Neoplastic AIDS-associated Kaposi's sarcoma cell line KSY-1 cannot transdifferentiate into capillaries

• Published in: Journal of human virology Vol. 2; no. 5; p. 315
• Main Authors: Lunardi-Iskandar, Y, Wernert, N, Cong, T H, Samnang, S, Bryant, J L, Vandenbunder, B, Stéhelin, D
• Format: Journal Article
• Language: English
• Published: United States 01.09.1999
• Subjects: Acquired Immunodeficiency Syndrome - complications; Animals; Antisense Elements (Genetics); Capillaries; Female; Humans; In Situ Hybridization; Male; Mice; Mice, Nude; Mice, SCID; Neoplasm Transplantation; Neovascularization, Pathologic; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-ets; Sarcoma, Kaposi - blood supply; Sarcoma, Kaposi - etiology; Sarcoma, Kaposi - pathology; Species Specificity; Transcription Factors; Tumor Cells, Cultured
• ISSN: 1090-9508

Kaposi's sarcoma (KS) is an acquired immunodeficiency syndrome (AIDS)-defining neoplasm histologically characterized by proliferation of spindle cells, inflammatory cells, and abundant neovascularization. When the malignant cell line KSY-1 derived from an AIDS-KS tumor is transplanted subcutaneously into nude mice, prominent neovascular features develop. Using this mouse model of neoplastic KS, we set out to determine, using c-ets 1 markers specific for mouse or human tissues, whether vascular growth and inflammatory infiltrate induced by the transplanted KSY-1 cells is of host cell or transplant origin. KS tumors were induced by subcutaneous inoculation of 5 x 10(6) KSY-1 cells/200 microL in immunodeficient mice, and species-specific mouse and human riboprobes of the c-ets 1 protooncogene were used for in situ hybridization to define cell of origin. Five different tumors were examined. Tissue sections from all cases were hybridized with radiolabeled riboprobes for the presence of both mouse and human c-ets 1 mRNA. Tumor cells were labeled with the human c-ets 1 probe, whereas neovascular and inflammatory tissues were of mouse origin. The finding that vascular but not tumor cells are of host origin supports the model of tumor-induced vascularization via a mechanism of tumor cell-derived cytokine-medicated pathogenesis.