Roles of inflammation in cancer initiation, progression, and metastasis

Front Biosci (Schol Ed). 2010 Jan 1;2:176-83. doi: 10.2741/s55.

Abstract

Inflammatory cells and signals contribute to the initiation and development of cancer. In fact, persistent inflammatory conditions resulting from infection or injury can exist before a normal cell is transformed into a cancer cell. Situations of chronic inflammation can promote genomic instability leading to DNA damage, oncogene activation, or impaired function of a tumor suppressor. Alternatively, cancer development unrelated to inflammation can stimulate the development of an inflammatory microenvironment that promotes tumor cell proliferation. Whether chronic or tumor-derived, inflammation and inflammation-related stimuli within the tumor microenvironment permits proliferation and survival of cancer cells, promotes blood and lymphatic vessel formation, and aids in invasion and metastasis. The inflammatory status of the tumor microenvironment can act to quell the body's natural immune response and effectively ameliorate a positive response to many commonly used anti-cancer antibodies and chemotherapeutic agents. New evidence suggests that the molecular pathways and consequences of inflammation specifically related to the tumor microenvironment are starting to be understood. This new information implicates novel cellular targets that could lead to improved diagnosis and treatment for a variety of solid malignancies.

MeSH terms

  • Cytokines / metabolism*
  • Disease Progression
  • Drug Delivery Systems
  • Humans
  • Hypoxia-Inducible Factor 1 / metabolism
  • Inflammation / complications*
  • Inflammation / metabolism
  • NF-kappa B / metabolism
  • Neoplasm Metastasis / physiopathology*
  • Neoplasms / etiology*
  • Neoplasms / physiopathology
  • Nitric Oxide Synthase Type II / metabolism
  • Prostaglandin-Endoperoxide Synthases / metabolism
  • Signal Transduction / physiology*

Substances

  • Cytokines
  • Hypoxia-Inducible Factor 1
  • NF-kappa B
  • Nitric Oxide Synthase Type II
  • Prostaglandin-Endoperoxide Synthases