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与散发性和家族性迪格奥尔格综合征相关的22q11区域的微缺失。

Microdeletions within 22q11 associated with sporadic and familial DiGeorge syndrome.

作者信息

Scambler P J, Carey A H, Wyse R K, Roach S, Dumanski J P, Nordenskjold M, Williamson R

机构信息

Department of Biochemistry and Molecular Genetics, St. Mary's Hospital Medical School, London, United Kingdom.

出版信息

Genomics. 1991 May;10(1):201-6. doi: 10.1016/0888-7543(91)90501-5.

Abstract

DiGeorge syndrome (DGS) is a developmental field defect of the third and fourth pharyngeal pouches. It is associated with deletion of 22q11 in 11% of cases. Molecular genetic analysis with probes from 22q11-pter reveals that a subset of markers is hemizygous in DGS patients with normal karyotypes. There is no apparent difference in the phenotype or the severity of the disorder between patients with the smallest detectable submicroscopic deletion and those with the largest cytogenetically visible abnormality. A microdeletion was found in a mildly affected child and in the severely affected child of a mildly affected father. Dysmorphology, especially cardiac outflow tract anomalies, resulting from 22q11 deletion may be more common than currently realized since chromosomes are unlikely to be checked if the complete spectrum of DGS is not present. Antenatal diagnosis, through detection of hemizygosity at 22q11, will be a possibility for mildly affected parents unwilling to risk the birth of a severely affected child.

摘要

迪乔治综合征(DGS)是第三和第四咽囊的发育性场缺陷。11%的病例与22q11缺失有关。用来自22q11 - pter的探针进行分子遗传分析表明,在核型正常的DGS患者中,一部分标记是半合子的。在可检测到的最小亚显微缺失患者和具有最大细胞遗传学可见异常的患者之间,该疾病的表型或严重程度没有明显差异。在一名轻度受影响的儿童及其轻度受影响父亲的严重受影响儿童中发现了微缺失。由于如果不存在DGS的完整谱系,染色体不太可能被检查,因此由22q11缺失导致的畸形,尤其是心脏流出道异常,可能比目前认识到的更为常见。对于不愿冒险生育严重受影响孩子的轻度受影响父母来说,通过检测22q11半合子进行产前诊断将成为可能。

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