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We identify LOY as a recurrent, functionally consequential alteration affecting \u223c50% of male PDAC patients across two independent cohorts, with strong enrichment in advanced disease and, critically, in the basal subtype, establishing LOY as a clinically actionable biomarker. Comprehensive genomic profiling positions LOY as a distinct genetic event associated with TP53 mutations, implicating it in aggressive tumor evolution. Integrative analyses across bulk tumors, single-cell datasets and CRISPR-engineered PDAC models converge on epithelial-to-mesenchymal transition (EMT) as the dominant LOY-driven program. Y-chromosome deletion alone induces EMT transcriptional states, mesenchymal morphology and enhanced metastatic ability. Mechanistically, LOY disrupts epigenetic regulation through loss of Y-linked chromatin modifiers, reshaping DNA methylation at EMT- and basal-defining loci and reducing chemotherapy sensitivity. These findings establish LOY as a causal genetic driver of PDAC progression and a clinically accessible biomarker with direct therapeutic relevance.<\/jats:p>","DOI":"10.64898\/2026.10.06.756936","type":"posted-content","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T08:30:24Z","timestamp":1791361824000},"source":"Crossref","is-referenced-by-count":0,"title":["Loss of the Y chromosome drives basal identity and metastatic potential via epigenetic reprogramming in pancreatic cancer"],"prefix":"10.64898","author":[{"given":"Madeleine","family":"Dorsch","sequence":"first","affiliation":[{"name":"Department of Medical Oncology, West German Cancer Center, University Hospital Essen at the University Duisburg-Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix E. 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