Joyce C A, Zorich B, Pike S J, Barber J C, Dennis N R
Genetics Laboratory, Salisbury District Hospital, UK.
J Med Genet. 1996 Dec;33(12):986-92. doi: 10.1136/jmg.33.12.986.
Fluorescence in situ hybridisation (FISH) and conventional chromosome analysis were performed on a series of 52 patients with classical Williams-Beuren syndrome (WBS), suspected WBS, or supravalvular aortic stenosis (SVAS). In the classical WBS group, 22/23 (96%) had a submicroscopic deletion of the elastin locus on chromosome 7, but the remaining patient had a unique interstitial deletion of chromosome 11 (del(11)(q13.5q14.2)). In the suspected WBS group 2/22 (9%) patients had elastin deletions but a third patient had a complex karyotype including a ring chromosome 22 with a deletion of the long arm (r(22)(p11-->q13)). In the SVAS group, 1/7 (14%) had an elastin gene deletion, despite having normal development and minimal signs of WBS. Overall, some patients with submicroscopic elastin deletions have fewer features of Williams-Beuren syndrome than those with other cytogenetic abnormalities. These results, therefore, emphasise the importance of a combined conventional and molecular cytogenetic approach to diagnosis and suggest that the degree to which submicroscopic deletions of chromosome 7 extend beyond the elastin locus may explain some of the phenotypic variability found in Williams-Beuren syndrome.
对52例患有典型威廉姆斯-贝伦综合征(WBS)、疑似WBS或瓣上主动脉狭窄(SVAS)的患者进行了荧光原位杂交(FISH)和传统染色体分析。在典型WBS组中,22/23(96%)患者在7号染色体上存在弹力蛋白基因座的亚显微缺失,但其余1例患者在11号染色体上存在独特的间质缺失(del(11)(q13.5q14.2))。在疑似WBS组中,2/22(9%)患者存在弹力蛋白缺失,但第3例患者具有复杂核型,包括一条22号环状染色体且长臂缺失(r(22)(p11-->q13))。在SVAS组中,1/7(14%)患者存在弹力蛋白基因缺失,尽管其发育正常且仅有轻微的WBS体征。总体而言,一些存在亚显微弹力蛋白缺失的患者比那些具有其他细胞遗传学异常的患者具有更少的威廉姆斯-贝伦综合征特征。因此,这些结果强调了传统和分子细胞遗传学联合诊断方法的重要性,并表明7号染色体亚显微缺失超出弹力蛋白基因座的程度可能解释了威廉姆斯-贝伦综合征中发现的一些表型变异性。