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Blood, Vol. 92 No. 9 (November 1), 1998:
pp. 3388-3393
Coexpression of Erythropoietin and Vascular Endothelial Growth
Factor in Nervous System Tumors Associated With von Hippel-Lindau
Tumor Suppressor Gene Loss of Function
Marion Krieg,
Hugo H. Marti, and
Karl
H. Plate
From the Department of Neuropathology, Freiburg
University Medical School, Freiburg; and the Department
of Molecular Cell Biology, Max-Planck Institute for
Physiological and Clinical Research, Bad Nauheim,
Germany.
Hemangioblastomas are highly vascular tumors of the central nervous
system that overexpress the hypoxia-inducible gene, vascular endothelial growth factor (VEGF), as a consequence of mutational inactivation of the von Hippel-Lindau tumor suppressor gene (VHL). Previous reports showed that hemangioblastomas can also express erythropoietin (Epo), which is also hypoxia-inducible. However, Epo
expression in hemangioblastomas was observed only in individual cases,
and the analyses were mainly based on indirect determination of
erythropoiesis-stimulating activity. Therefore, we analyzed a series of
11 hemangioblastomas for Epo, VEGF, and VHL expression by Northern blot
analysis and compared the results with normal brain and glioblastomas.
Surprisingly, we observed Epo mRNA expression in all hemangioblastoma
specimens analyzed, but in none of four glioblastomas. In contrast,
VEGF mRNA was expressed in all hemangioblastomas and all glioblastomas.
In situ hybridization revealed neoplastic stromal cells as Epo- and
VEGF-producing cells in hemangioblastomas. These results suggest that
in the nonhypoxic microenvironment of hemangioblastoma, Epo, similar to
VEGF, might be negatively regulated by the VHL gene product.
© 1998 by The American Society of Hematology.
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