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Blood, 15 September 2004, Vol. 104, No. 6, pp. 1769-1777. Prepublished online as a Blood First Edition Paper on June 8, 2004; DOI 10.1182/blood-2003-11-3952. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-11-3952v1 104/6/1769    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 Göthert, J. R. Articles by Begley, C. G. Search for Related Content PubMed PubMed Citation Articles by Göthert, J. R. Articles by Begley, C. G. Related Collections Hematopoiesis and Stem Cells Hemostasis, Thrombosis, and Vascular Biology Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium Joachim R. Göthert, Sonja E. Gustin, J. Anke M. van Eekelen, Uli Schmidt, Mark A. Hall, Stephen M. Jane, Anthony R. Green, Berthold Göttgens, David J. Izon, and C. Glenn Begley From the Division of Cancer Biology, Telethon Institute for Child Health Research, Centre for Child Health Research and Western Australian Institute for Medical Research (WAIMR), University of Western Australia, West Perth, WA, Australia; Rotary Bone Marrow Research Laboratory, Royal Melbourne Hospital, Parkville, Victoria, Australia; and The University of Cambridge, Department of Haematology, Cambridge Institute for Medical Research, Cambridge, United Kingdom. Tumor growth is dependent in part on "neoangiogenesis." Functional involvement of bone marrow (BM)-derived cells in this process has been demonstrated. However, it remains controversial as to whether tumor endothelium itself is BM derived. Here we sought to address this issue with an endothelial-specific, inducible transgenic model. We generated Cretransgenic mice (endothelial-SCL-Cre-ERT) using the tamoxifen-inducible Cre-ERT recombinase driven by the 5' endothelial enhancer of the stem cell leukemia (SCL) locus. These mice were intercrossed with Cre reporter strains in which -galactosidase (LacZ) or enhanced yellow fluorescent protein (EYFP) are expressed upon Cre-mediated recombination. After tamoxifen administration, endothelial LacZ staining was observed in embryonic and adult tissues. Cre-mediated recombination was also observed in newly generated tumor endothelium. In adult BM cells we could only detect trace amounts of recombination by flow cytometry. Subsequently, BM from endothelial-SCL-Cre-ERT;R26R mice was transplanted into irradiated recipients. When tumors were grown in recipient mice, which received tamoxifen, no tumor LacZ staining was detected. However, when tumors were grown in endothelial-SCL-Cre-ERT;R26R mice 3 weeks after the cessation of tamoxifen treatment, there was widespread endothelial LacZ staining present. Thus, this genetic model strongly suggests that BM cells do not contribute to tumor endothelium and demonstrates the lineage relation between pre-existing endothelium and newly generated tumor endothelial cells. (Blood. 2004;104:1769-1777) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. Pula, U. Mayr, C. Evans, M. Prokopi, D. S. Vara, X. Yin, Z. Astroulakis, Q. Xiao, J. Hill, Q. Xu, et al. Proteomics Identifies Thymidine Phosphorylase As a Key Regulator of the Angiogenic Potential of Colony-Forming Units and Endothelial Progenitor Cell Cultures Circ. Res., January 2, 2009; 104(1): 32 - 40. [Abstract] [Full Text] [PDF] S. Obi, K. Yamamoto, N. Shimizu, S. Kumagaya, T. Masumura, T. Sokabe, T. Asahara, and J. Ando Fluid shear stress induces arterial differentiation of endothelial progenitor cells J Appl Physiol, January 1, 2009; 106(1): 203 - 211. [Abstract] [Full Text] [PDF] J. Ma and D. J. 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