title: Inflammation and neural signaling:  etiologic mechanisms of the cancer treatment-related symptom cluster.
abstract: OBJECTIVE
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors: School of Nursing, MGH Institute of Health Professions, Boston, Massachusetts 02129, USA. ljwood@mghihp.edu
authors: Lisa J
authors: LJ
authors: Wood
authors: Kristianna
authors: K
authors: Weymann
mesh_terms: D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D003072:Cognition Disorders / Q000139:chemically induced / Q000150:complications; D005221:Fatigue / Q000139:chemically induced / Q000150:complications; D006801:Humans; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology; D055809:Illness Behavior / Q000187:drug effects*; D007249:Inflammation / Q000097:blood / Q000139:chemically induced* / Q000150:complications; D053583:Interleukin-1beta / Q000097:blood / Q000187:drug effects* / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood / Q000502:physiology; D019964:Mood Disorders / Q000139:chemically induced; D009369:Neoplasms / Q000150:complications / Q000188:drug therapy*; D011788:Quality of Life; D018123:Receptors, Interleukin / Q000097:blood / Q000187:drug effects / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood / Q000187:drug effects / Q000502:physiology; D018434:Sickness Impact Profile; D015398:Signal Transduction / Q000187:drug effects*; D013577:Syndrome
chemical_list: D000970:Antineoplastic Agents; D053583:Interleukin-1beta; D015850:Interleukin-6; D018123:Receptors, Interleukin; D018124:Receptors, Tumor Necrosis Factor