Baird P N, Groves N, Haber D A, Housman D E, Cowell J K
ICRF Oncology Group, Institute of Child Health, London, UK.
Oncogene. 1992 Nov;7(11):2141-9.
Individuals with constitutional, heterozygous deletions of chromosome region 11p13 are predisposed to the development of Wilms' tumour, indicating the site of the tumour predisposition gene. The WT1 gene is a candidate for this cancer predisposition gene. If this gene is truly involved in tumorigenesis it would be expected to be mutant in tumour tissue from patients with 11p13 deletions. We have used single-stranded conformation polymorphism (SSCP) and polymerase chain reaction sequencing to test this hypothesis in an exon-by-exon analysis of the gene. Four tumours were analysed, two of which were from unilaterally affected individuals and two from a bilaterally affected patient. SSCP analysis identified mutations in the two unilateral tumours which, on sequencing, were shown to involve a 10-bp insertion in exon 7 and a single base pair change in exon 8. Both mutations result in the generation of premature stop codons and the predicted proteins would lack part of the zinc finger motif. Despite complete sequencing of the WT1 gene in both of the bilateral tumours, no mutations were identified. These results possibly suggest that WT1 may not be involved in tumorigenesis in all tumours. All four tumours retained heterozygosity in the 11p15 region, making it unlikely that a second recessive oncogene in this region was involved in tumorigenicity.
具有11p13染色体区域先天性杂合缺失的个体易患威尔姆斯瘤,这表明了肿瘤易感基因的位置。WT1基因是这种癌症易感基因的候选基因。如果该基因真的参与肿瘤发生,那么预计在11p13缺失患者的肿瘤组织中会发生突变。我们使用单链构象多态性(SSCP)和聚合酶链反应测序,通过对该基因进行逐个外显子分析来检验这一假设。分析了4个肿瘤,其中2个来自单侧患病个体,2个来自双侧患病患者。SSCP分析在2个单侧肿瘤中鉴定出突变,测序显示这些突变涉及外显子7中的10个碱基对插入和外显子8中的单个碱基对改变。这两个突变均导致产生过早的终止密码子,预测的蛋白质将缺少部分锌指基序。尽管对两个双侧肿瘤中的WT1基因进行了完整测序,但未鉴定出突变。这些结果可能表明WT1可能并非在所有肿瘤的肿瘤发生中都起作用。所有4个肿瘤在11p15区域均保持杂合性,这使得该区域不太可能存在第二个隐性致癌基因参与致瘤性。