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Although most of aCPs are driven by somatic mutations in \u03b2-catenin (\n                    <jats:italic>CTNNB1<\/jats:italic>\n                    ), some cases remain genetically unresolved. Here, we show that disruption of the Wnt-antagonist and tumour suppressor adenomatous polyposis coli (\n                    <jats:italic>Apc<\/jats:italic>\n                    ) leads to pituitary tumours that present all classic molecular and histopathological hallmarks of aCPs. Mechanistically, we show that a hypomorphic allele of\n                    <jats:italic>Apc<\/jats:italic>\n                    leads to tumour development and that bi-allelic loss of\n                    <jats:italic>Apc<\/jats:italic>\n                    in the Sox2+ve pituitary stem cells can initiate aCP formation. Apc-driven tumour-initiating cells show a distinct transcriptional signature of p21-mediated senescence-associated secretory phenotype (SASP) with methylomic analyses revealing shared epigenetic alteration of SASP-like inflammatory programme across aCP subtypes. Our data demonstrate a causal role of disruption of\n                    <jats:italic>Apc<\/jats:italic>\n                    in driving aCPs, reinforcing the importance of genetic testing for mutations in\n                    <jats:italic>APC<\/jats:italic>\n                    in patients with aCP. Furthermore, our work highlights the need to screen patients with familial adenomatous polyposis (FAP) or the spectrum of\n                    <jats:italic>APC<\/jats:italic>\n                    -pathogenic syndromes for aCP development early in life.\n                  <\/jats:p>","DOI":"10.1038\/s44321-026-00525-2","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T06:13:06Z","timestamp":1791526386000},"page":"4386-4412","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Apc-deficient pituitary stem cells drive adamantinomatous craniopharyngioma through senescence-associated inflammation"],"prefix":"10.1038","volume":"18","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0744-5275","authenticated-orcid":false,"given":"James","family":"Blackburn","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4585-6924","authenticated-orcid":false,"given":"James G","family":"Nicholson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-2404-021X","authenticated-orcid":false,"given":"Laura","family":"Gomez-Corral","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingyi","family":"Xue","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashutosh","family":"Rai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryan Padraig","family":"Finn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachael J L","family":"Tan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kalyana C","family":"Chakravarthi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelica","family":"Gualtieri","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charlotte L","family":"Hall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabor","family":"Czibik","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pinaki","family":"Dutta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4101-9432","authenticated-orcid":false,"given":"M\u00e1rta","family":"Korbonits","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federico","family":"Roncaroli","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7354-5691","authenticated-orcid":false,"given":"Shannon W","family":"Davis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6793-3118","authenticated-orcid":false,"given":"Carles","family":"Gaston-Massuet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,9]]},"reference":[{"key":"525_CR1","doi-asserted-by":"publisher","first-page":"978","DOI":"10.1038\/ncb2784","volume":"15","author":"JC Acosta","year":"2013","unstructured":"Acosta JC, Banito A, Wuestefeld T, Georgilis A, Janich P, Morton JP, Athineos D, Kang TW, Lasitschka F, Andrulis M et al (2013) A complex secretory program orchestrated by the inflammasome controls paracrine senescence. 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