title: Review article: immune suppression and colorectal cancer.
abstract: BACKGROUND
  Advances in immunology and molecular biology have shown that colorectal cancer is potentially immunogenic and that host immune responses influence survival. However, immune surveillance and activation is frequently ineffective in preventing and/or controlling tumour growth.
  
  
  OBJECTIVE
  To discuss potential ways in which colorectal cancer induces immune suppression, its effect upon prognosis and avenues for therapeutic development.
  
  
  METHODS
  A literature review was undertaken for evidence of colorectal cancer-induced immune suppression using PubMed and Medline searches. Further studies were identified from the reference lists of identified papers.
  
  
  RESULTS
  Immune suppression occurs at a molecular and cellular level and can result in a shift from cellular to humoral immunity. Several mechanisms for immune suppression have been described affecting innate and adaptive immunity with suppression linked to poorer clinical outcome.
  
  
  CONCLUSIONS
  Colorectal cancer causes direct inhibition of the host's immune response with a detrimental effect upon prognosis. Immunotherapy offers a therapeutic strategy to counteract these effects with promising results seen particularly in precancerous conditions and early tumours. This review strongly suggests that immunotherapy should be incorporated into adjuvant therapeutic trials for stage 2 tumours and be considered as adjuvant treatment in conjunction with standard chemotherapy regimes for advanced disease.
authors.affiliation: Institution Colorectal Surgery Unit & Division of Oncology, St George's Hospital, Blackshaw Road, London, UK.
authors.forename: C
authors.initials: C
authors.lastname: Evans
authors.forename: A G
authors.initials: AG
authors.lastname: Dalgleish
authors.forename: D
authors.initials: D
authors.lastname: Kumar
mesh_terms: D017209:Apoptosis / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D015179:Colorectal Neoplasms / Q000276:immunology*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015536:Down-Regulation / Q000276:immunology; D006680:HLA Antigens / Q000032:analysis; D059951:HLA-G Antigens; D006632:Histamine / Q000276:immunology; D015395:Histocompatibility Antigens Class I / Q000032:analysis / Q000276:immunology; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology*; D016753:Interleukin-10 / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology; D042461:Vascular Endothelial Growth Factor A / Q000276:immunology
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; D016753:Interleukin-10; D006632:Histamine; D051546:Cyclooxygenase 2