Angiogenesis seems to be important both in the pathogenesis of acute myelogenous 
leukemia (AML) and for the susceptibility of AML blasts to chemotherapy. Recent 
clinical studies even suggest that antiangiogenic therapy can induce disease 
control in patients with AML relapse. In this context we have investigated the 
profile of the systemic component of angiogenic regulation in AML by 
characterizing the serum levels of (i) the angiogenic regulators angiogenin, 
basic fibroblast growth factor (bFGF) and endostatin; (ii) the endothelial cell 
marker soluble (s) E-selectin. Patients with untreated AML had increased levels 
of angiogenin, endostatin and sE-selectin, whereas the levels of bFGF were not 
significantly altered. The systemic levels of the proangiogenic bFGF, the 
antiangiogenic endostatin and the endothelial cell marker sE-selectin showed 
significant correlations, whereas angiogenin and sE-selectin levels were not 
correlated. Furthermore, intensive chemotherapy resulted in decreased systemic 
levels of the 2 proangiogenic mediators angiogenin and bFGF, whereas endostatin 
levels remained high after treatment. Although angiogenin normally is a part of 
the acute phase reaction, its systemic levels were not altered when patients 
with chemotherapy-induced cytopenia developed complicating bacterial infections. 
Our results suggest that intensive chemotherapy can modulate the systemic 
component of angiogenic regulation in AML patients.