Szuhai Károly, Ijszenga Marije, Tanke Hans J, Rosenberg Carla, Hogendoorn Pancras C W
Department of Molecular Cell Biology, Leiden University Medical Center, PO Box 9600, 2300RC, Leiden, The Netherlands.
Cancer Genet Cytogenet. 2006 Apr 15;166(2):173-9. doi: 10.1016/j.cancergencyto.2005.11.006.
Most Ewing family tumors are identified by the characteristic translocation t(11;22)(q24;q12), resulting in a fusion protein EWS/FLI1 that acts as an aberrant transcription factor. In a minority of cases, the EWS gene is fused to another member of the ETS gene (ERG, ETV1, E1AF, and FEV). Though the oncogenic transforming capability of the EWS/FLI1 protein is highly suggestive, the exact pathway behind remains to be elucidated. The availability of cell lines may help in the understanding of underlying cellular processes. In this study, we have established two new Ewing sarcoma cell lines and characterized them with molecular cytogenetic tools. This technology was also applied on four other previously published Ewing sarcoma cell lines. Our findings in relation to previous data on similar tumors are discussed.
大多数尤因家族肿瘤可通过特征性易位t(11;22)(q24;q12)得以识别，该易位会产生一种融合蛋白EWS/FLI1，其作为一种异常转录因子发挥作用。在少数情况下，EWS基因会与ETS基因的另一个成员（ERG、ETV1、E1AF和FEV）融合。尽管EWS/FLI1蛋白的致癌转化能力极具提示性，但其背后的确切途径仍有待阐明。细胞系的可用性可能有助于理解潜在的细胞过程。在本研究中，我们建立了两个新的尤因肉瘤细胞系，并用分子细胞遗传学工具对其进行了表征。该技术还应用于其他四个先前发表的尤因肉瘤细胞系。我们讨论了与先前关于类似肿瘤的数据相关的研究结果。
