Journal
CELL
Volume 162, Issue 6, Pages 1365-1378Publisher
CELL PRESS
DOI: 10.1016/j.cell.2015.08.031
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Funding
- Cooperative Research Centre for Biomarker Translation
- NHMRC [541901, 1058190]
- NHMRC Career Development Fellowship
- Swiss National Science Foundation grants
- NHMRC Development Grant [1075504]
- National Health and Medical Research Council of Australia [1075504, 1058190] Funding Source: NHMRC
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The cytokine TWEAK and its cognate receptor Fn14 are members of the TNF/TNFR superfamily and are upregulated in tumors. We found that Fn14, when expressed in tumors, causes cachexia and that antibodies against Fn14 dramatically extended lifespan by inhibiting tumor-induced weight loss although having only moderate inhibitory effects on tumor growth. Anti-Fn14 antibodies prevented tumorinduced inflammation and loss of fat and muscle mass. Fn14 signaling in the tumor, rather than host, is responsible for inducing this cachexia because tumors in Fn14- andTWEAK-deficient hosts developed cachexia that was comparable to that of wild-type mice. These results extend the role of Fn14 in wound repair and muscle development to involvement in the etiology of cachexia and indicate that Fn14 antibodies may be a promising approach to treat cachexia, thereby extending lifespan and improving quality of life for cancer patients.
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