Tumor cells and tumor-associated macrophages: secreted proteins as potential targets for therapy

Clin Dev Immunol. 2011;2011:565187. doi: 10.1155/2011/565187. Epub 2011 Nov 17.

Abstract

Inflammatory pathways, meant to defend the organism against infection and injury, as a byproduct, can promote an environment which favors tumor growth and metastasis. Tumor-associated macrophages (TAMs), which constitute a significant part of the tumor-infiltrating immune cells, have been linked to the growth, angiogenesis, and metastasis of a variety of cancers, most likely through polarization of TAMs to the M2 (alternative) phenotype. The interaction between tumor cells and macrophages provides opportunities for therapy. This paper will discuss secreted proteins as targets for intervention.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Communication / immunology*
  • Cell Differentiation / immunology
  • Chemokine CCL2 / antagonists & inhibitors
  • Chemokine CCL2 / immunology
  • Chemokine CCL2 / metabolism
  • Clinical Trials as Topic
  • Cyclooxygenase 2 / immunology
  • Cyclooxygenase 2 / metabolism
  • Female
  • Humans
  • Interleukin-12 / immunology
  • Interleukin-12 / metabolism
  • Interleukin-6 / immunology
  • Interleukin-6 / metabolism
  • Macrophage Activation*
  • Macrophage Colony-Stimulating Factor / antagonists & inhibitors
  • Macrophage Colony-Stimulating Factor / immunology
  • Macrophage Colony-Stimulating Factor / metabolism
  • Macrophages / immunology*
  • Matrix Metalloproteinases / immunology
  • Matrix Metalloproteinases / metabolism
  • Mice
  • Neoplasm Invasiveness
  • Neoplasms / immunology*
  • Neoplasms / pathology*
  • Neoplasms / therapy
  • Receptor, Macrophage Colony-Stimulating Factor / immunology
  • Receptor, Macrophage Colony-Stimulating Factor / metabolism
  • Receptors, Tumor Necrosis Factor, Type I / immunology
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Receptors, Tumor Necrosis Factor, Type II / immunology
  • Receptors, Tumor Necrosis Factor, Type II / metabolism
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CCL2
  • Interleukin-6
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Tumor Necrosis Factor-alpha
  • Interleukin-12
  • Macrophage Colony-Stimulating Factor
  • Cyclooxygenase 2
  • Receptor, Macrophage Colony-Stimulating Factor
  • Matrix Metalloproteinases