Anti-tumor activities of the angiogenesis inhibitors interferon-inducible protein-10 and the calreticulin fragment vasostatin

Cancer Immunol Immunother. 2002 Sep;51(7):358-66. doi: 10.1007/s00262-002-0294-2. Epub 2002 Jul 3.

Abstract

Tumor growth depends upon an adequate supply of oxygen and nutrients achieved through angiogenesis and maintenance of an intact tumor vasculature. Therapy with individual agents that target new vessel formation or existing vessels has suppressed experimental tumor growth, but rarely resulted in the eradication of tumors. We therefore tested the combined anti-tumor activity of vasostatin and interferon-inducible protein-10 (IP-10), agents that differently target the tumor vasculature. Vasostatin, a selective and direct inhibitor of endothelial cell proliferation, significantly reduced Burkitt tumor growth and tumor vessel density. IP-10, an "angiotoxic" chemokine, caused vascular damage and focal necrosis in Burkitt tumors. When combined, vasostatin plus IP-10 reduced tumor growth more effectively than each agent alone, but complete tumor regression was not observed. Microscopically, these tumors displayed focal necrosis and reduction in vessel density. Combination therapy with the inhibitors of angiogenesis vasostatin and IP-10 is effective in reducing the rate of tumor growth but fails to induce tumor regression, suggesting that curative treatment may require supplemental drugs targeting directly the tumor cells.

MeSH terms

  • Actins / analysis
  • Angiogenesis Inhibitors / therapeutic use*
  • Animals
  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects
  • Burkitt Lymphoma / drug therapy*
  • Burkitt Lymphoma / prevention & control
  • Calcium-Binding Proteins / therapeutic use*
  • Calreticulin
  • Cell Division / drug effects
  • Chemokine CXCL10 / therapeutic use*
  • Drug Evaluation, Preclinical
  • Drug Synergism
  • Endothelium, Vascular / drug effects
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Muscle, Smooth, Vascular / drug effects
  • Neovascularization, Pathologic / drug therapy*
  • Peptide Fragments / therapeutic use*
  • Platelet Endothelial Cell Adhesion Molecule-1 / analysis
  • Recombinant Fusion Proteins / therapeutic use
  • Ribonucleoproteins / therapeutic use*
  • Xenograft Model Antitumor Assays

Substances

  • Actins
  • Angiogenesis Inhibitors
  • Antineoplastic Agents
  • Calcium-Binding Proteins
  • Calreticulin
  • Chemokine CXCL10
  • Peptide Fragments
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Recombinant Fusion Proteins
  • Ribonucleoproteins
  • vasostatin