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MatchTypeWhy
Bonetto, AndreaPerson Why?
ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.Academic Article Why?
STAT3 in the systemic inflammation of cancer cachexia.Academic Article Why?
?-hydroxy-?-methylbutyrate (HMB) attenuates muscle and body weight loss in experimental cancer cachexia.Academic Article Why?
The urgent need to improve childhood cancer cachexia.Academic Article Why?
FoxP1 is a transcriptional repressor associated with cancer cachexia that induces skeletal muscle wasting and weakness.Academic Article Why?
IGF-1 is downregulated in experimental cancer cachexia.Academic Article Why?
PDK4 drives metabolic alterations and muscle atrophy in cancer cachexia.Academic Article Why?
Reduced rDNA transcription diminishes skeletal muscle ribosomal capacity and protein synthesis in cancer cachexia.Academic Article Why?
Role of myokines and osteokines in cancer cachexia.Academic Article Why?
STAT3 activation in skeletal muscle links muscle wasting and the acute phase response in cancer cachexia.Academic Article Why?
The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia.Academic Article Why?
Tumor-derived IL-6 and trans-signaling among tumor, fat, and muscle mediate pancreatic cancer cachexia.Academic Article Why?
Postoperative consequences of cancer cachexia after head and neck free flap reconstruction.Academic Article Why?
Impairment of aryl hydrocarbon receptor signalling promotes hepatic disorders in cancer cachexia.Academic Article Why?
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