{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T10:15:29Z","timestamp":1779963329220,"version":"3.53.1"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,5,26]],"date-time":"2026-05-26T00:00:00Z","timestamp":1779753600000},"content-version":"vor","delay-in-days":25,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P50 CA217694"],"award-info":[{"award-number":["P50 CA217694"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["P30 CA008748"],"award-info":[{"award-number":["P30 CA008748"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100017050","name":"Cycle for Survival","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100017050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100019543","name":"Kristen Ann Carr Fund","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100019543","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Genes Chromosomes &amp;amp; Cancer"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions are rare but recurrent driver events in a spectrum of mostly pediatric and young adult mesenchymal soft tissue tumors, including infantile fibrosarcoma, lipofibromatosis\u2010like neural tumors, and other kinase fusion spindle cell neoplasms. Their clinicopathologic spectrum, co\u2010occurring secondary genomic events, and frequency among various sarcoma histotypes remain incompletely characterized. The purpose of this study is to comprehensively investigate the incidence and structural variants of\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions among a large clinicopathologic and molecular sarcoma cohort. The additional goal was to distinguish primary driver\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions from potential passenger events and correlate with sarcoma histotypes. We identified a total of 24 cases harboring\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions, with 18 (75%) occurring in canonical\n                    <jats:italic>BRAF<\/jats:italic>\n                    \u2010driven histotypes, including kinase\u2010associated spindle cell tumors (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200912), myxoinflammatory fibroblastic sarcoma (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093), GIST (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092) and one hybrid nerve sheath tumor. The remaining six cases were detected in various established pathologic entities (undifferentiated pleomorphic sarcoma, angiosarcoma, embryonal rhabdomyosarcoma, dedifferentiated liposarcoma, PEComa), likely as secondary or passenger events. Among the 12 kinase\u2010associated spindle cell tumors, the most common histologies included tumors resembling infantile fibrosarcoma (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20094), malignant peripheral nerve sheath tumor (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20093), lipofibromatosis (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092), and myoid\/pericytic lesions (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092). This predominant group had a wide age range at diagnosis (median 15.5\u2009years), a predilection for soft tissues of extremities, trunk, and head\/neck and showed CD34 and S100 co\u2010expression in 45% of cases. In this group,\n                    <jats:italic>BRAF<\/jats:italic>\n                    breakpoints clustered in exons 8\u201311 retaining an intact kinase domain, and fusion partners were diverse (\n                    <jats:italic>AGK<\/jats:italic>\n                    ,\n                    <jats:italic>AHNAK<\/jats:italic>\n                    ,\n                    <jats:italic>NRF1<\/jats:italic>\n                    ,\n                    <jats:italic>PAK2<\/jats:italic>\n                    ,\n                    <jats:italic>TMEM245<\/jats:italic>\n                    ,\n                    <jats:italic>FNBP1<\/jats:italic>\n                    ,\n                    <jats:italic>STEAP4<\/jats:italic>\n                    ,\n                    <jats:italic>TSC1<\/jats:italic>\n                    ,\n                    <jats:italic>KIAA1549<\/jats:italic>\n                    ). Tumor mutation burden was consistently low, with\n                    <jats:italic>CDKN2A<\/jats:italic>\n                    homozygous deletion being the only recurrent secondary event (4\/5 cases profiled). Among the five patients with follow\u2010up (median 34\u2009months), one patient died of disease, with two developing local recurrences at 5 and 84\u2009months. The\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions occurring in non\u2010canonical histotypes had similar breakpoint patterns and various partners. These results highlight the heterogeneity of mesenchymal neoplasms harboring\n                    <jats:italic>BRAF<\/jats:italic>\n                    fusions, including both driver and likely secondary genetic events, which often require a comprehensive approach that integrates clinical, histopathologic, and detailed molecular data, for a definitive classification.\n                  <\/jats:p>","DOI":"10.1002\/gcc.70144","type":"journal-article","created":{"date-parts":[[2026,5,27]],"date-time":"2026-05-27T04:25:40Z","timestamp":1779855940000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Comprehensive Clinicopathologic and Molecular Analysis of Mesenchymal Tumors With\n                    <scp>\n                      <i>BRAF<\/i>\n                    <\/scp>\n                    Fusions"],"prefix":"10.1002","volume":"65","author":[{"given":"Maximus C. F.","family":"Yeung","sequence":"first","affiliation":[{"name":"Department of Pathology, School of Clinical Medicine, LKS Faculty of Medicine The University of Hong Kong, Queen Mary Hospital  Hong Kong SAR China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9717-8205","authenticated-orcid":false,"given":"Cristina R.","family":"Antonescu","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center  New York New York 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