van Kessel A G, Nusse R, Slater R, Tetteroo P, Hagemeijer A
Cancer Genet Cytogenet. 1985 Feb 1;15(1-2):79-84. doi: 10.1016/0165-4608(85)90132-3.
Hybrid cell lines, obtained after fusion of rodent cells with leukocytes from a patient with the aniridia-Wilms' tumor syndrome and carrying a specific constitutional deletion in chromosome #11 (del.11p13), were assayed for the presence of the c-Ha-ras1 oncogene. This sequence has recently been assigned to the p-arm of chromosome #11 and, hence, has been suggested to be involved in the development of renal tumors in patients with this syndrome. Positive hybridization of a cellular Ha-ras1 probe to hybrid cell DNA was observed, irrespective of whether the normal chromosome #11 or its deleted homologue was present. The results presented here suggest that c-Ha-ras1 is located outside the region 11p12-11p14, bounded by the chromosomal breakpoints observed in the patient used. Therefore, we conclude that predisposition of aniridia patients to develop Wilms' tumors is not due to a constitutional deletion of one of the c-Ha-ras1 alleles.
将啮齿动物细胞与患有无虹膜-威尔姆斯瘤综合征患者的白细胞融合后获得的杂交细胞系,携带11号染色体上特定的结构性缺失(del.11p13),检测其是否存在c-Ha-ras1癌基因。该序列最近已被定位到11号染色体的p臂上,因此,有人提出它与该综合征患者肾肿瘤的发生有关。观察到细胞Ha-ras1探针与杂交细胞DNA呈阳性杂交,无论正常的11号染色体还是其缺失的同源染色体是否存在。此处给出的结果表明,c-Ha-ras1位于11p12 - 11p14区域之外,该区域由所用患者中观察到的染色体断点界定。因此,我们得出结论,无虹膜患者易患威尔姆斯瘤并非由于c-Ha-ras1等位基因之一的结构性缺失。