外显子组测序
杂合子丢失
医学
非整倍体
遗传学
基因检测
突变
外显子组
遗传异质性
疾病基因鉴定
复合杂合度
遗传性疾病
血缘关系
核型
等位基因
马赛克
生物
生物信息学
癌症综合征
染色体异常
基因
遗传咨询
智力残疾
比较基因组杂交
遗传倾向
基因缺失
作者
Cristina Pellicer Viudes,Mercè Borràs,Susana Enrique Madrid,Berta Diago García,Armando Carlos Maruenda Jiménez,Paula Guzmán Tena,Maria Leticia Vazquez Alvarez,Victoria Cañadas Olmo,Dolores Tío Guillamón,María Amparo Edo Tena,Edurne Novella-Maestre,Purificación Marín Reina
标识
DOI:10.1515/jpem-2025-0643
摘要
Abstract Objectives Mosaic variegated aneuploidy syndrome 2 (MVA2) is an uncommon autosomal recessive genetic condition caused by mutations in the CEP57 gene. It is characterized by intrauterine growth restriction, severe short stature, facial dysmorphism, and skeletal abnormalities. Most affected individuals also show congenital cardiac defects and delayed development. To date, only 16 patients have been reported. Case presentation We report a 6-year-old girl of consanguineous Moroccan parents, presenting with severe short stature, clinodactyly, and dysmorphic facial features including prominent forehead, triangular face, micro-retrognathia, and low set ears. Neurodevelopment was initially normal, but mild intellectual disability was then noted. Genetic testing including karyotype, array-CGH, and Silver–Russell syndrome were normal. Finally, whole exome sequencing revealed a homozygous c.834_844dupCAATGTTCAGC variant in CEP57 , classified as likely pathogenic. Familial segregation confirmed heterozygosity in both parents and siblings. Conclusions This report describes a novel homozygous variant of CEP57 , expanding the clinical and genetic spectrum of MVA2 syndrome. Although, karyotype should be firstly requested if MVA is suspected, whole exome sequencing is crucial. Growth hormone therapy shows limited response in this syndrome, and the association with cancer predisposition should be further studied.
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