Cancer cachexia: mediators, signaling, and metabolic pathways.

By K. Fearon, D. Glass, D. Guttridge. Cell Metabolism, 2012

1,139 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/75b0e2433612a58ad8f9d67ccc0d2bf3bbccbcea

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In Molecular Biology

1. E. Wagner

In Physiology

1. R. Zechner

Citations in the corpus

• A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy (2012, neutral): “Myo-PGC-1a4 Mice Show Resistance to CancerInducedCachexiawith ImprovedGlucose Tolerance and Preserved Muscle Mass Cancer cachexia is a very important complication of manymalignancies, resulting in severe muscle wasting and negatively affecting patient outcome (Fearon et al., 2012).”
• A switch from white to brown fat increases energy expenditure in cancer-associated cachexia. (2014, background): “WAT atrophy represents one of the hallmarks of cachexia and is caused by b-adrenergic activation and/or inflammatory cytokine-induced lipolysis (Das et al., 2011; Fearon et al., 2012).”