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The aim of this study was to evaluate the prevalence of genetic defects in pediatric PAs through germline and tumor testing, and to describe genotype-phenotype correlations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Fifty-four pediatric patients with PAs and available germline and\/or tumor samples were studied. Germline and\/or tumor sequencing were reviewed for variants in genes previously associated with pituitary tumorigenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Germline genetic testing revealed a pathogenic variant in\n                      <jats:italic>AIP<\/jats:italic>\n                      gene in 2 patients with growth hormone excess (GHE) and a likely pathogenic variant in\n                      <jats:italic>CDKN2A<\/jats:italic>\n                      in a patient with Cushing\u2019s disease (CD). Somatic gene sequencing identified pathogenic variants in\n                      <jats:italic>GNAS<\/jats:italic>\n                      in 4\/7 patients (57.1%) with GHE. 6\/38 patients (15.8%) with CD had pathogenic variants in\n                      <jats:italic>USP8<\/jats:italic>\n                      gene, and in one tumor pathogenic variants in\n                      <jats:italic>PRKAR1A<\/jats:italic>\n                      ,\n                      <jats:italic>TP53<\/jats:italic>\n                      and\n                      <jats:italic>MEN1<\/jats:italic>\n                      genes were identified. Overall, pathogenic\/likely pathogenic germline or somatic variants were identified in 14\/54 patients (25.9%). When evaluating the genotype-phenotype correlations in patients with CD, patients with somatic\n                      <jats:italic>USP8<\/jats:italic>\n                      pathogenic variants had larger tumors (median size: 9.5\u00a0mm [6.5, 13.3] vs. 6\u00a0mm [4.0, 7.0],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.048), trend towards higher incidence of cavernous sinus invasion (50% vs. 12.5%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.06), and higher risk of non-remission after surgery (33.3% vs. 0%,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.021) compared to patients without\n                      <jats:italic>USP8<\/jats:italic>\n                      variants.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Somatic\n                      <jats:italic>USP8<\/jats:italic>\n                      pathogenic variants correlate with worse tumor behavior and patient outcomes in pediatric-onset CD. Unlike GH-secreting PAs, the genetic basis of the majority of pediatric corticotroph PAs remains unclear. Further studies are needed to explore the genetic drivers of pediatric CD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>ClinicalTrials.gov ID<\/jats:title>\n                    <jats:p>NCT00001595, NCT03206099.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s11102-025-01557-6","type":"journal-article","created":{"date-parts":[[2025,8,14]],"date-time":"2025-08-14T16:53:58Z","timestamp":1755190438000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Genetic evaluation of pediatric pituitary adenomas and USP8-related genotype-phenotype correlations in Cushing\u2019s disease"],"prefix":"10.1007","volume":"28","author":[{"given":"Rida","family":"Zainab","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sukhvir","family":"Kaur","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin","family":"Lack","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Morgan","family":"Similuk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mayank","family":"Tandon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajarshi","family":"Ghosh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryce A.","family":"Seifert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mari","family":"Tokita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chelsi","family":"Flippo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia","family":"Yan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Walkiewicz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prashant","family":"Chittiboina","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2882-4584","authenticated-orcid":false,"given":"Christina","family":"Tatsi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,8,14]]},"reference":[{"key":"1557_CR1","doi-asserted-by":"publisher","first-page":"655","DOI":"10.1530\/EJE-15-0189","volume":"173","author":"TT Agustsson","year":"2015","unstructured":"Agustsson TT, Baldvinsdottir T, Jonasson JG, Olafsdottir E, Steinthorsdottir V, Sigurdsson G et al (2015) The epidemiology of pituitary adenomas in iceland, 1955\u20132012: a nationwide population-based study. 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