CCL2 and neoplasm: Pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, IL-8, interferon-γ (IFN-γ), monocyte chemoattractant protein-1 (MCP-1), and other catabolic factors (activin and myostatin) are released into circulation by the tumor [37]. These signals can, in turn, activate metabolic pathways that increase proteolysis and/or decrease protein synthesis, which culminate in SKM wasting [22]. TNF-α is a major mediator of muscle catabolism associated with poor nutritional status in PDAC patients [22,38].