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20p11.2 区域导致全垂体功能减退症的划分。

Delineation of a region responsible for panhypopituitarism in 20p11.2.

机构信息

Service de Génétique Médicale, Hôpital de l'Archet II, CHU Nice, Nice Cedex 3, France.

出版信息

Am J Med Genet A. 2013 Jul;161A(7):1547-54. doi: 10.1002/ajmg.a.35921. Epub 2013 May 8.

DOI:10.1002/ajmg.a.35921
PMID:23657910
Abstract

We report on the case of a young woman with a de novo 20p11.21p11.23 deletion, discovered by array-CGH. She has behavioral troubles with autistic traits, intellectual disability, panhypopituitarism, severe hypoglycemia, epilepsy, and scoliosis. The majority of the reported 20p deletions are located on the 20p12 region, covering the JAG1 gene responsible for the Alagille syndrome. More proximal deletions are even rarer, with very few cases described in the literature to date. The deletion carried by our patient is, to our knowledge, the smallest described de novo proximal 20p11.2 deletion. It was first discovered by 0.5 Mb BAC array-CGH, further delineated using an oligonucleotide array, and finally confirmed by fluorescence in situ hybridization. The deletion is 4.22 Mb in size, with the exact location on chr20: 19.810.034-24.031.344 (Feb. 2009, GRCh37/hg19). In light of the other reported cases that display genomic and phenotypic overlap with our patient, we discuss the phenotype of our patient, in order to further delineate the 20p proximal deletion phenotype. We propose a minimal critical region responsible for panhypopituitarism with global developmental delay, intellectual disability, scoliosis and facial dysmorphism. Moreover, considering the deleted genes, we highlight the impact of the deletion of this minimal critical region on the Shh signaling pathway.

摘要

我们报告了一例新发生的 20p11.21p11.23 缺失的年轻女性病例,该缺失是通过 array-CGH 发现的。她存在行为问题,伴有自闭症特征、智力障碍、全垂体功能减退、严重低血糖、癫痫和脊柱侧凸。大多数报道的 20p 缺失位于 20p12 区域,该区域包含导致 Alagille 综合征的 JAG1 基因。更靠近的缺失更为罕见,迄今为止,文献中仅描述了极少数病例。我们患者携带的缺失是迄今为止描述的最小的新发近端 20p11.2 缺失。该缺失首先通过 0.5Mb BAC array-CGH 发现,随后通过寡核苷酸 array 进一步描绘,最后通过荧光原位杂交确认。该缺失大小为 4.22Mb,确切位置在 chr20:19.810.034-24.031.344(2009 年 2 月,GRCh37/hg19)。鉴于其他报道的病例与我们的患者存在基因组和表型重叠,我们讨论了我们患者的表型,以进一步描绘近端 20p 缺失的表型。我们提出了一个最小的关键区域,负责全垂体功能减退、全面发育迟缓、智力障碍、脊柱侧凸和面部畸形。此外,考虑到缺失的基因,我们强调了该最小关键区域缺失对 Shh 信号通路的影响。

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