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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1508-1514. Prepublished online as a Blood First Edition Paper on October 14, 2004; DOI 10.1182/blood-2004-06-2246. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: 2004-06-2246v1 105/4/1508    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Criscuoli, M. L. Articles by Eliceiri, B. P. Search for Related Content PubMed PubMed Citation Articles by Criscuoli, M. L. Articles by Eliceiri, B. P. Related Collections Hemostasis, Thrombosis, and Vascular Biology Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Tumor metastasis but not tumor growth is dependent on Src-mediated vascular permeability Michele L. Criscuoli, Mai Nguyen, and Brian P. Eliceiri From the Division of Cancer Biology, La Jolla Institute for Molecular Medicine, San Diego, CA. Vascular endothelial growth factor (VEGF)–induced vascular permeability (VP) is a hallmark of tumor growth and metastasis. Previous studies have shown a requirement for Src kinase in VEGF-mediated VP and signaling in blood vessels. In this study, we have examined the effect of Src-mediated reduced VP on tumor growth and metastasis. The growth and spontaneous metastasis of VEGF-expressing tumor cells were determined in Src-knockout (src–/–) or control mice (src+/+ or src+/–). In comparison to control mice, src-null mice had a significant reduction in tumor-induced VP as well as a subsequent reduction in spontaneous metastasis. In contrast, primary tumor weight and vascular density were unchanged between src-null and control mice. Consistent with a role for Src in the extravasation of tumor cells from the circulation, direct intravenous injection of lung carcinoma cells resulted in a more than 2-fold reduction in lung tumor burden in src-null mice compared to control mice. The comparison of the results from the experimental metastasis and the spontaneous metastasis models suggests that there are defects in VP in the primary site of Src-deficient mice and that there may be an essential role for Src and Src-mediated VP in tumor metastasis to the lung. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. L. Van Sluis, T. M.H. Niers, C. T. Esmon, W. Tigchelaar, D. J. Richel, H. R. 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