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MLL2 镶嵌突变和 Kabuki 综合征患者的基因内缺失-重复。

MLL2 mosaic mutations and intragenic deletion-duplications in patients with Kabuki syndrome.

机构信息

Department of Genetic Medicine, St Mary's Hospital, Manchester Academic Health Sciences Centre (MAHSC), University of Manchester, Manchester, UK.

出版信息

Clin Genet. 2013 May;83(5):467-71. doi: 10.1111/j.1399-0004.2012.01955.x. Epub 2012 Sep 18.

Abstract

Kabuki syndrome (KS) is a rare multi-system disorder that can result in a variety of congenital malformations, typical dysmorphism and variable learning disability. It is caused by MLL2 point mutations in the majority of the cases and, rarely by deletions involving KDM6A. Nearly one third of cases remain unsolved. Here, we expand the known genetic basis of KS by presenting five typical patients with the condition, all of whom have novel MLL2 mutation types- two patients with mosaic small deletions, one with a mosaic whole-gene deletion, one with a multi-exon deletion and one with an intragenic multi-exon duplication. We recommend MLL2 dosage studies for all patients with typical KS, where traditional Sanger sequencing fails to identify mutations. The prevalence of such MLL2 mutations in KS may be comparable with deletions involving KDM6A. These findings may be helpful in understanding the mutational mechanism of MLL2 and the disease mechanism of KS.

摘要

歌舞伎综合征(KS)是一种罕见的多系统疾病,可导致多种先天性畸形、典型的发育异常和不同程度的学习障碍。大多数情况下是由于 MLL2 点突变引起的,极少数情况下是由于涉及 KDM6A 的缺失引起的。近三分之一的病例仍未解决。在这里,我们通过介绍五名具有典型 KS 表现的患者,扩展了 KS 的已知遗传基础,他们均具有新的 MLL2 突变类型-两名患者存在镶嵌性小缺失,一名患者存在镶嵌性全基因缺失,一名患者存在多外显子缺失,一名患者存在基因内多外显子重复。我们建议对所有具有典型 KS 的患者进行 MLL2 剂量研究,在传统的 Sanger 测序无法识别突变的情况下,这种方法非常有效。在 KS 中,此类 MLL2 突变的发生率可能与涉及 KDM6A 的缺失相当。这些发现可能有助于理解 MLL2 的突变机制和 KS 的疾病机制。

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