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[Cancer Research 64, 6845-6848, October 1, 2004]
© 2004 American Association for Cancer Research

Advances in Brief

Schedule-dependent Inhibition of Hypoxia-inducible Factor-1{alpha} Protein Accumulation, Angiogenesis, and Tumor Growth by Topotecan in U251-HRE Glioblastoma Xenografts

Annamaria Rapisarda1, Jessica Zalek1, Melinda Hollingshead2, Till Braunschweig3, Badarch Uranchimeg1, Carrie A. Bonomi1, Suzanne D. Borgel1, John P. Carter1, Stephen M. Hewitt3, Robert H. Shoemaker2 and Giovanni Melillo1

1 Science Applications International Corporation–Frederick, Inc., National Cancer Institute at Frederick, Frederick, Maryland; 2 Developmental Therapeutics Program, National Cancer Institute at Frederick, Frederick, Maryland; and 3 Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Advanced Technology Center, Bethesda, Maryland

We have previously shown that topotecan, a topoisomerase I poison, inhibits hypoxia-inducible factor (HIF)-1{alpha} protein accumulation by a DNA damage-independent mechanism. Here, we report that daily administration of topotecan inhibits HIF-1{alpha} protein expression in U251-HRE glioblastoma xenografts. Concomitant with HIF-1{alpha} inhibition, topotecan caused a significant tumor growth inhibition associated with a marked decrease of angiogenesis and expression of HIF-1 target genes in tumor tissue. These results provide a compelling rationale for testing topotecan in clinical trials to target HIF-1 in cancer patients.




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