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Tumor Biology and Carcinogenesis Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion, Division of Basic Sciences, National Cancer Institute, NIH, Building 37, Room 2D02, Bethesda, Maryland 20892
In this study, we used a self-contained tetracycline-regulated retroviral vector system to elucidate the role of vascular endothelial growth factor (VEGF) in controlling s.c. growth of human T-47D breast carcinoma cells. VEGF expression was tightly regulated by this system, both in vitro and in nude mouse xenografts. A 2.4-fold increase in tumor volume was associated with VEGF overexpression. Tumor growth was almost completely inhibited when VEGF was suppressed from the time of T-47D cell inoculation, and a 6-fold reduction in tumor volume was observed when VEGF suppression was started in 175-mm3 tumors. However, no growth inhibition was observed when VEGF suppression was started in 820-mm3 tumors. In these tumors, basic fibroblast growth factor and transforming growth factor 
RNA expression was detected after VEGF was switched off. These findings demonstrate that VEGF is critical for the initial s.c. growth of T-47D breast carcinoma cells, whereas other angiogenic factors can compensate for the loss of VEGF after the tumors have reached a certain size.
1 Present address: Third Department of Internal Medicine, Nara Medical University, Shijo-cho 840, Kashihara, Nara 634, Japan.
2 To whom requests for reprints should be addressed, at Tumor Biology and Carcinogenesis Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion, Division of Basic Sciences, National Cancer Institute, NIH, Building 37, Room 2D02, Bethesda, MD 20892. Phone: (301) 496-1982; Fax: (301) 402-0153; E-mail: thorgeiu@dc37a.nci.nih.gov.
Received 6/11/97. Accepted 7/31/97.
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