Angiogenesis plays a key role in solid tumor growth. The purpose of this wo
rk was to study angiogenesis in acute myeloid leukemia (AML), We stained bo
ne marrow samples from 20 adult patients with untreated AML and 20 normal c
ontrols using endothelial cell markers (ULEX-E and von Willebrand factor [v
WF]). The number of vessels per millimeter length of bone marrow core biops
y specimen was scored by light microscopy. Using ULEX-E staining, AML marro
ws had (average+/-SEM) 8.3+/-3.6 vessels/mm (range, 3.7-19.3), whereas norm
al marrows had 4.3 +/- 1.8 vessels/mm (range, 1.6-7.9). A similar differenc
e was noted using VWF staining (8.6 +/- 3.0 vessels/mm vs 4.9 +/- 2.2 vesse
ls/mm in AML vs normal bone marrows, respectively). The differences between
the numbers of vessels/mm in AML and normal marrows were highly significan
t (P<.0001 for both ULEX-E and vWF staining). When analyzed by FAB category
, there was no difference in the average number of vessels/mm among the dif
ferent subgroups of AML, Using reverse transcriptase polymerase chain react
ion, we observed that the HL-60 and U937 human AML cell lines and 4 of 4 fr
eshly isolated AML cells from untreated patients expressed mRNA for vascula
r endothelial growth factor (VEGF). Both cell lines as well as all fresh AM
L isolates tested expressed VEGF protein. Basic fibroblast growth factor wa
s expressed only in HL-60 cells and in only 3 of 4 fresh AML samples. These
observations suggest that angiogenesis may play a role in the pathogenesis
of AML, inhibition of angiogenesis could constitute a novel strategy for t
he treatment of AML, (C) 2000 by The American Society of Hematology.