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Here, we identify serum amyloid A1 (SAA1) as a mediator of tumor- to-host communication acting through Toll-like receptor 4 (TLR4). Tumor-derived SAA1 was elevated in human PDAC and in a mouse PDAC model and disrupted both myofiber and muscle stem cell (MuSC) homeostasis. Genetic reduction of tumor-derived SAA1 uncoupled tumor progression from host wasting, preserving muscle mass and function and prolonging survival without affecting primary tumor growth. Mechanistically, SAA1-TLR4 signaling drove multicellular remodeling of the skeletal muscle microenvironment. Therapeutic TLR4 inhibition after cachexia onset restored muscle mass, function and MuSC abundance and prolonged survival independently of tumor growth. Conservation of SAA1-TLR4 signaling in human skeletal muscle identifies a therapeutically actionable tumor\u2013host pathway and demonstrates that host deterioration can be targeted independently of tumor progression.<\/jats:p>","DOI":"10.64898\/2026.09.04.748998","type":"posted-content","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T15:15:11Z","timestamp":1788966911000},"source":"Crossref","is-referenced-by-count":0,"title":["Tumor-derived SAA1-TLR4 signaling drives tumor-to-muscle communication in pancreatic cancer cachexia"],"prefix":"10.64898","author":[{"given":"Gabriele","family":"Guarnaccia","sequence":"first","affiliation":[{"name":"Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037 USA"},{"name":"Cardiovascular and Muscular Diseases Center, Sanford Burnham Prebys Medical Discovery Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037 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