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Due to its rarity, the molecular landscape remains incompletely characterized. We aimed to expand the current understanding of the genetic alterations in sialoblastoma through comprehensive molecular analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Five sialoblastoma cases were retrieved from four institutional archives. Clinical and pathologic review was performed, and targeted next-generation sequencing was conducted using clinically validated panels. Copy number analysis was performed on four cases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The cohort included five patients with tumors located in parotid gland (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20092), minor salivary glands (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20092), and submandibular gland (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20091). Four patients were diagnosed before 6 months of age. Histologically, all tumors showed solid organoid nests with primitive basaloid cells, dense fibrous stroma, and mitotic activity ranging from 8 to 25 per 10 high-power fields. Recurrent\n                      <jats:italic>FGFR2<\/jats:italic>\n                      p.C382R variants were identified in 80% (4\/5) of cases. Additional alterations were seen in\n                      <jats:italic>FGFR2<\/jats:italic>\n                      p.C382R mutated tumors, including\n                      <jats:italic>PIK3CA<\/jats:italic>\n                      hotspot mutations in two cases (p.R88Q, p.R38H) and a truncating\n                      <jats:italic>FGFR2<\/jats:italic>\n                      variant (p.L776Rfs) in one. The single tumor that lacked\n                      <jats:italic>FGFR2<\/jats:italic>\n                      mutations harbored a\n                      <jats:italic>CTNNB1<\/jats:italic>\n                      p.I35T variant and showed more favorable histologic features. Copy number analysis revealed recurrent whole-chromosome gains of chromosomes 8, 10, and 11.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      A distinct subset of sialoblastoma has\n                      <jats:italic>FGFR2<\/jats:italic>\n                      p.C382R hotspot mutation as the predominant driver mutation. Tumors with this mutation tend to have solid growth pattern, aggressive histologic features, and clinical behavior. The identification of concurrent genomic alterations expands the molecular landscape of this rare tumor. The detection of alternative drivers, such as\n                      <jats:italic>CTNNB1<\/jats:italic>\n                      hotspot mutations typical of basal cell adenoma, also suggests that a subset of sialoblastoma may represent other salivary gland tumors presenting in infancy.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s12105-025-01838-3","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T08:00:04Z","timestamp":1756972804000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Recurrent FGFR2 and PIK3CA Mutations in Sialoblastoma"],"prefix":"10.1007","volume":"19","author":[{"given":"Selene C.","family":"Koo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingqun","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quynh T.","family":"Tran","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rita","family":"Alaggio","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandra","family":"Stracuzzi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pauline M.","family":"Chou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin J.","family":"Wilkins","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brent A.","family":"Orr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faizan","family":"Malik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,9,4]]},"reference":[{"key":"1838_CR1","doi-asserted-by":"publisher","first-page":"44","DOI":"10.1016\/j.ijporl.2016.04.037","volume":"87","author":"AL Irace","year":"2016","unstructured":"Irace AL, Adil EA, Archer NM, Silvera VM, Perez-Atayde A, Rahbar R (2016) Pediatric sialoblastoma: evaluation and management. 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