Kaneko Y, Kondo K, Rowley J D, Moohr J W, Maurer H S
Cancer Genet Cytogenet. 1983 Oct;10(2):191-7. doi: 10.1016/0165-4608(83)90124-3.
We studied chromosomes in Wilms' tumor cells of two patients without aniridia who had a normal constitutional karyotype. In both tumors, trisomy for 1q occurred as the result of a t(1;16), although the breakpoints in each chromosome differed in the two tumors. No 11p rearrangements could be detected, whereas in our previous patient an interstitial deletion of 11p13 was present in all tumor cells. Thus, trisomy for 1q may be another pathway leading to the development of Wilms' tumor, although the effect of the deletion of 16q cannot be assessed at present.
我们研究了两名无虹膜且染色体核型正常的患者的肾母细胞瘤细胞中的染色体。在这两个肿瘤中，1q三体是由t(1;16)导致的，尽管两个肿瘤中每条染色体的断点不同。未检测到11p重排，而在我们之前的患者中，所有肿瘤细胞中均存在11p13的间质缺失。因此，1q三体可能是导致肾母细胞瘤发生的另一条途径，尽管目前无法评估16q缺失的影响。
