{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T07:58:04Z","timestamp":1790841484820,"version":"4.1.0"},"reference-count":9,"publisher":"American Association for Cancer Research (AACR)","issue":"10","content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,10,1]]},"abstract":"<jats:title>Summary:<\/jats:title>\n                  <jats:p>Cancer cachexia is increasingly recognized as a coordinated, tumor-induced, unsustainable alteration in interorgan communication. Machado and colleagues identify a new molecular mechanism that promotes cachexia, in which tumor-secreted ADAMTSL4 drives tissue wasting by promoting local activation of latent TGF\u03b21, revealing post-secretory control of ligand activation as a potential therapeutic vulnerability in cancer cachexia.<\/jats:p>\n                  <jats:p>See related article by Machado et al., p. 2172<\/jats:p>","DOI":"10.1158\/2159-8290.cd-26-1661","type":"journal-article","created":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T07:13:33Z","timestamp":1790838813000},"page":"1964-1966","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Activity over Abundance: ADAMTSL4 Unlocks Latent TGF\u03b21 in Cancer 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