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与 8p11.21 染色体缺失相关的全球发育迟缓及遗传性血影细胞性溶血性贫血,该缺失区域包含 KAT6A 和 ANK1 基因。

Global retardation and hereditary spherocytosis associated with a novel deletion of chromosome 8p11.21 encompassing KAT6A and ANK1.

机构信息

Department of Pediatrics, Jinhua Central Hospital, #351 Mingyue Street, Jinhua, 321000, Zhejiang Province, China.

Department of Pediatrics, Jinhua Central Hospital, #351 Mingyue Street, Jinhua, 321000, Zhejiang Province, China.

出版信息

Eur J Med Genet. 2020 Dec;63(12):104082. doi: 10.1016/j.ejmg.2020.104082. Epub 2020 Oct 13.

Abstract

The loss of heterozygosity localized at chromosome segment 8p11.2 causes a contiguous gene syndrome, which mostly combined phenotype of Kallmann syndrome and hereditary spherocytosis. It has been documented that this combined phenotype is in association with both the deletion of the fibroblast growth factor receptor 1 (FGFR1) and ankyrin 1 (ANK1) genes. Here, we described a 6-year-old girl with microcephaly, global developmental delay, mental retardation, and hereditary spherocytosis, associated with a heterozygous pathogenic microdeletion of 1.9 Mb size at 8p11.21. Molecular analysis confirmed that the identified microdeletion contained two OMIM (Online Mendelian Inheritance in Man)genes, including ANK1 and lysine acetyltransferase 6 A (KAT6A), but not FGFR1. Therefore, the simultaneous occurrence of mild developmental delay and distinctive facial in this patient was associated with the pathogenic variation of the KAT6A.

摘要

8p11.2 染色体片段的杂合性缺失导致连续基因综合征,其主要表现为 Kallmann 综合征和遗传性球形红细胞增多症的联合表型。已有文献证明,这种联合表型与成纤维细胞生长因子受体 1(FGFR1)和锚蛋白 1(ANK1)基因的缺失有关。在这里,我们描述了一名 6 岁女孩,她患有小头畸形、全面发育迟缓、智力障碍和遗传性球形红细胞增多症,与 8p11.21 处大小为 1.9 Mb 的杂合致病性微缺失有关。分子分析证实,所鉴定的微缺失包含两个 OMIM(在线孟德尔遗传数据库)基因,包括 ANK1 和赖氨酸乙酰转移酶 6A(KAT6A),但不包括 FGFR1。因此,该患者轻度发育迟缓伴独特面部特征的同时发生与 KAT6A 的致病性变异有关。

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