The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium
Abstract
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 β-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)
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De Palma, M., Venneri, M. A., Galli, R., Sergi, L. S., Politi, L. S., Sampaolesi, M., & Naldini, L. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.08.002 · Cited by 1,311
Liver sinusoidal endothelial cells: Physiology and role in liver diseases
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Kioi, M., Vogel, H., Schultz, G., Hoffman, R. M., Harsh, G. R., & Brown, J. M. (2010) · Journal of Clinical Investigation · doi:10.1172/jci40283 · Cited by 773
ADAR1 is essential for the maintenance of hematopoiesis and suppression of interferon signaling
Hartner, J. C., Walkley, C. R., Lu, J., & Orkin, S. H. (2009) · Nature Immunology · doi:10.1038/ni.1680 · Cited by 490
Kidd, S., Spaeth, E., Watson, K., Burks, J., Lu, H., Klopp, A., Andreeff, M., & Marini, F. C. (2012) · PLoS ONE · doi:10.1371/journal.pone.0030563 · Cited by 371
Metadata
- Authors
- Göthert, J. R., Gustin, S. E., van Eekelen, J. A. M., Schmidt, U., Hall, M. A., Jane, S. M., Green, A. R., Göttgens, B., Izon, D. J., & Begley, C. G.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2004-09-15
- Volume
- 104
- Issue
- 6
- Pages
- 1769-1777
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2109947902
- Cited by
- 285
- References
- 57
- FWCI
- 7.33
- Type
- journal article
- Language
- en
- Open access
- closed
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- Göthert, J. R., Gustin, S. E., van Eekelen, J. A. M., Schmidt, U., Hall, M. A., Jane, S. M., Green, A. R., Göttgens, B., Izon, D. J., & Begley, C. G. (2004). Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium. Blood. https://doi.org/10.1182/blood-2003-11-3952
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