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日本 KBG 综合征患者 16q24.3 处存在 ANKRD11 的从头缺失。

A de novo deletion at 16q24.3 involving ANKRD11 in a Japanese patient with KBG syndrome.

机构信息

Department of Human Genetics, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

出版信息

Am J Med Genet A. 2013 May;161A(5):1073-7. doi: 10.1002/ajmg.a.35661. Epub 2013 Mar 5.

Abstract

KBG syndrome is a rare autosomal dominant congenital syndrome comprising developmental delay with various neurological involvements, macrodontia of the upper central incisors, characteristic facial dysmorphism, and skeletal anomalies. ANKRD11 was recently identified as the gene responsible for this syndrome. To date, there have been only five KBG syndrome families described, each carrying a single base substitution or a 1- to 14-bp deletion of this gene. Here, we present a patient with clinically confirmed KBG syndrome carrying a de novo 690-kb deletion at 16q24.3 involving part of ANKRD11. He had characteristic facial appearance, macrodontia of the upper central incisors, hand anomalies, delayed bone age and intellectual impairment without autistic features. Interestingly, the deleted region overlaps with the critical region for 16q24.3 microdeletion syndrome. We discuss the clinical entities of KBG syndrome and 16q24.3 microdeletion syndrome from a clinical and genetic point of view.

摘要

KBG 综合征是一种罕见的常染色体显性遗传性先天综合征,其特征包括发育迟缓、伴有多种神经系统受累的巨门齿、特征性的面部畸形和骨骼异常。ANKRD11 最近被确定为该综合征的致病基因。迄今为止,已有五个 KBG 综合征家族被描述,每个家族均携带该基因的单个碱基替换或 1 至 14 个碱基的缺失。在这里,我们介绍了一个经临床证实的 KBG 综合征患者,其携带 16q24.3 上的 690-kb 缺失,涉及部分 ANKRD11。他具有典型的面部特征、上门牙巨大、手部畸形、骨龄延迟和智力障碍但无自闭症特征。有趣的是,缺失区域与 16q24.3 微缺失综合征的关键区域重叠。我们从临床和遗传的角度讨论了 KBG 综合征和 16q24.3 微缺失综合征的临床实体。

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