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Notable progress in understanding of the molecular background of cPAs has been made recently but biology of CCAs remains poorly recognized. Results of our previous study suggested distinct frequency of the known recurrent mutations in CCAs than in sparsely and densely granulated cPAs. Thus, the aim was to determine the prevalence of\n                      <jats:italic>USP8<\/jats:italic>\n                      ,\n                      <jats:italic>USP48<\/jats:italic>\n                      ,\n                      <jats:italic>BRAF<\/jats:italic>\n                      and\n                      <jats:italic>TP53<\/jats:italic>\n                      variants in a relatively large retrospective group of patients diagnosed with CCA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      DNA was isolated from formalin-fixed and paraffin-embedded tissue of 29 CCAs (14 clinically functioning and 15 nonfunctioning). Sanger sequencing was used for the identification of\n                      <jats:italic>USP8<\/jats:italic>\n                      ,\n                      <jats:italic>USP48<\/jats:italic>\n                      ,\n                      <jats:italic>BRAF<\/jats:italic>\n                      hotspot variants, while semiconductor sequencing with Ion AmpliSeq TP53 Panel was used for analysis of\n                      <jats:italic>TP53<\/jats:italic>\n                      sequence.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>USP8<\/jats:italic>\n                      variants were found in 2 CCA patients with Cushing\u2019s disease (CD), whereas 3\n                      <jats:italic>TP53<\/jats:italic>\n                      variants were identified in 1 CCA patient with CD and 2 patients with clinically nonfunctioning CCAs.\n                      <jats:italic>USP8<\/jats:italic>\n                      variants are less frequent in clinically functioning CCAs than functioning sparsely and densely granulated corticotroph tumors (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0271).\n                      <jats:italic>TP53<\/jats:italic>\n                      variants are more common in CCAs as compared to other histological subtypes (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0164). One\n                      <jats:italic>BRAF<\/jats:italic>\n                      V600E variant and no\n                      <jats:italic>USP48<\/jats:italic>\n                      variant were found.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      CCAs have slightly distinct mutational profile then other histological subtypes of cPAs. Since clinical relevance of\n                      <jats:italic>TP53<\/jats:italic>\n                      variants in corticotroph tumors was already documented, testing toward\n                      <jats:italic>TP53<\/jats:italic>\n                      sequence changes in patients with CCAs should be considered.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11102-025-01566-5","type":"journal-article","created":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T18:51:39Z","timestamp":1759690299000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["USP8, USP48, BRAF and TP53 mutations in crooke cell adenoma"],"prefix":"10.1007","volume":"28","author":[{"given":"Paulina","family":"Kober","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Szczepaniak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monika","family":"P\u0119kul","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalia","family":"Rusetska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beata J.","family":"Mossakowska","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Artur","family":"Kowalik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Maksymowicz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grzegorz","family":"Zieli\u0144ski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacek","family":"Kunicki","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mateusz","family":"Bujko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,10,5]]},"reference":[{"key":"1566_CR1","unstructured":"WHO (2022) Classification of tumours editorial board. 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