Cytogenetics Unit, IRCCS "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Italy.
Medical Genetics Unit and Laboratory of Medical Genetics, Ospedale Pediatrico Bambino Gesù, IRCCS, Rome, Italy.
Am J Med Genet A. 2018 Nov;176(11):2501-2508. doi: 10.1002/ajmg.a.40512. Epub 2018 Sep 23.
Wolf-Hirschhorn syndrome is a well-defined disorder due to 4p16.3 deletion, characterized by distinct facial features, intellectual disability, prenatal and postnatal growth retardation, and seizures. Genotype-phenotype correlations based on differently sized deletions have been attempted, and some candidate genes have been suggested. We report on clinical characteristics of three patients with pure interstitial submicroscopic 4p16.3 deletions, ranging in size from 68 to 166 kb, involving WHSCR1 and/or part of WHSCR2, and review published cases with overlapping 4p16.3 losses. The present study highlights a major role of NSD2 gene in the pathogenesis of the WHS main features and predicts that loss-of-function mutations affecting NSD2 gene could result in microcephaly, prenatal and postnatal growth retardation, psychomotor and language delay, and craniofacial features. Absent seizures in all subjects corroborate the suggestion that this specific feature is causally linked with at least one additional causative gene. Finally, we suggest that mir-943 could play a role in the pathogenesis of CHD in some of these patients.
Wolf-Hirschhorn 综合征是一种由于 4p16.3 缺失引起的明确疾病,其特征为独特的面部特征、智力障碍、产前和产后生长迟缓以及癫痫发作。已经尝试了基于不同大小缺失的基因型-表型相关性研究,并提出了一些候选基因。我们报告了 3 名纯间质亚微观 4p16.3 缺失患者的临床特征,缺失大小从 68 到 166kb 不等,涉及 WHSCR1 和/或 WHSCR2 的一部分,并回顾了具有重叠 4p16.3 缺失的已发表病例。本研究强调了 NSD2 基因在 Wolf-Hirschhorn 综合征主要特征发病机制中的主要作用,并预测影响 NSD2 基因的功能丧失突变可能导致小头畸形、产前和产后生长迟缓、精神运动和语言延迟以及颅面特征。所有患者均无癫痫发作,这进一步证实了这一特定特征与至少一个额外的致病基因有关。最后,我们建议 mir-943 可能在这些患者中的一些 CHD 发病机制中发挥作用。