Abstract
Abstract An important concept in tumor angiogenesis has been that tumor blood vessels contain genetically normal and stable endothelial cells (ECs), unlike tumor cells, which typically display genetic instability. Chromosomal aberration in human tumor endothelial cells (hTECs) in carcinoma has not yet been investigated. Here we isolated TECs from 20 human renal cell carcinomas (RCCs) and analyzed their cytogenetic abnormalities. The degree of aneuploidy was analyzed by fluorescence in situ hybridization using chromosome 7 and chromosome 8 DNA probes in isolated hTECs. In human RCCs, 22-58% (median 33%) of uncultured hTECs were aneuploid, whereas normal ECs were diploid. The mechanisms of TEC aneuploidy were studied using mouse TECs (mTECs) isolated from xenografts of human epithelial tumors. To investigate the contribution of progenitor cells to aneuploidy in mTECs, CD133 positive and CD133 negative mTECs were compared for aneuploidy. CD133 positive mTECs showed aneuploidy more frequently than CD133 negative mTECs. This is the first report showing cytogenetic abnormality of hTECs in carcinoma, contrary to traditional belief. It is suggested that cytogenetic alterations in tumor vessels of carcinoma can occur and may play a signicant role in modifying tumor-stromal interactions. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1308.
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