The role of inflammatory pathways in cancer-associated cachexia and radiation resistance

Dysregulated inflammatory responses are key contributors to a multitude of chronic ailments, including cancer. Evidence indicates that disease progression in cancer is dependent on the complex interaction between the tumor and the host microenvironment. Most recently, the inflammatory response has been suggested to be critical, as both the tumor and microenvironment compartments produce cytokines that act on numerous target sites, where they foster a complex cascade of biologic outcomes. Patients with cancer-associated cachexia (CAC) suffer from a dramatic loss of skeletal muscle and adipose tissue, ultimately precluding them from many forms of therapeutic intervention, including radiotherapy. The cytokines that have been linked to the promotion of the cachectic response may also participate in radiation resistance. The major changes at the cytokine level are, in part, due to transcriptional regulatory alterations possibly due to epigenetic modifications. Herein we discuss the role of inflammatory pathways in CAC and examine the potential link between cachexia induction and radiation resistance.