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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 309-313
Evidence of increased angiogenesis in patients with acute myeloid
leukemia
Jerry W. Hussong,
George M. Rodgers, and
Paul J. Shami
From the Department of Pathology, ARUP Laboratories, and Divisions
of Hematology and Oncology, Department of Medicine, University of Utah
and Salt Lake City VA Medical Centers, Salt Lake City, UT.
Angiogenesis plays a key role in solid tumor growth. The purpose of
this work was to study angiogenesis in acute myeloid leukemia (AML). We
stained bone marrow samples from 20 adult patients with untreated AML
and 20 normal controls using endothelial cell markers (ULEX-E and von
Willebrand factor [vWF]). The number of vessels per millimeter length
of bone marrow core biopsy specimen was scored by light microscopy.
Using ULEX-E staining, AML marrows had (average ± SEM)
8.3 ± 3.6 vessels/mm (range, 3.7-19.3), whereas normal marrows had
4.3 ± 1.8 vessels/mm (range, 1.6-7.9). A similar difference was
noted using vWF staining (8.6 ± 3.0 vessels/mm vs 4.9 ± 2.2
vessels/mm in AML vs normal bone marrows, respectively). The
differences between the numbers of vessels/mm in AML and normal marrows
were highly significant (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 different subgroups of AML.
Using reverse transcriptase polymerase chain reaction, we observed that
the HL-60 and U937 human AML cell lines and 4 of 4 freshly isolated AML
cells from untreated patients expressed mRNA for vascular endothelial
growth factor (VEGF). Both cell lines as well as all fresh AML isolates
tested expressed VEGF protein. Basic fibroblast growth factor was
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 the treatment of AML. (Blood. 2000;95:309-313).
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