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[Cancer Research 59, 3374-3378, July 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 3374-3378, July 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Blockade of the Vascular Endothelial Growth Factor Stress Response Increases the Antitumor Effects of Ionizing Radiation1

David H. Gorski, Michael A. Beckett, Nora T. Jaskowiak, Douglas P. Calvin, Helena J. Mauceri, Rabih M. Salloum, Saraswathy Seetharam, Ann Koons, Danielle M. Hari, Donald W. Kufe and Ralph R. Weichselbaum2

Departments of Radiation and Cellular Oncology [D. H. G., M. A. B., D. P. C., H. J. M., S. S., A. K., D. M. H., R. R. W.] and Surgery [N. T. J., R. M. S.], University of Chicago, Chicago, Illinois 60637, and Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115 [D. W. K.]

The family of vascular endothelial growth factor (VEGF) proteins include potent and specific mitogens for vascular endothelial cells that function in the regulation of angiogenesis. Inhibition of VEGF-induced angiogenesis, either by neutralizing antibodies or a dominant-negative soluble receptor, blocks the growth of primary and metastatic experimental tumors. Here we report that VEGF expression is induced in Lewis lung carcinomas (LLCs) both in vitro and in vivo after exposure to ionizing radiation (IR) and in human tumor cell lines (Seg-1 esophageal adenocarcinoma, SQ20B squamous cell carcinoma, T98 and U87 glioblastomas, and U1 melanoma) in vitro. The biological significance of IR-induced VEGF production is supported by our finding that treatment of tumor-bearing mice (LLC, Seg-1, SQ20B, and U87) with a neutralizing antibody to VEGF-165 before irradiation is associated with a greater than additive antitumor effect. In vitro, the addition of VEGF decreases IR-induced killing of human umbilical vein endothelial cells, and the anti-VEGF treatment potentiates IR-induced lethality of human umbilical vein endothelial cells. Neither recombinant VEGF protein nor neutralizing antibody to VEGF affects the radiosensitivity of tumor cells. These findings support a model in which induction of VEGF by IR contributes to the protection of tumor blood vessels from radiation-mediated cytotoxicity and thereby to tumor radioresistance.




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