{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T13:54:14Z","timestamp":1791986054357,"version":"4.4.0"},"reference-count":81,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"14","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Adv."],"published-print":{"date-parts":[[2023,4,7]]},"abstract":"<jats:p>\n                    The mechanisms underlying\n                    <jats:italic>ETS<\/jats:italic>\n                    -driven prostate cancer initiation and progression remain poorly understood due to a lack of model systems that recapitulate this phenotype. We generated a genetically engineered mouse with prostate-specific expression of the\n                    <jats:italic>ETS<\/jats:italic>\n                    factor, ETV4, at lower and higher protein dosage through mutation of its degron. Lower-level expression of ETV4 caused mild luminal cell expansion without histologic abnormalities, and higher-level expression of stabilized ETV4 caused prostatic intraepithelial neoplasia (mPIN) with 100% penetrance within 1 week. Tumor progression was limited by p53-mediated senescence and\n                    <jats:italic>Trp53<\/jats:italic>\n                    deletion cooperated with stabilized ETV4. The neoplastic cells expressed differentiation markers such as Nkx3.1 recapitulating luminal gene expression features of untreated human prostate cancer. Single-cell and bulk RNA sequencing showed that stabilized ETV4 induced a previously unidentified  luminal-derived expression cluster with signatures of cell cycle, senescence, and epithelial-to-mesenchymal transition. These data suggest that\n                    <jats:italic>ETS<\/jats:italic>\n                    overexpression alone, at sufficient dosage, can initiate prostate neoplasia.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adc9446","type":"journal-article","created":{"date-parts":[[2023,4,5]],"date-time":"2023-04-05T13:58:37Z","timestamp":1680703117000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":25,"title":["ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8777-4580","authenticated-orcid":true,"given":"Dan","family":"Li","sequence":"first","affiliation":[{"name":"Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New\u00a0York, NY 10065, 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