Initiation of angiogenic Kaposi's sarcoma lesions.
A new mouse model reported in this issue of Cancer Cell implies that VEGF/KDR-mediated paracrine effects induced by the lytic cycle vGPCR signaling protein encoded by human Kaposi's sarcoma-associated herpesvirus (KSHV or HHV8) may be involved in promoting the proliferation of the KSHV latently infected spindle endothelial cells of Kaposi's sarcoma.
Hayward
Gary S
GS
Viral Oncology Program, Sydney Kimmel Oncology Center, Bunting-Blaustein Building, 1650 Orleans Street, CRB 3M09, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. ghayward@jhmi.edu
D000818:Animals; D002471:Cell Transformation, Neoplastic; D019288:Herpesvirus 8, Human / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D051379:Mice; D023421:Models, Animal; D009389:Neovascularization, Pathologic; D019707:Receptors, Chemokine / Q000378:metabolism*; D012514:Sarcoma, Kaposi / Q000473:pathology* / Q000821:virology*; D014764:Viral Proteins / Q000378:metabolism*
C105181:ORF74 protein, Human herpesvirus 8; D019707:Receptors, Chemokine; D014764:Viral Proteins