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To survive this metabolic stress, PDAC cells activate lysosome-centered nutrient acquisition and recycling programs, including macroautophagy, RAS-driven macropinocytosis, and receptor-mediated endocytosis, that traffic intracellular and extracellular cargo to lysosomes for degradation and metabolite export. These pathways are reinforced by oncogenic signaling and MiT\/TFE-dependent lysosomal biogenesis, and they support core outputs of tumor metabolism such as iron bioavailability, amino acid and nucleotide pools, lipid homeostasis, and immune evasion. Lysosomal programs in nonmalignant compartments (fibroblasts, stellate cells, and immune cells) further shape nutrient exchange, matrix production, and whole-body metabolism, positioning the lysosome as a key node at the tumor\u2013host interface. Although genetic and pharmacologic blockade of autophagy\/lysosome function can produce potent antitumor effects in preclinical models, clinical trials with lysosomotropic agents have shown limited benefit, highlighting challenges in target engagement, biomarkers, and rational combination strategies. Here we review current tools and concepts for interrogating lysosomal flux in PDAC, integrate emerging insights from systemic metabolism and dietary interventions, and outline therapeutic opportunities for more effectively exploiting lysosome dependence in pancreatic cancer.<\/jats:p>","DOI":"10.1101\/gad.353702.126","type":"journal-article","created":{"date-parts":[[2026,8,6]],"date-time":"2026-08-06T15:10:15Z","timestamp":1786029015000},"page":"1578-1597","source":"Crossref","is-referenced-by-count":2,"title":["Lysosomal metabolism in pancreatic cancer and its crosstalk with host physiology"],"prefix":"10.1101","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1872-2661","authenticated-orcid":false,"given":"Caleb","family":"Cheng","sequence":"first","affiliation":[{"name":"Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA;"},{"name":"Medical Scientist Training Program, University of Michigan, Ann Arbor, Michigan 48109, USA;"},{"name":"Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, Michigan 48109, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-5325-4007","authenticated-orcid":false,"given":"R\u00fcya","family":"Pakkan","sequence":"additional","affiliation":[{"name":"Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9282-3415","authenticated-orcid":false,"given":"Arul M.","family":"Chinnaiyan","sequence":"additional","affiliation":[{"name":"Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA;"},{"name":"Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA;"},{"name":"Rogel Cancer Center, University of Michigan, Ann Arbor, Michigan 48109, USA;"},{"name":"Howard Hughes Medical Institute, University of 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