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 TGFβ1, revealing post-secretory control of ligand activation as a potential therapeutic vulnerability in cancer cachexia. See related article by Machado et al., p. 2172.
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