Increased angiogenesis and Fas-ligand expression are independent processes in acute myeloid leukemia

Leuk Res. 2001 Dec;25(12):1067-73. doi: 10.1016/s0145-2126(01)00082-0.

Abstract

We evaluated the clinical significance of tumor angiogenesis and Fas-ligand (FasL) expression using parameters including the microvessel count (MVC), vascular endothelial growth factor (VEGF) level, and FasL expression in patients with acute myeloid leukemia (AML). Paraffin-embedded bone marrow (BM) sections from 43 AML patients at diagnosis, 20 patients after subsequent induction therapy, and 18 controls with non-invasive lymphoma were stained immunohistochemically for von Willebrand factor (vWF) and FasL. VEGF in BM mononuclear cells from 32 AML patients at diagnosis and 10 controls, including bone marrow transplantation donors, was assayed by an ELISA method. We found that the mean MVC, VEGF level, and FasL expression in AML patients at diagnosis were significantly higher than those of controls, with a significant correlation between the MVC and VEGF levels (r=0.43). However, there were no correlations between FasL expression and MVC or VEGF level. The mean MVC and FasL expression after induction therapy were lower than those evaluated at diagnosis, but were higher than those of controls. There was a correlation between the MVC and percentage of BM blasts (r=0.479), but no correlation between the MVC, VEGF level, or FasL expression and other hematologic or clinical variables. Our findings provide evidence of increased angiogenesis and tumor immune escape in AML, and both angiogenesis and tumor immune escape are independent processes in AML.

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Bone Marrow / chemistry
  • Endothelial Growth Factors / analysis*
  • Fas Ligand Protein
  • Female
  • Humans
  • Immunohistochemistry
  • Leukemia, Myeloid, Acute / blood*
  • Leukemia, Myeloid, Acute / metabolism
  • Lymphokines / analysis*
  • Male
  • Membrane Glycoproteins / analysis*
  • Middle Aged
  • Neovascularization, Pathologic / etiology*
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Substances

  • Endothelial Growth Factors
  • FASLG protein, human
  • Fas Ligand Protein
  • Lymphokines
  • Membrane Glycoproteins
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors