Vascular endothelial growth factor and its relationship to inflammatory mediators

Clin Cancer Res. 2007 May 15;13(10):2825-30. doi: 10.1158/1078-0432.CCR-06-2416.

Abstract

Inflammation occurs in response to host injury or infection, as the result of an autoimmune disease, or in response to the development of a tumor. Although the immune system may be helpful in fighting the tumor, it may also fuel the tumorigenic process. In fact, recent data suggest a strong link between chronic inflammation, angiogenesis, and the development of cancer. For example, inflammation and scarring caused by recurring infections with Mycobacterium tuberculosis may be a cause for cancers of the lung. Inflammatory breast cancer exhibits increased angiogenesis and lymphangiogenesis and has a higher metastatic potential than noninflammatory breast cancer. Nonsteroidal anti-inflammatory drugs have been proposed as preventives for the development of colon carcinoma and ovarian cancer. Inhibition of nuclear factor-kappaB contributes to the proposed mechanism of action. Inflammatory cytokines, including interleukin-6, serve as autocrine and paracrine growth factors for several cancers, and high levels of these cytokines may correlate with a poor prognosis and increased production of angiogenic factors. The state of the art of our understanding of this critical interaction is reviewed.

Publication types

  • Review

MeSH terms

  • Humans
  • Immune System / metabolism
  • Inflammation / complications*
  • Inflammation / immunology
  • Inflammation Mediators / metabolism*
  • Neoplasms / blood supply*
  • Neoplasms / immunology*
  • Neovascularization, Pathologic / immunology*
  • Vascular Endothelial Growth Factor A / metabolism*

Substances

  • Inflammation Mediators
  • Vascular Endothelial Growth Factor A