PR 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