Inflammation and cancer: an ancient link with novel potentials

Int J Cancer. 2007 Dec 1;121(11):2373-80. doi: 10.1002/ijc.23173.

Abstract

Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Mediators of the inflammatory response, e.g., cytokines, free radicals, prostaglandins and growth factors, can induce genetic and epigenetic changes including point mutations in tumor suppressor genes, DNA methylation and post-translational modifications, causing alterations in critical pathways responsible for maintaining the normal cellular homeostasis and leading to the development and progression of cancer. Recent discovery of an interaction between microRNAs and innate immunity during inflammation has further strengthened the association between inflammation and cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Chronic Disease
  • Cyclooxygenase 2 / metabolism
  • Cytokines / metabolism
  • DNA Methylation
  • Disease Progression
  • Epigenesis, Genetic
  • Free Radicals / adverse effects
  • Genes, p53 / genetics
  • Humans
  • Immunity, Innate
  • Inflammation / complications*
  • Inflammation / microbiology
  • Inflammation / parasitology
  • Inflammation / virology
  • Inflammation Mediators / adverse effects
  • Inflammation Mediators / metabolism*
  • Intercellular Signaling Peptides and Proteins / metabolism
  • MicroRNAs
  • NF-kappa B / metabolism
  • Neoplasms / etiology*
  • Neoplasms / genetics
  • Neoplasms / immunology
  • Neoplasms / metabolism*
  • Neoplasms / microbiology
  • Neoplasms / virology
  • Nitric Oxide Synthase / metabolism
  • Point Mutation
  • Prostaglandins / metabolism
  • Risk Assessment
  • Risk Factors
  • Signal Transduction

Substances

  • Cytokines
  • Free Radicals
  • Inflammation Mediators
  • Intercellular Signaling Peptides and Proteins
  • MicroRNAs
  • NF-kappa B
  • Prostaglandins
  • Nitric Oxide Synthase
  • Cyclooxygenase 2