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[Cancer Research 59, 5412-5416, November 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 5412-5416, November 1, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Antiangiogenic Therapy Targeting the Tyrosine Kinase Receptor for Vascular Endothelial Growth Factor Receptor Inhibits the Growth of Colon Cancer Liver Metastasis and Induces Tumor and Endothelial Cell Apoptosis1

Raymond M. Shaheen, Darren W. Davis, Wenbiao Liu, Brian K. Zebrowski, Michael R. Wilson, Corazon D. Bucana, David J. McConkey, Gerald McMahon and Lee M. Ellis2

Departments of Surgical Oncology [R. M. S., B. K. Z., L. M. E.] and Cancer Biology [D. W. D., W. L., M. R. W., C. D. B., D. J. M., L. M. E.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, and SUGEN, Inc., South San Francisco, California 94080 [G. M.]

Increased vascular endothelial growth factor (VEGF) expression is associated with colon cancer metastases. We hypothesized that inhibition of VEGF receptor activity could inhibit colon cancer liver metastases. BALB/c mice underwent splenic injection with CT-26 colon cancer cells to generate metastases. Mice received daily i.p. injections of vehicle, tyrosine kinase inhibitor for Flk-1/KDR (SU5416) or tyrosine kinase inhibitor for VEGF, basic fibroblast growth factor, and platelet-derived growth factor receptors (SU6668). SU5416 and SU6668 respectively inhibited metastases (48.1% and 55.3%), microvessel formation (42.0% and 36.2%), and cell proliferation (24.4% and 27.3%) and increased tumor cell (by 2.6- and 4.3-fold) and endothelial cell (by 18.6- and 81.4-fold) apoptosis (P < 0.001). VEGF receptor inhibitors increased endothelial cell apoptosis, suggesting that VEGF may serve as an endothelial survival factor.




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