Coppes M J, Sohl H, Teshima I E, Mutirangura A, Ledbetter D H, Weksberg R
Department of Cancer Biology, Cleveland Clinic Foundation, Ohio.
J Pediatr. 1993 May;122(5 Pt 1):730-3. doi: 10.1016/s0022-3476(06)80015-6.
The development of Wilms tumor in a patient with Prader-Willi syndrome prompted us to determine the parental origin of the genes implicated in both disorders because of the sex-specific parent-of-origin effects previously demonstrated for both conditions. A paternal chromosome 15q11-q13 deletion was demonstrated, but no changes were demonstrated in a limited analysis of chromosome 11p, which harbors two Wilms tumor suppressor genes, WT1 and WT2.
一名患有普拉德-威利综合征的患者发生了肾母细胞瘤，鉴于先前已证实这两种病症都存在性别特异性的亲本来源效应，这促使我们去确定与这两种病症相关的基因的亲本来源。结果证实存在父源15号染色体q11-q13缺失，但在对含有两个肾母细胞瘤抑制基因WT1和WT2的11号染色体p臂进行的有限分析中未发现变化。
