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U.S.A."],"published-print":{"date-parts":[[2026,10,6]]},"abstract":"<jats:p>\n                    Pituitary adenomas constitute up to 20% of primary brain tumors, yet somatic mutations are only found in 15% of pituitary adenomas. Epigenomic dysregulation has been proposed as a tumorigenic mechanism in pituitary adenomas causing Cushing\u2019s disease (CD). We created paired datasets of human CD adenomas and en-route margin adult human pituitary glands, and assayed their chromatin accessibility, DNA methylation, transcriptomic, proteomic, and phospho-proteomic landscapes. In CD adenomas, we found epigenetic reactivation of a neurodevelopmental phosphoprotein program typically lost in the postnatal pituitary gland. CD cells overexpressed\n                    <jats:italic toggle=\"yes\">PPP1R17<\/jats:italic>\n                    , an endogenous inhibitor of the protein phosphatase PP2A. Mechanistically, PPP1R17 overexpression in normal murine pituitary cells recapitulated the adenoma phenotype, and the resulting hyperproliferation was reversed in a PP2A-dependent manner by fingolimod, an FDA-approved small molecule, both in vitro and in vivo. Our findings highlight kinase-phosphatase imbalance as a targetable mechanism in CD.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2528513123","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:18:26Z","timestamp":1790698706000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":0,"title":["Phosphoproteomic dysregulation promotes tumor proliferation in Cushing\u2019s disease"],"prefix":"10.1073","volume":"123","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6229-3190","authenticated-orcid":false,"given":"David T.","family":"Asuzu","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01s5ya894","id-type":"ROR","asserted-by":"publisher"}],"name":"Neurosurgery Unit for Pituitary and Inheritable Diseases, National Institute of Neurological Disorders and 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