The paradox of pro-inflammatory cytokines in cancer

Cancer Metastasis Rev. 2006 Sep;25(3):307-13. doi: 10.1007/s10555-006-9000-8.


Cytokines such as IL-1 and TNF are primarily pro-inflammatory. The inflammation induced by these cytokines is reflected in the type of genes they induce. In the pathogenesis of carcinogenesis as well as tumor growth and spread, cytokines such as IL-1 and TNF induce chemokines that attract neutrophils. Neutrophils are key players in the production of reactive oxygen species and carcinogenesis. Another aspect of pro-inflammatory cytokines is the induction of adhesion molecules and metalloproteinases, both of which provide mechanisms for tumor invasion. Blocking cytokines, however, will reduce tumor growth and spread if administered at sufficient concentrations and will require parenteral therapy. However, blocking cytokines will not kill tumor cells nor prevent carcinogenesis. Blocking cytokines is best as an adjunct therapy together with tumorocidal drugs.

Publication types

  • Review

MeSH terms

  • Cytokines / physiology*
  • Dinoprostone / physiology
  • Humans
  • Immunologic Surveillance*
  • Infections / immunology
  • Inflammation / immunology
  • Interleukin-1 / physiology*
  • Interleukin-18 / physiology
  • Neoplasms / genetics
  • Neoplasms / immunology*
  • Neoplasms / pathology
  • Oncogenes / genetics
  • Tumor Necrosis Factor-alpha / physiology*


  • Cytokines
  • Interleukin-1
  • Interleukin-18
  • Tumor Necrosis Factor-alpha
  • Dinoprostone