肿瘤性艾滋病相关卡波西肉瘤细胞系KSY-1不能转分化为毛细血管。

Journal of human virology Pub Date : 1999-09-01
Y Lunardi-Iskandar, N Wernert, T H Cong, S Samnang, J L Bryant, B Vandenbunder, D Stéhelin
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引用次数: 0

摘要

目的:卡波西肉瘤(KS)是一种获得性免疫缺陷综合征(AIDS)定义的肿瘤,其组织学特征为梭形细胞、炎症细胞增生和丰富的新生血管。当从AIDS-KS肿瘤中提取的恶性细胞系KSY-1皮下移植到裸鼠体内时,出现了明显的新血管特征。使用这种小鼠肿瘤KS模型,我们开始使用小鼠或人体组织特异性的c-ets 1标记物来确定移植的KSY-1细胞诱导的血管生长和炎症浸润是宿主细胞还是移植细胞。研究设计/方法:免疫缺陷小鼠皮下接种5 × 10(6)个KSY-1细胞/200微l诱导KS肿瘤,用物种特异性小鼠和人c-ets -1原癌基因的核糖探针原位杂交确定细胞来源。结果:检查了5种不同的肿瘤。用放射性标记的核探针对所有病例的组织切片进行杂交,以确定小鼠和人c-ets 1mrna的存在。肿瘤细胞用人c-ets - 1探针标记,而新生血管和炎症组织则来自小鼠。结论:血管细胞而非肿瘤细胞来源于宿主的发现,通过肿瘤细胞衍生的细胞因子药物致病机制支持肿瘤诱导血管化模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neoplastic AIDS-associated Kaposi's sarcoma cell line KSY-1 cannot transdifferentiate into capillaries.

Objective: 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.

Study design/methods: 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.

Results: 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.

Conclusions: 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.

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