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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1310-1318. Prepublished online as a Blood First Edition Paper on October 7, 2004; DOI 10.1182/blood-2004-03-0933. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-03-0933v1 105/3/1310    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 Masood, R. Articles by Gill, P. S. Search for Related Content PubMed PubMed Citation Articles by Masood, R. Articles by Gill, P. S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Neoplasia Cell Adhesion and Motility Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Ephrin B2 expression in Kaposi sarcoma is induced by human herpesvirus type 8: phenotype switch from venous to arterial endothelium Rizwan Masood, Guangbin Xia, D. Lynne Smith, Piergips Scalia, Jonathan G. Still, Anil Tulpule, and Parkash S. Gill From the Departments of Medicine and Pathology, University of Southern California Keck School of Medicine, Los Angeles, CA. Kaposi sarcoma (KS) is an angioproliferative tumor derived from endothelial cells in which tumor cells form aberrant vascular structures. Ephrin B2 and ephrin B4 (EphB4) are artery- and vein-specific proteins, respectively, with critical roles in vessel maturation. We investigated whether the disorganized KS vasculature was due to unbalanced expression of ephrin B2 and EphB4. Secondly, we wished to determine if human herpesvirus type 8 (HHV-8), the viral agent associated with KS, regulates ephrin B2 and EphB4. An arterial phenotype was observed in KS tissue and cell lines, as shown by abundant expression of ephrin B2 with little or no EphB4. Infection of venous endothelial cells with HHV-8 resulted in a phenotype switch from EphB4 to ephrin B2, similar to that seen with vascular endothelial growth factor (VEGF). The HHV-8 effect on ephrin B2 expression was reproduced with the HHV-8-specific viral G-protein-coupled receptor. We also showed that ephrin B2 expression is required for KS cell viability by knock down with siRNA. KS is the first example of a human tumor with a predominantly arterial phenotype. This predominance can be attributed to expression of HHV-8 proteins and their downstream effects. Ephrin B2 is thus an important novel factor in KS biology and a potential target for therapy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Talk amongst yourselves William Wachsman Blood 2005 105: 913-914. [Full Text] [PDF] This article has been cited by other articles: J. M. Phillips and J. I. Goodman Identification of Genes that May Play Critical Roles in Phenobarbital (PB)-Induced Liver Tumorigenesis due to Altered DNA Methylation Toxicol. Sci., July 1, 2008; 104(1): 86 - 99. [Abstract] [Full Text] [PDF] F. A. Kudo, A. Muto, S. P. Maloney, J. M. Pimiento, S. Bergaya, T. N. Fitzgerald, T. S. Westvik, J. C. Frattini, C. K. Breuer, C. H. Cha, et al. Venous Identity Is Lost but Arterial Identity Is Not Gained During Vein Graft Adaptation Arterioscler. Thromb. Vasc. Biol., July 1, 2007; 27(7): 1562 - 1571. [Abstract] [Full Text] [PDF] F.-C. Ye, D. J. Blackbourn, M. Mengel, J.-P. Xie, L.-W. Qian, W. Greene, I-T. 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Receptor Tyrosine Kinase EphB4 Is a Survival Factor in Breast Cancer Am. J. Pathol., July 1, 2006; 169(1): 279 - 293. [Abstract] [Full Text] [PDF] G. Xia, S. R. Kumar, R. Masood, M. Koss, C. Templeman, D. Quinn, S. Zhu, R. Reddy, V. Krasnoperov, and P. S. Gill Up-Regulation of EphB4 in Mesothelioma and Its Biological Significance Clin. Cancer Res., June 15, 2005; 11(12): 4305 - 4315. [Abstract] [Full Text] [PDF]

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