Cachexia is a syndrome characterized by continuous, involuntary weight loss and systemic inflammation. Several mediators that are either host- or tumor-derived, such as pro-inflammatory cytokines, have been implicated in the pathogenesis of cancer cachexia.

The compensatory humoral system that typically reduces the excessive production of pro-inflammatory cytokines in order to maintain homeostasis is also highly activated in patients with cancer cachexia. The above observations, along with cachexia, suggest that conditions similar to SIRS (systemic inflammatory response syndrome) and CARS (compensatory anti-inflammatory response syndrome), or to mixed anti-inflammatory response syndrome (MARS), may exist in cachexia. The typical immunological status of patients with cancer cachexia has been demonstrated to be suppressed cell-mediated immunity, and a Th2-dominant condition and myeloid-derived suppressor cells: MDSCs are major causes of this suppression.

Several therapies and strategies have been proposed with regard to anti-inflammatory treatments. However, no effective therapy against cancer cachexia is currently available. Further studies on the molecular mechanisms of inflammation, and the development of new anti-inflammatory agents, are required.