Spengler Sabrina, Begemann Matthias, Binder Gerhard, Eggermann Thomas
Institute of Human Genetics, RWTH Aachen, Aachen, Germany.
Genet Test Mol Biomarkers. 2011 Oct;15(10):725-6. doi: 10.1089/gtmb.2011.0013. Epub 2011 May 25.
Silver-Russell syndrome (SRS) is a congenital imprinting disorder mainly characterized by growth restriction, a triangular shaped face, a relative macrocephaly, and asymmetry of the body and the limbs. In 7%-10% of the patients a maternal uniparental disomy of chromosome 7 (upd(7)mat) can be observed; a hypomethylation of the imprinting control region 1 (ICR1) in 11p15 is present in >38% of patients. Methylation-specific multiplex ligation-dependent probe amplification is a well-established method for the detection of (epi)mutations in 11p15. In routine diagnostics, DNA samples derived from leukocytes are used for this testing approach. We now analyzed buccal smear DNA taken from both cheek sides of 8 carriers of an ICR1 hypomethylation and 25 SRS patients without 11p15 epimutaton or upd(7)mat to check whether (i) the epimutation can be detected in other tissues and (ii) the detection rate can be increased. Indeed, the ICR1 hypomethylation diagnosed in blood cells could be confirmed in the buccal swab DNA of all 11p15 epimutation carriers, but we could not discover any further carriers among the patients without 11p15 epimutation and upd(7)mat in lymphocytes. Thus, the overall detection rate for the 11p15 epimutation could not be increased by including further tissues originating from different germ layers. We rather assume that other-so far unknown-(genetic) factors are contributing to the etiology of SRS that escape the current diagnostic procedures.
Silver-Russell综合征(SRS)是一种先天性印记障碍,主要特征为生长受限、三角形脸、相对巨头畸形以及身体和四肢不对称。7%-10%的患者可观察到母源7号染色体单亲二倍体(upd(7)mat);超过38%的患者存在11p15印记控制区1(ICR1)的低甲基化。甲基化特异性多重连接依赖探针扩增是检测11p15(表观)突变的成熟方法。在常规诊断中,来自白细胞的DNA样本用于这种检测方法。我们现在分析了8例ICR1低甲基化携带者以及25例无11p15表观突变或upd(7)mat的SRS患者双侧脸颊的口腔涂片DNA,以检查(i)是否能在其他组织中检测到表观突变,以及(ii)检测率是否能提高。事实上,在所有11p15表观突变携带者的口腔拭子DNA中都证实了血细胞中诊断出的ICR1低甲基化,但在淋巴细胞中无11p15表观突变和upd(7)mat的患者中未发现更多携带者。因此,纳入源自不同胚层的更多组织并不能提高11p15表观突变的总体检测率。我们宁可认为其他迄今未知的(遗传)因素导致了SRS的病因,而这些因素逃过了当前的诊断程序。