Baujat Geneviève, Rio Marlène, Rossignol Sylvie, Sanlaville Damien, Lyonnet Stanislas, Le Merrer Martine, Munnich Arnold, Gicquel Christine, Cormier-Daire Valérie, Colleaux Laurence
INSERM U393 and Département de Génétique, Hôpital Necker-Enfants Malades, Paris, France.
Am J Hum Genet. 2004 Apr;74(4):715-20. doi: 10.1086/383093. Epub 2004 Mar 1.
Sotos syndrome is an overgrowth syndrome characterized by pre- and postnatal overgrowth, macrocephaly, advanced bone age, variable degrees of mental retardation, and typical facial features. Defects of the NSD1 gene account for >or=60% of cases of Sotos syndrome, whereas the disease-causing mechanism of other cases remains unknown. Beckwith-Wiedemann syndrome (BWS) is a distinct overgrowth condition characterized by macroglossia, abdominal-wall defects, visceromegaly, embryonic tumors, hemihyperplasia, ear anomalies, renal anomalies, and neonatal hypoglycemia. Deregulation of imprinted growth-regulatory genes within the 11p15 region is the major cause of BWS, whereas the molecular defect underlying a significant proportion of sporadic BWS cases remains unknown. Owing to clinical overlaps between the two syndromes, we investigated whether unexplained cases of Sotos syndrome could be related to 11p15 anomalies and, conversely, whether unexplained BWS cases could be related to NSD1 deletions or mutations. Two 11p15 anomalies were identified in a series of 20 patients with Sotos syndrome, and two NSD1 mutations were identified in a series of 52 patients with BWS. These results suggest that the two disorders may have more similarities than previously thought and that NSD1 could be involved in imprinting of the chromosome 11p15 region.
索托斯综合征是一种过度生长综合征,其特征为出生前后过度生长、巨头畸形、骨龄超前、不同程度的智力迟钝以及典型的面部特征。NSD1基因缺陷占索托斯综合征病例的60%以上,而其他病例的致病机制仍不清楚。贝克威思-维德曼综合征(BWS)是一种独特的过度生长疾病,其特征为巨舌症、腹壁缺损、内脏肿大、胚胎肿瘤、半身肥大、耳部异常、肾脏异常以及新生儿低血糖。11p15区域内印迹生长调节基因的失调是BWS的主要病因,而相当一部分散发性BWS病例的分子缺陷仍不清楚。由于这两种综合征在临床上存在重叠,我们研究了原因不明的索托斯综合征病例是否可能与11p15异常有关,反之,原因不明的BWS病例是否可能与NSD1缺失或突变有关。在一组20例索托斯综合征患者中发现了两个11p15异常,在一组52例BWS患者中发现了两个NSD1突变。这些结果表明,这两种疾病可能比以前认为的有更多相似之处,并且NSD1可能参与11p15区域的印迹过程。