Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Support Palliat Care. 2013 Mar;7(1):54-9. doi: 10.1097/SPC.0b013e32835dabe3.

Inflammation and neural signaling: etiologic mechanisms of the cancer treatment-related symptom cluster.

Author information

  • 1School of Nursing, MGH Institute of Health Professions, Boston, Massachusetts 02129, USA.



Cancer patients undergoing treatment with cytotoxic chemotherapeutic agents (CCAs) often experience a cluster of treatment-related symptoms, which include fatigue, loss of appetite, disturbed sleep, depressed mood, cognitive difficulties, and changes in body composition. This symptom cluster collectively referred to herein as cancer treatment-related symptoms (CTRSs) decrease quality of life, and physical and social functioning. The preclinical and clinical studies described in this review represent important progress in understanding potential underlying mechanisms of CTRS.


Recent studies support a role for CCA-induced interleukin-1β (IL-1β) signaling in the cause of CTRS. CCAs may share a common ability to activate intracellular stress response pathways to trigger the synthesis, processing, and release of IL-1β from immune cells. Fatigue, sleep disturbance, and cognitive difficulties in cancer patients exposed to CCAs correlate with plasma levels of IL-6, IL-1 receptor antagonist, and soluble tumor necrosis factor receptor-I/II, surrogate markers of IL-1β-mediated central nervous system (CNS) inflammation. Additional preclinical work suggests IL-1β-mediated CNS inflammation may cause CTRS by altering hypothalamic and hippocampal functioning.


Although additional research is necessary to further establish the link between CCA exposure, IL-1β-mediated inflammatory processes and CTRS, these data provide hints for future studies and therapeutic approaches in ameliorating these symptoms in cancer patients.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins Icon for PubMed Central
    Loading ...
    Write to the Help Desk